This document discusses various types of toxic drug interactions that can occur when two or more drugs are taken together. It describes pharmacodynamic interactions, which occur when drugs have similar pharmacological effects or side effects, and pharmacokinetic interactions, which occur when one drug alters the absorption, metabolism or excretion of another drug. It notes that while many drug interactions are harmless, interactions with drugs that have a narrow therapeutic index or require careful dosage control can be more problematic. The document provides several examples of specific drug interactions to watch out for.
ADE
INCIDENCE OF ADR
GREADING OF SEVERITY OF ADR
CLASSIFICATIONS
PHARMACOVIGILANCE
CATAGORIES
CAUSES OF ADR
DRUG INDUCED HEPATIC DYSFUNCTION
DRUG INDUCED ENDOCRINE DYSFUNCTION
DRUG INDUCED PHERIPHERAL NEUROPATHY
MANAGEMENT OF ADR
Naranjo
WHO-UMC
Bayesian:
Bayesian
Expert Opinion:
CIOMS
Most commonly used:
Naranjo
WHO-UMC
Naranjo Causality Assessment Scale
Criteria Score
1. Previous conclusive reports on this reaction 0
1. Previous conclusive reports on this reaction +1
2. The adverse event appeared after the suspected drug was administered. +2
3. The adverse reaction improved when the drug was discontinued or a specific antagonist was administered. +1
4. The adverse reaction reappeared when the drug was readministered. +2
5. Alternative causes that could solely have
This document discusses drug interactions, which occur when the pharmacological activity of one drug is altered by another substance like another drug, food, or disease. It describes the main types of interactions as drug-drug, drug-food, drug-chemical, drug-test, and drug-disease. Interactions can be undesirable or beneficial. The three main mechanisms are pharmaceutical, pharmacokinetic, and pharmacodynamic. Pharmacokinetic interactions alter absorption, distribution, metabolism, or excretion of a drug. Pharmacodynamic interactions involve drugs with similar, opposing, additive, antagonistic, or synergistic effects. Managing interactions requires identifying risks, reviewing drug history, monitoring therapy, and educating patients.
Role of Clinical Pharmacist in Emergency DepartmentArslan Tahir
This document outlines the role of a clinical pharmacist in an emergency department. It begins by defining clinical pharmacists and their duties in assessing patients' medication statuses and ensuring optimal medication therapy. The emergency department is described as a high-risk environment where pharmacists can play an important role. Several studies are cited showing medication errors and adverse drug events are common in emergency departments. The document then discusses strategies to optimize the emergency pharmacist's role, such as maintaining high visibility, focusing on patients, and surveillance of medication orders. It also covers the education and training requirements and activities emergency pharmacists can perform, such as medication reviews, toxicology support, and education. A sample job description is provided as well. In conclusion, the document
Patient Counselling is needed for
Better patient understanding to their illness and role of medication.
Improve medication adherence.
Improve dosage regimen adherence.
More effective Drug treatment.
Reduce incidence of adverse drug effect and unnecessary healthcare cost.
ADR reporting.
Improve quality of life for patient.
Raising image of Pharmacist & its profession.
ADE
INCIDENCE OF ADR
GREADING OF SEVERITY OF ADR
CLASSIFICATIONS
PHARMACOVIGILANCE
CATAGORIES
CAUSES OF ADR
DRUG INDUCED HEPATIC DYSFUNCTION
DRUG INDUCED ENDOCRINE DYSFUNCTION
DRUG INDUCED PHERIPHERAL NEUROPATHY
MANAGEMENT OF ADR
Naranjo
WHO-UMC
Bayesian:
Bayesian
Expert Opinion:
CIOMS
Most commonly used:
Naranjo
WHO-UMC
Naranjo Causality Assessment Scale
Criteria Score
1. Previous conclusive reports on this reaction 0
1. Previous conclusive reports on this reaction +1
2. The adverse event appeared after the suspected drug was administered. +2
3. The adverse reaction improved when the drug was discontinued or a specific antagonist was administered. +1
4. The adverse reaction reappeared when the drug was readministered. +2
5. Alternative causes that could solely have
This document discusses drug interactions, which occur when the pharmacological activity of one drug is altered by another substance like another drug, food, or disease. It describes the main types of interactions as drug-drug, drug-food, drug-chemical, drug-test, and drug-disease. Interactions can be undesirable or beneficial. The three main mechanisms are pharmaceutical, pharmacokinetic, and pharmacodynamic. Pharmacokinetic interactions alter absorption, distribution, metabolism, or excretion of a drug. Pharmacodynamic interactions involve drugs with similar, opposing, additive, antagonistic, or synergistic effects. Managing interactions requires identifying risks, reviewing drug history, monitoring therapy, and educating patients.
Role of Clinical Pharmacist in Emergency DepartmentArslan Tahir
This document outlines the role of a clinical pharmacist in an emergency department. It begins by defining clinical pharmacists and their duties in assessing patients' medication statuses and ensuring optimal medication therapy. The emergency department is described as a high-risk environment where pharmacists can play an important role. Several studies are cited showing medication errors and adverse drug events are common in emergency departments. The document then discusses strategies to optimize the emergency pharmacist's role, such as maintaining high visibility, focusing on patients, and surveillance of medication orders. It also covers the education and training requirements and activities emergency pharmacists can perform, such as medication reviews, toxicology support, and education. A sample job description is provided as well. In conclusion, the document
Patient Counselling is needed for
Better patient understanding to their illness and role of medication.
Improve medication adherence.
Improve dosage regimen adherence.
More effective Drug treatment.
Reduce incidence of adverse drug effect and unnecessary healthcare cost.
ADR reporting.
Improve quality of life for patient.
Raising image of Pharmacist & its profession.
Pharmacy & self medication by prof. amrutkar rakesh d.RakeshAmrutkar
This document discusses various topics related to pharmacy and self-medication. It defines pharmacy as the art and science of preparing and dispensing medications. It also defines drugs and discusses the origins, nomenclature, and scope of pharmacy. The document outlines pharmacist careers and pharmacy education. It discusses pharmacy ethics, good dispensing practices, and defines self-medication as the use of non-prescription medicines without a doctor's guidance. The document notes some conditions commonly treated with self-medication and discusses both the potential benefits and risks of self-medication.
Ward rounds involve medical practitioners and health professionals visiting hospital inpatients at their bedside to review health progress. The document discusses goals and benefits of clinical pharmacists participating in ward rounds, such as gaining understanding of patient status, providing drug therapy expertise, optimizing treatment, detecting adverse reactions, assisting with discharge planning, and strengthening inter-professional relationships. Participation also provides learning opportunities for pharmacists to see how drugs are used and their effects on patients.
This document discusses adverse drug reactions (ADRs), defined as any undesirable or unintended consequence of drug administration. ADRs are classified as either predictable (type A) or unpredictable (type B) reactions. Predictable reactions include excessive pharmacological effects, secondary pharmacological effects, and rebound effects on drug discontinuation. Unpredictable reactions include allergic drug reactions, idiosyncrasy, and genetically determined toxicity. The document also covers ADR detection methods like patient interviews, ADR reporting approaches, and ADR management based on reaction severity and importance of continued treatment.
Medications are an important tool for preventing illness and disability in older populations, but they can also cause medication-related problems (MRPs). MRPs are undesirable events involving drug therapy that interfere with patient outcomes. Common symptoms of MRPs include changes in speech, falls, confusion, loss of appetite, weakness, incontinence, insomnia, and Parkinson's-like symptoms. Older adults are more at risk for MRPs due to multiple chronic diseases, medications, prescribers, and age-related physiological changes. The presentation provides tips for preventing MRPs such as designating a medication manager, keeping an accurate medication list, consulting providers before starting new medications, and developing routines for administering medications to patients
Adverse drug reactions are unwanted effects that occur when taking medications. They can range from mild to severe or life-threatening. Monitoring adverse drug reactions involves identifying suspected reactions, assessing the causality between the drug and reaction, documenting the details of the case, and reporting serious reactions to regulatory authorities. Serious adverse reactions must be reported within 14 days, while investigators report them to sponsors and ethics committees within 24 hours and 7 days respectively to ensure patient safety.
This document discusses drug interactions, including definitions, types, mechanisms, high risk patients, and how to handle interactions. It notes the main types are drug-drug, herbal-drug, food-drug, and drink-drug interactions. Mechanisms include effects on absorption, distribution, metabolism, and excretion. Absorption can be affected by changes in pH, bacteria, insoluble complexes, or motility. Metabolism interactions involve enzyme induction or inhibition. The document provides examples of interactions and notes some drugs are more prone to interactions. It outlines approaches to preventing or managing interactions.
The document discusses drug information centers and poison information centers. It provides details on:
- The history and development of the first drug information centers (DICs) and poison control centers (PCCs) in the 1960s in the US and other countries.
- The aims of DICs and PCCs, which include providing drug and poison information to health professionals, developing guidelines, education programs, and participating in research.
- The staffing of DICs and PCCs, which usually includes pharmacists, pharmacy technicians, toxicologists, and others with library sciences backgrounds.
- The processes DICs use to respond to drug information requests, which follow a systematic approach of
This document discusses the etiology, pathophysiology, clinical presentation, and management of nausea, vomiting, dyspepsia, and diarrhea. It begins by describing nausea and vomiting as common symptoms of gastrointestinal disorders. It then discusses the etiology, pathophysiology involving the vomiting center and various neurotransmitter systems, and pharmacological management including antacids, H2 receptor antagonists, and serotonin antagonists. Next, it covers dyspepsia including definition, causes, pathophysiology, clinical presentation, and management with antacids, H2 receptor antagonists, and proton pump inhibitors. Finally, it addresses diarrhea by defining it, discussing pathophysiological mechanisms, and outlining non-pharmacological and pharmacological treatment
Pharmacovigilance AND ADVERSE DRUG REACTIONS.
MONITORING REPORTING ROLE OF PHARMACIST.
CLASSIFICATION OF ADR. MECHANISM OF ADR
ROLE OF PHARMACIST IN MANAGING ADR. AUGMENTED, BIZZARE, CONTINOUS, DELAYED, END OF TREATMENT, ABCD, ABCDE.
Al Azhar University | Faculty of Pharmacy | Class of 2018 Graduation Project (Drug Interactions).
in both parameters Drug Drug Interactions and Drug Food Interactions.
A drug interaction is a situation in which a substance (usually another drug) affects the activity of a drug when both are administered together.
This document provides information about adverse drug reactions. It begins with defining an adverse drug reaction as an unintended effect of a drug occurring at normal doses. Adverse drug reactions are common, with 3% of medical admissions due to them. It then classifies adverse drug reactions and discusses various types like predictable reactions, allergic reactions, and interactions. It describes methods for detecting adverse drug reactions like spontaneous reporting, record linkage studies, cohort studies, and case control studies.
Drug interactions their types, examples and roleYousra Ashraf
Drug interactions occur when two or more substances administered together alter their effects on the body. There are two main types of drug interactions - pharmacodynamic interactions, which involve drugs acting on the same receptors or tissues, and pharmacokinetic interactions, which alter a drug's absorption, distribution, metabolism, or excretion. Common examples of drug-drug interactions include aspirin increasing the effects of anticoagulants like warfarin and antibiotics affecting blood thinners. Food and disease can also interact with drugs. It is important for pharmacists to monitor for potential interactions and advise patients.
This document defines key terms related to adverse drug reactions (ADRs), including what constitutes an ADR, adverse event, and serious ADR. It classifies ADRs into different types (A, B, C, D, E), such as expected/unexpected, allergic, chronic effects, and end of treatment effects. The objectives of ADR monitoring are outlined as detecting the nature and frequency of reactions to assist regulators, educate healthcare professionals, and initiate further studies.
This document discusses adverse drug reactions (ADRs). It begins by defining ADRs according to the WHO as any unintended and noxious response to a drug. It then provides a brief history of notable ADR events. The document goes on to classify ADRs based on factors like onset, type of reaction, and severity. It describes each type of reaction with examples. Finally, it discusses other drug-related concepts like side effects, toxicity, dependence, and teratogenicity.
This document provides information about over-the-counter (OTC) medications. It defines OTC medications as drugs that are safe for use by the general public without a prescription from a doctor. OTC medications have little pharmacological activity and are primarily used for symptomatic relief rather than as prescription drug substitutes. The document discusses the classification of medications as either prescription-controlled or prescription decontrolled/OTC. It also covers OTC drug labeling requirements, proper OTC drug use, common types of OTC drugs, risks of OTC drug use, and the process of counseling patients on OTC medication selection and use.
Establishing a drug information centerkatta amulya
This document discusses establishing a drug information center. It begins by introducing the main functions of a drug information center which is to provide written or verbal drug-related information to healthcare professionals and the public. It then classifies drug information centers into hospital based, industry based, and community based. The document outlines the need for drug information centers by discussing their primary function of responding to drug therapy inquiries and services like drug evaluation, education, and pharmacovigilance. It also covers staffing, resources, literature databases, and concludes by emphasizing the importance of efficient drug information centers for optimal patient care.
This document discusses dispensing in pharmacy practice. Dispensing involves interpreting prescriptions to supply appropriate medicines to patients. It describes the key activities in dispensing like receiving prescriptions, checking for completeness and legality, filling prescriptions, and providing directions for patients. It emphasizes the importance of a well-organized dispensing environment and carefully checking prescriptions to avoid errors due to illegibility or similar drug names. Dispensers must concentrate to ensure the correct medicines are accurately dispensed.
The document discusses important drug-drug interactions, including their intensity, mechanism, and management. It defines drug-drug interactions as when taking two drugs together causes a change in one drug's effects on the body. Interactions can be pharmacodynamic, involving receptor-level or intracellular effects, or pharmacokinetic, altering a drug's absorption, distribution, metabolism, or excretion. The document provides examples of serious interactions to avoid or monitor closely, outlines approaches to minimizing interactions, and poses sample cases to identify and manage interactions.
This document discusses drug interactions, which occur when two or more drugs are taken at the same time and one drug affects the activity of another. It provides examples of synergistic, antagonistic, and minor drug interactions. It also discusses the four main sites where drug interactions can occur: outside the body during administration, during absorption in the gastrointestinal tract, at the distribution and binding sites in plasma proteins and receptors, and during metabolism by the liver and excretion by the kidneys. Numerous specific drug combinations that can have clinically significant interactions are outlined for each site.
Pharmacy & self medication by prof. amrutkar rakesh d.RakeshAmrutkar
This document discusses various topics related to pharmacy and self-medication. It defines pharmacy as the art and science of preparing and dispensing medications. It also defines drugs and discusses the origins, nomenclature, and scope of pharmacy. The document outlines pharmacist careers and pharmacy education. It discusses pharmacy ethics, good dispensing practices, and defines self-medication as the use of non-prescription medicines without a doctor's guidance. The document notes some conditions commonly treated with self-medication and discusses both the potential benefits and risks of self-medication.
Ward rounds involve medical practitioners and health professionals visiting hospital inpatients at their bedside to review health progress. The document discusses goals and benefits of clinical pharmacists participating in ward rounds, such as gaining understanding of patient status, providing drug therapy expertise, optimizing treatment, detecting adverse reactions, assisting with discharge planning, and strengthening inter-professional relationships. Participation also provides learning opportunities for pharmacists to see how drugs are used and their effects on patients.
This document discusses adverse drug reactions (ADRs), defined as any undesirable or unintended consequence of drug administration. ADRs are classified as either predictable (type A) or unpredictable (type B) reactions. Predictable reactions include excessive pharmacological effects, secondary pharmacological effects, and rebound effects on drug discontinuation. Unpredictable reactions include allergic drug reactions, idiosyncrasy, and genetically determined toxicity. The document also covers ADR detection methods like patient interviews, ADR reporting approaches, and ADR management based on reaction severity and importance of continued treatment.
Medications are an important tool for preventing illness and disability in older populations, but they can also cause medication-related problems (MRPs). MRPs are undesirable events involving drug therapy that interfere with patient outcomes. Common symptoms of MRPs include changes in speech, falls, confusion, loss of appetite, weakness, incontinence, insomnia, and Parkinson's-like symptoms. Older adults are more at risk for MRPs due to multiple chronic diseases, medications, prescribers, and age-related physiological changes. The presentation provides tips for preventing MRPs such as designating a medication manager, keeping an accurate medication list, consulting providers before starting new medications, and developing routines for administering medications to patients
Adverse drug reactions are unwanted effects that occur when taking medications. They can range from mild to severe or life-threatening. Monitoring adverse drug reactions involves identifying suspected reactions, assessing the causality between the drug and reaction, documenting the details of the case, and reporting serious reactions to regulatory authorities. Serious adverse reactions must be reported within 14 days, while investigators report them to sponsors and ethics committees within 24 hours and 7 days respectively to ensure patient safety.
This document discusses drug interactions, including definitions, types, mechanisms, high risk patients, and how to handle interactions. It notes the main types are drug-drug, herbal-drug, food-drug, and drink-drug interactions. Mechanisms include effects on absorption, distribution, metabolism, and excretion. Absorption can be affected by changes in pH, bacteria, insoluble complexes, or motility. Metabolism interactions involve enzyme induction or inhibition. The document provides examples of interactions and notes some drugs are more prone to interactions. It outlines approaches to preventing or managing interactions.
The document discusses drug information centers and poison information centers. It provides details on:
- The history and development of the first drug information centers (DICs) and poison control centers (PCCs) in the 1960s in the US and other countries.
- The aims of DICs and PCCs, which include providing drug and poison information to health professionals, developing guidelines, education programs, and participating in research.
- The staffing of DICs and PCCs, which usually includes pharmacists, pharmacy technicians, toxicologists, and others with library sciences backgrounds.
- The processes DICs use to respond to drug information requests, which follow a systematic approach of
This document discusses the etiology, pathophysiology, clinical presentation, and management of nausea, vomiting, dyspepsia, and diarrhea. It begins by describing nausea and vomiting as common symptoms of gastrointestinal disorders. It then discusses the etiology, pathophysiology involving the vomiting center and various neurotransmitter systems, and pharmacological management including antacids, H2 receptor antagonists, and serotonin antagonists. Next, it covers dyspepsia including definition, causes, pathophysiology, clinical presentation, and management with antacids, H2 receptor antagonists, and proton pump inhibitors. Finally, it addresses diarrhea by defining it, discussing pathophysiological mechanisms, and outlining non-pharmacological and pharmacological treatment
Pharmacovigilance AND ADVERSE DRUG REACTIONS.
MONITORING REPORTING ROLE OF PHARMACIST.
CLASSIFICATION OF ADR. MECHANISM OF ADR
ROLE OF PHARMACIST IN MANAGING ADR. AUGMENTED, BIZZARE, CONTINOUS, DELAYED, END OF TREATMENT, ABCD, ABCDE.
Al Azhar University | Faculty of Pharmacy | Class of 2018 Graduation Project (Drug Interactions).
in both parameters Drug Drug Interactions and Drug Food Interactions.
A drug interaction is a situation in which a substance (usually another drug) affects the activity of a drug when both are administered together.
This document provides information about adverse drug reactions. It begins with defining an adverse drug reaction as an unintended effect of a drug occurring at normal doses. Adverse drug reactions are common, with 3% of medical admissions due to them. It then classifies adverse drug reactions and discusses various types like predictable reactions, allergic reactions, and interactions. It describes methods for detecting adverse drug reactions like spontaneous reporting, record linkage studies, cohort studies, and case control studies.
Drug interactions their types, examples and roleYousra Ashraf
Drug interactions occur when two or more substances administered together alter their effects on the body. There are two main types of drug interactions - pharmacodynamic interactions, which involve drugs acting on the same receptors or tissues, and pharmacokinetic interactions, which alter a drug's absorption, distribution, metabolism, or excretion. Common examples of drug-drug interactions include aspirin increasing the effects of anticoagulants like warfarin and antibiotics affecting blood thinners. Food and disease can also interact with drugs. It is important for pharmacists to monitor for potential interactions and advise patients.
This document defines key terms related to adverse drug reactions (ADRs), including what constitutes an ADR, adverse event, and serious ADR. It classifies ADRs into different types (A, B, C, D, E), such as expected/unexpected, allergic, chronic effects, and end of treatment effects. The objectives of ADR monitoring are outlined as detecting the nature and frequency of reactions to assist regulators, educate healthcare professionals, and initiate further studies.
This document discusses adverse drug reactions (ADRs). It begins by defining ADRs according to the WHO as any unintended and noxious response to a drug. It then provides a brief history of notable ADR events. The document goes on to classify ADRs based on factors like onset, type of reaction, and severity. It describes each type of reaction with examples. Finally, it discusses other drug-related concepts like side effects, toxicity, dependence, and teratogenicity.
This document provides information about over-the-counter (OTC) medications. It defines OTC medications as drugs that are safe for use by the general public without a prescription from a doctor. OTC medications have little pharmacological activity and are primarily used for symptomatic relief rather than as prescription drug substitutes. The document discusses the classification of medications as either prescription-controlled or prescription decontrolled/OTC. It also covers OTC drug labeling requirements, proper OTC drug use, common types of OTC drugs, risks of OTC drug use, and the process of counseling patients on OTC medication selection and use.
Establishing a drug information centerkatta amulya
This document discusses establishing a drug information center. It begins by introducing the main functions of a drug information center which is to provide written or verbal drug-related information to healthcare professionals and the public. It then classifies drug information centers into hospital based, industry based, and community based. The document outlines the need for drug information centers by discussing their primary function of responding to drug therapy inquiries and services like drug evaluation, education, and pharmacovigilance. It also covers staffing, resources, literature databases, and concludes by emphasizing the importance of efficient drug information centers for optimal patient care.
This document discusses dispensing in pharmacy practice. Dispensing involves interpreting prescriptions to supply appropriate medicines to patients. It describes the key activities in dispensing like receiving prescriptions, checking for completeness and legality, filling prescriptions, and providing directions for patients. It emphasizes the importance of a well-organized dispensing environment and carefully checking prescriptions to avoid errors due to illegibility or similar drug names. Dispensers must concentrate to ensure the correct medicines are accurately dispensed.
The document discusses important drug-drug interactions, including their intensity, mechanism, and management. It defines drug-drug interactions as when taking two drugs together causes a change in one drug's effects on the body. Interactions can be pharmacodynamic, involving receptor-level or intracellular effects, or pharmacokinetic, altering a drug's absorption, distribution, metabolism, or excretion. The document provides examples of serious interactions to avoid or monitor closely, outlines approaches to minimizing interactions, and poses sample cases to identify and manage interactions.
This document discusses drug interactions, which occur when two or more drugs are taken at the same time and one drug affects the activity of another. It provides examples of synergistic, antagonistic, and minor drug interactions. It also discusses the four main sites where drug interactions can occur: outside the body during administration, during absorption in the gastrointestinal tract, at the distribution and binding sites in plasma proteins and receptors, and during metabolism by the liver and excretion by the kidneys. Numerous specific drug combinations that can have clinically significant interactions are outlined for each site.
This document provides information on adverse drug reactions (ADRs), including:
1. It defines ADRs and differentiates them from adverse drug events, and outlines some common causes of events that are excluded from being considered ADRs.
2. It describes various types and classifications of ADRs, including by intensity/severity, outcome, mechanism of production, and pharmacoepidemiological criteria.
3. It discusses methods of pharmacovigilance for detecting ADRs and standards for determining the imputability or likelihood that a reaction was caused by a drug.
Imipramine tablets bp 25mg smpc taj pharmaceuticalsTaj Pharma
IMIPRAMINE Taj Pharma : Uses, Side Effects, Interactions, Pictures, Warnings, IMIPRAMINE Dosage & Rx Info | IMIPRAMINE Uses, Side Effects -: Indications, Side Effects, Warnings, IMIPRAMINE - Drug Information - Taj Pharma, IMIPRAMINE dose Taj pharmaceuticals IMIPRAMINE interactions, Taj Pharmaceutical IMIPRAMINE contraindications, IMIPRAMINE price, IMIPRAMINE Taj Pharma IMIPRAMINE TABLETS BP 25mg SMPC- Taj Pharma . Stay connected to all updated on IMIPRAMINE Taj Pharmaceuticals Taj pharmaceuticals Hyderabad.
Herbal-drug and herb-food interactions are common. Pharmacokinetic interactions occur when an herbal supplement shares the same absorption, distribution, metabolism, or excretion mechanisms as a drug, potentially changing the drug's concentration. Pharmacodynamic interactions involve direct effects of an herbal supplement on a drug's mechanism of action. Some potentially clinically significant interactions include St. John's Wort decreasing serum levels of drugs metabolized by CYP450 enzymes, kava potentiating central nervous system depressants, and ginkgo increasing bleeding risk when taken with anticoagulants or antiplatelets. Close monitoring is recommended when taking herbs and drugs together.
Chlorphenamine maleate tablets smpc taj pharmaceuticalsTaj Pharma
Chlorphenamine maleate Taj Pharma : Uses, Side Effects, Interactions, Pictures, Warnings, Chlorphenamine maleate Dosage & Rx Info | Chlorphenamine maleate Uses, Side Effects -: Indications, Side Effects, Warnings, Chlorphenamine maleate - Drug Information - Taj Pharma, Chlorphenamine maleate dose Taj pharmaceuticals Chlorphenamine maleate interactions, Taj Pharmaceutical Chlorphenamine maleate contraindications, Chlorphenamine maleate price, Chlorphenamine maleate Taj Pharma Chlorphenamine maleate Tablets SMPC- Taj Pharma . Stay connected to all updated on Chlorphenamine maleate Taj Pharmaceuticals Taj pharmaceuticals Hyderabad.
This document summarizes various types of adverse drug effects including pharmacological toxicity, idiosyncratic reactions, drug allergies, hepatotoxicity, nephrotoxicity, drug interactions, photosensitization, and local pain and tissue injuries. It discusses the mechanisms, clinical signs, and management of these adverse effects for different drug classes in veterinary medicine. Risk factors, treatment approaches, and ways to minimize adverse reactions are also covered.
Drug interactions can occur when two or more drugs are taken simultaneously and modify each other's effects. Interactions can be pharmacokinetic, affecting absorption, distribution, metabolism or excretion of the drugs. They can also be pharmacodynamic if the drugs affect the same receptor sites. Common causes of interactions include effects on drug metabolizing enzymes like CYP450 and drug transporters, protein binding displacement, and additive pharmacodynamic effects. It is important for doctors to consider potential interactions when prescribing multiple medications to a patient. While many interactions can be managed safely, they should be avoided if possible due to risks of toxic effects or reduced treatment effectiveness.
this presentation helps you describing drugs for patients attending dental clinic regarding their medical problems and drugs they use for their illness.
This document discusses the mechanisms of action, side effects, and clinical management of anticoagulant drugs including heparin, warfarin, and newer oral anticoagulants. It describes how heparin and related drugs act as indirect thrombin inhibitors by enhancing the effects of antithrombin, while direct thrombin inhibitors and factor Xa inhibitors act by directly binding to and inhibiting specific coagulation proteins. The side effects of bleeding and heparin-induced thrombocytopenia are reviewed for heparin, as are methods for reversing its effects. Drug interactions and toxicity are discussed for warfarin along with reversal of its anticoagulant effects.
This document provides basic drug information about Sintrom, which contains the active ingredient acenocoumarol. It is used to treat and prevent thromboembolic diseases. The tablets come in a 4 mg dose. It works by inhibiting the production of vitamin K-dependent clotting factors in the liver. Its effects can be seen within 36-72 hours and it has a narrow therapeutic index, so regular coagulation monitoring and dose adjustments are required for safe use. Common side effects include bleeding, while an overdose can cause serious or fatal hemorrhage.
Fluconazole 150 mg capsule smpc taj pharmaceuticalsTaj Pharma
Fluconazole Taj Pharma : Uses, Side Effects, Interactions, Pictures, Warnings, Fluconazole Dosage & Rx Info | Fluconazole Uses, Side Effects -: Indications, Side Effects, Warnings, Fluconazole - Drug Information - Taj Pharma, Fluconazole dose Taj pharmaceuticals Fluconazole interactions, Taj Pharmaceutical Fluconazole contraindications, Fluconazole price, Fluconazole Taj Pharma Fluconazole 150 mg Capsule SMPC- Taj Pharma . Stay connected to all updated on Fluconazole Taj Pharmaceuticals Taj pharmaceuticals Hyderabad.
Theophylline Extended-Release Tablets 100mg, 200mg, 300mg, 400mg Taj Pharma: Uses, Side Effects, Interactions, Pictures, Warnings, Theophylline Dosage & Rx Info | Theophylline Uses, Side Effects Theophylline: Indications, Side Effects, Warnings, Theophylline -Drug Information –Taj Pharma, Theophylline dose Taj pharmaceuticals Theophylline interactions, Taj Pharmaceutical Theophylline contraindications, Theophylline price, Theophylline Taj Pharma Theophylline SmPC-Taj Pharma Stay connected to all updated on Theophylline Taj Pharmaceuticals Mumbai. Patient Information Leaflets, SmPC.
This document discusses pharmacovigilance, which involves monitoring medicines to detect and prevent adverse effects. It defines pharmacovigilance and describes its aims to improve patient safety and public health related to medicine use. The document outlines the scope of pharmacovigilance and objectives to improve care, health, assess medicine benefits and risks, and promote education. It also discusses adverse drug reactions, types A-F, factors affecting reactions like patient characteristics and medicine properties, and the role of pharmacists in managing reactions.
pharmacovigilance- clinical pharmacy pharm-DAnusha Are
This document discusses pharmacovigilance, which involves monitoring medicines to detect and prevent adverse drug reactions. It defines pharmacovigilance and describes its aims to improve patient safety, public health, and understanding of drug risks and benefits. The document outlines the scope of pharmacovigilance and objectives to improve care, health, risk assessment, and education. It also discusses adverse drug reactions, common causes, types based on predictability and onset, severity classifications, and the role of pharmacists in managing reactions.
This document provides information on acute poisoning, including definitions, common causes, general management approaches, and specific management for certain types of poisoning. It discusses paracetamol poisoning, organophosphorus insecticide poisoning, and opiate poisoning. For paracetamol poisoning, it outlines treatment with acetylcysteine or alternative treatments based on time since ingestion. For organophosphorus poisoning, it describes the triphasic illness and recommends atropine as the antidote. The document provides detailed guidance on assessment, monitoring, supportive care and specific treatments for acute poisoning.
This document provides a historical overview of local anesthesia techniques from the 18th century introduction of chemical compounds to modern developments. It discusses key events and discoveries such as the first use of nitrous oxide and ether for dental procedures. The era of inhalation anesthesia gave way to injection techniques using hypodermic syringes and localized drugs like cocaine and procaine. Modern techniques for mandibular nerve blocks and vasoconstrictors that prolong anesthesia are also covered. The document concludes with sections on interactions, side effects, contraindications and toxicity of local anesthetic drugs and recommended maximum dosing.
Similar to Pharmacology drug interaction hand book f (20)
Are you looking for a long-lasting solution to your missing tooth?
Dental implants are the most common type of method for replacing the missing tooth. Unlike dentures or bridges, implants are surgically placed in the jawbone. In layman’s terms, a dental implant is similar to the natural root of the tooth. It offers a stable foundation for the artificial tooth giving it the look, feel, and function similar to the natural tooth.
Lecture 6 -- Memory 2015.pptlearning occurs when a stimulus (unconditioned st...AyushGadhvi1
learning occurs when a stimulus (unconditioned stimulus) eliciting a response (unconditioned response) • is paired with another stimulus (conditioned stimulus)
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
Test bank for karp s cell and molecular biology 9th edition by gerald karp.pdfrightmanforbloodline
Test bank for karp s cell and molecular biology 9th edition by gerald karp.pdf
Test bank for karp s cell and molecular biology 9th edition by gerald karp.pdf
Test bank for karp s cell and molecular biology 9th edition by gerald karp.pdf
Know the difference between Endodontics and Orthodontics.Gokuldas Hospital
Your smile is beautiful.
Let’s be honest. Maintaining that beautiful smile is not an easy task. It is more than brushing and flossing. Sometimes, you might encounter dental issues that need special dental care. These issues can range anywhere from misalignment of the jaw to pain in the root of teeth.
These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
DECLARATION OF HELSINKI - History and principlesanaghabharat01
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5-hydroxytryptamine or 5-HT or Serotonin is a neurotransmitter that serves a range of roles in the human body. It is sometimes referred to as the happy chemical since it promotes overall well-being and happiness.
It is mostly found in the brain, intestines, and blood platelets.
5-HT is utilised to transport messages between nerve cells, is known to be involved in smooth muscle contraction, and adds to overall well-being and pleasure, among other benefits. 5-HT regulates the body's sleep-wake cycles and internal clock by acting as a precursor to melatonin.
It is hypothesised to regulate hunger, emotions, motor, cognitive, and autonomic processes.
The skin is the largest organ and its health plays a vital role among the other sense organs. The skin concerns like acne breakout, psoriasis, or anything similar along the lines, finding a qualified and experienced dermatologist becomes paramount.
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2. Interactions
Two or more drugs given at the same time may exert their effects
independently or may interact. The interaction may be potentiation or antagonism
of one drug by another, or occasionally some other effect.
Pharmacodynamic interactions
These are interactions between drugs which have similar or antagonistic
pharmacological effects or side effects. They may be due to competition at
receptor sites, or occur between drugs acting on the same physiological system.
They are usually predictable from a knowledge of the pharmacology of the
interacting drugs; in general, those demonstrated with one drug are likely to occur
with related drugs. They occur to a greater or lesser extent in most patients who
receive the interacting drugs.
Pharmacokinetic interactions
These occur when one drug alters the absorption, distribution, metabolism,
or excretion of another, thus increasing or reducing the amount of drug available
to produce its pharmacological effects. They are not easily predicted and many of
them affect only a small proportion of patients taking the combination of drugs.
Pharmacokinetic interactions occurring with one drug cannot be assumed to occur
with related drugs unless their pharmacokinetic properties are known to be
similar.
Relative importance of interactions
Many drug interactions are harmless and many of those which are
potentially harmful only occur in a small proportion of patients; moreover, the
severity of an interaction varies from one patient to another. Drugs with a small
therapeutic ratio (e.g. phenytoin) and those which require careful control of
dosage (e.g. anticoagulants, antihypertensives, and antidiabetics) are most often
involved. Patients at increased risk from drug interactions include the elderly and
those with impaired renal or liver function.
1.ALLOPURINOL
Antivirals: allopurinol increases plasma concentration of didanosine (risk of
toxicity)—avoid concomitant use.
Cytotoxics: allopurinol enhances effects and increases toxicity of azathioprine
and mercaptopurine (reduce dose of azathioprine and mercaptopurine to one
quarter of usual dose); avoidance of allopurinol advised by manufacturer of
capecitabine.
2
3. 2.ALPHA BLOCKERS
Antidepressants: enhanced hypotensive effect when alpha-blockers given with
MAOIs; manufacturer of indoramin advises avoid concomitant use with MAOIs.
Antivirals: plasma concentration of alfuzosin possibly increased by ritonavir—
avoid concomitant use.
Sildenafil: enhanced hypotensive effect when alphablockers given with sildenafil
(avoid alpha-blockers for 4 hours after sildenafil).
Sympathomimetics: avoid concomitant use of tolazoline with adrenaline
(epinephrine) or dopamine.
Tadalafil: enhanced hypotensive effect when alphablockers given with tadalafil—
avoid concomitant use.
Memantine: increased risk of CNS toxicity when amantadine given with
memantine (manufacturer of memantine advises avoid concomitant use); effects
of dopaminergics possibly enhanced by memantine.
3.AMIODARONE
Anti-arrhythmics: increased myocardial depression when anti-arrhythmics given
with other antiarrhythmics; increased risk of ventricular arrhythmias when
amiodarone given with disopyramide—avoid concomitant use; amiodarone
increases plasma concentration of flecainide (halve dose of flecainide).
.Antibacterials
erythromycin—avoid concomitant use; increased risk of ventricular arrhythmias
when amiodarone given with levofloxacin or moxifloxacin—avoid concomitant use;
increased risk of ventricular arrhythmias when amiodarone given with
sulfamethoxazole and trimethoprim (as co-trimoxazole) — avoid concomitant use
of co-trimoxazole.
Antidepressants: increased risk of ventricular arrhythmias when amiodarone
given with tricyclics— avoid concomitant use arrhythmias when amiodarone given
with pentamidine isetionate—avoid concomitant use.
Antimalarials: avoidance of amiodarone advised by manufacturer of artemether/
lumefantrine (risk of ventricular arrhythmias); increased risk of ventricular
arrhythmias when amiodarone given with chloroquine and hydroxychloroquine,
mefloquine or quinine—avoid concomitant use.
Antipsychotics: increased risk of ventricular arrhythmias when anti-arrhythmics
that prolong the QT interval given with antipsychotics that prolong the QT interval;
increased risk of ventricular arrhythmias when amiodarone given with benperidol—
manufacturer of benperidol advises avoid concomitant use; increased risk of
ventricular arrhythmias when amiodarone given with amisulpride, haloperidol,
phenothiazines, pimozide, sertindole or zuclopenthixol—avoid concomitant use;
increased risk of ventricular arrhythmias when amiodarone given with sulpiride.
Antivirals: plasma concentration of amiodarone possibly increased by atazanavir;
plasma concentration of amiodarone possibly increased by fosamprenavir
(increased risk of ventricular arrhythmias—avoid concomitant use); plasma
concentration of amiodarone possibly increased by indinavir—avoid concomitant
3
4. use; increased risk of ventricular arrhythmias when amiodarone given with
nelfinavir—avoid concomitant use; plasma concentration of amiodarone increased
by ritonavir (increased risk of ventricular arrhythmias—avoid concomitant use).
Beta-blockers: increased risk of bradycardia, AV block and myocardial depression
when amiodarone given with beta-blockers; increased myocardial depression when
anti-arrhythmics given with beta-blockers; increased risk of ventricular
arrhythmias when amiodarone given with sotalol—avoid concomitant use.
Pentamidine Isetionate: increased risk of ventricular arrhythmias when
amiodarone given with pentamidine isetionate — avoid concomitant use.
Corticosteroids: increased risk of hypokalaemia whenamphotericin given with
corticosteroids—avoidconcomitant use unless corticosteroids needed to control
reactions.
4.ANAESTHETICS GENERAL
Cytotoxics: nitrous oxide increases antifolate effect of methotrexate—avoid
concomitant use.
Memantine: increased risk of CNS toxicity when ketamine given with memantine
(manufacturer of memantine advises avoid concomitant use).
5.ANAKINRA
Infliximab: avoid concomitant use of anakinra with infliximab.
Antidepressants: avoidance of fluvoxamine advised by manufacturer of
reboxetine; possible increased serotonergic effects when SSRIs given with
duloxetine; fluvoxamine inhibits metabolism of duloxetine—avoid concomitant use;
citalopram, escitalopram, fluvoxamine or paroxetine should not be started until 2
weeks after stopping MAOIs, also MAOIs should not be started until at least 1
week after stopping citalopram, escitalopram, fluvoxamine or paroxetine; CNS
effects of SSRIs increased by MAOIs (risk of serious toxicity); sertraline should not
be started until 2 weeks after stopping MAOIs, also MAOIs should not be started
until at least 2 weeks after stopping sertraline; fluoxetine should not be started
until 2 weeks after stopping MAOIs, also MAOIs should not be started until at least
5 weeks after stopping fluoxetine; increased risk of CNS toxicity when
escitalopram given with moclobemide, preferably avoid concomitant use; after
stopping citalopram, fluvoxamine or paroxetine do not start moclobemide for at
least 1 week; after stopping fluoxetine do not start moclobemide for 5 weeks;
after stopping sertraline do not start moclobemide for 2 weeks; increased
serotonergic effects when SSRIs given with St John’s wort—avoid concomitant
use; SSRIs increase plasma concentration of some tricyclics; agitation and nausea
may occur when SSRIs given with tryptophan.
Anxiolytics and Hypnotics: fluvoxamine increases plasma concentration of some
benzodiazepines; fluvoxamine increases plasma concentration of melatonin—avoid
concomitant use; sedative effects possibly increased when sertraline given with
zolpidem.
6.ANTIDIPRESSANTS TRICYCLIC
4
5. Anti-arrhythmics: increased risk of ventricular arrhythmias when tricyclics given
with amiodarone— avoid concomitant use; increased risk of ventricular
arrhythmias when tricyclics given with disopyramide or flecainide; increased risk of
arrhythmias when tricyclics given with propafenone.
Antimalarials: avoidance of antidepressants advised by manufacturer of
artemether/lumefantrine.
Alcohol: increased sedation when tricyclic related antidepressants given with
alcohol.
Alpha -adrenoceptor Stimulants: avoidance of tricyclic- related antidepressants
advised by manufacturer of apraclonidine and brimonidine.
7.ANTI DIABETICS
Bosentan: increased risk of hepatotoxicity when glibenclamide given with
bosentan—avoid concomitant use.
Lipid-regulating Drugs: hypoglycaemic effect of acarbose possibly enhanced by
colestyramine; hypoglycaemic effect of nateglinide possibly enhanced by
gemfibrozil; increased risk of severe hypoglycaemia when repaglinide given with
gemfibrozil—avoid concomitant use; plasma concentration of rosiglitazone
increased by gemfibrozil (consider reducing dose of rosiglitazone); plasma
concentration of glibenclamide possibly increased by fluvastatin; may be improved
glucose tolerance and an additive effect when insulin or sulphonylureas given with
fibrates.
8.ANTI FUNGALS IMIDAZOLE
Anti-arrhythmics: increased risk of ventricular arrhythmias when ketoconazole
given with .disopyramide—avoid concomitant use.
Antibacterials: metabolism of ketoconazole accelerated by rifampicin (reduced
plasma concentration), also plasma concentration of rifampicin may be reduced by
ketoconazole; plasma concentration of ketoconazole possibly reduced by isoniazid;
avoidance of concomitant ketoconazole in severe renal and hepatic impairment
advised by manufacturer of telithromycin.
Anticoagulants: ketoconazole enhances anticoagulant effect of .coumarins;
miconazole enhances anticoagulant effect of .coumarins (miconazole oral gel and
possibly vaginal formulations absorbed); ketoconazole increases plasma
concentration of rivaroxaban—avoid concomitant use.
Antidiabetics: miconazole enhances hypoglycaemic effect of .gliclazide and
glipizide—avoid concomitant use; miconazole increases plasma concentration of
sulphonylureas.
Antihistamines: manufacturer of loratadine advises ketoconazole possibly
increases plasma concentration of loratadine; imidazoles possibly inhibit
metabolism of .mizolastine (avoid concomitant use); ketoconazole inhibits
metabolism of .mizolastine— avoid concomitant use.
Antimalarials: avoidance of imidazoles advised by manufacturer of artemether/
lumefantrine use.
5
6. Antimuscarinics: absorption of ketoconazole reduced by antimuscarinics;
ketoconazole increases plasma concentration of darifenacin—avoid concomitant
use; manufacturer of fesoterodine advises dose reduction when ketoconazole
given with fesoterodine —consult fesoterodine product literature; ketoconazole
increases plasma concentration of solifenacin; avoidance of ketoconazole advised
by manufacturer of tolterodine.
Antipsychotics: ketoconazole inhibits metabolism of aripiprazole (reduce dose of
aripiprazole); increased risk of ventricular arrhythmias when imidazoles given with
.pimozide—avoid concomitant use; imidazoles possibly increase plasma
concentration of quetiapine (reduce dose of quetiapine); increased risk of
ventricular arrhythmias when ketoconazole given with sertindole—avoid
concomitant use; possible increased risk of ventricular arrhythmias when
imidazoles given with sertindole—avoid concomitant use.
Antivirals: plasma concentration of both drugs increased when ketoconazole
given with darunavir; plasma concentration of ketoconazole increased by
fosamprenavir; ketoconazole increases plasma concentration of indinavir and
maraviroc (consider reducing dose of indinavir and maraviroc); plasma
concentration of ketoconazole reduced by nevirapine—avoid concomitant use;
combination of ketoconazole with ritonavir may increase plasma concentration of
either drug (or both); ketoconazole increases plasma concentration of saquinavir;
imidazoles possibly increase plasma concentration of saquinavir.
Cytotoxics: ketoconazole inhibits metabolism of erlotinib and sunitinib (increased
plasma concentration); ketoconazole increases plasma concentration of
bortezomib and imatinib; ketoconazole increases plasma concentration of lapatinib
and nilotinib— avoid concomitant use; ketoconazole increases plasma
concentration of active metabolite of temsirolimus—avoid concomitant use; in vitro
studies suggest a possible interaction between ketoconazole and docetaxel
(consult docetaxel product literature); ketoconazole reduces plasma concentration
of irinotecan (but concentration of active metabolite of irinotecan increased)—
avoid concomitant use.
Diuretics: ketoconazole increases plasma concentration of eplerenone—avoid
concomitant use.
Ergot Alkaloids: increased risk of ergotism when imidazoles given with
ergotamine and methysergide — avoid concomitant use.
5HT Agonists: ketoconazole increases plasma concentration of almotriptan
(increased risk of toxicity); ketoconazole increases plasma concentration of
eletriptan (risk of toxicity)—avoid concomitant use.
Ivabradine: ketoconazole increases plasma concentration of ivabradine—avoid
concomitant use.
Lipid-regulating Drugs: possible increased risk of myopathy when imidazoles
given with atorvastatin or simvastatin; increased risk of myopathy when
ketoconazole given with .simvastatin (avoid concomitant use); possible increased
risk of myopathy when miconazole given with .simvastatin—avoid concomitant
use.
6
7. Sirolimus: ketoconazole increases plasma concentration of sirolimus—avoid
concomitant use; miconazole increases plasma concentration of sirolimus.
Vardenafil: ketoconazole increases plasma concentration of vardenafil—avoid
concomitant use.
9.ANTI FUNGALS TRIAZOLE
Anti-arrhythmics: manufacturer of itraconazole advises avoid concomitant use
with disopyramide.
Antibacterials: plasma concentration of itraconazole increased by clarithromycin;
triazoles possibly increase plasma concentration of rifabutin (increased risk of
uveitis—reduce rifabutin dose); posaconazole increases plasma concentration of
rifabutin (also plasma concentration of posaconazole reduced); voriconazole
increases plasma concentration of rifabutin, also rifabutin reduces plasma
concentration of voriconazole (increase dose of voriconazole and also monitor for
rifabutin toxicity); fluconazole increases plasma concentration of rifabutin
(increased risk of uveitis—reduce rifabutindose); plasma concentration of
itraconazole reduced by rifabutin—avoid concomitant use; plasma concentration of
posaconazole reduced by rifampicin; plasma concentration of voriconazole reduced
by rifampicin—avoid concomitant use; metabolism of fluconazole and itraconazole
accelerated by rifampicin (reduced plasma concentration).
Antidepressants: avoidance of triazoles advised by manufacturer of reboxetine;
plasma concentration of voriconazole reduced by .St John’s wort—avoid
concomitant use of midazolam (risk of prolonged sedation); itraconazole increases
plasma concentration of buspirone (reduce dose of buspirone).
Antiepileptics: plasma concentration of itraconazole and posaconazole possibly
reduced by carbamazepine; fluconazole possibly increases plasma concentration of
carbamazepine; plasma concentration of voriconazole possibly reduced by
carbamazepine and primidone—avoid concomitant use; voriconazole increases
plasma concentration of phenytoin, also phenytoin reduces plasma concentration
of voriconazole (increase dose of voriconazole and also monitor for phenytoin
toxicity); plasma concentration of posaconazole reduced by phenytoin; plasma
concentration of itraconazole reduced by phenytoin—avoid concomitant use;
fluconazole increases plasma concentration of phenytoin (consider reducing dose
of phenytoin); plasma concentration of posaconazole possibly reduced by
primidone.
Antihistamines: itraconazole inhibits metabolism of mizolastine—avoid
concomitant use .
Antimalarials: avoidance of triazoles advised by manufacturer of artemether/
lumefantrine.
Antipsychotics: itraconazole possibly inhibits metabolism of aripiprazole (reduce
dose of aripiprazole); increased risk of ventricular arrhythmias when triazoles
given with pimozide—avoid concomitant use; triazoles possibly increase plasma
concentration of quetiapine (reduce dose of quetiapine); possible increased risk of
ventricular arrhythmias when triazoles given with sertindole—avoid concomitant
7
8. use; increased risk of ventricular arrhythmias when itraconazole given with
sertindole —avoid concomitant use.
Antivirals: posaconazole increases plasma concentration of atazanavir; plasma
concentration of itraconazole and posaconazole reduced by efavirenz; plasma
concentration of voriconazole reduced by efavirenz, also plasma concentration of
efavirenz increased (consider increasing voriconazole dose and reducing efavirenz
dose); plasma concentration of itraconazole possibly increased by fosamprenavir;
itraconazole increases plasma concentration of indinavir (consider reducing dose of
indinavir); fluconazole increases plasma concentration of nevirapine, ritonavir and
tipranavir; plasma concentration of voriconazole reduced by ritonavir—avoid
concomitant use; combination of itraconazole with ritonavir may increase plasma
concentration of either drug (or both); triazoles possibly increase plasma
concentration of saquinavir; fluconazole increases plasma concentration of
zidovudine (increased risk of toxicity).
Bosentan: fluconazole possibly increases plasma concentration of bosentan—
avoid concomitant use; itraconazole possibly increases plasma concentration of
bosentan.
Cytotoxics: itraconazole inhibits metabolism of busulfan (increased risk of
toxicity); itraconazole possibly increases side-effects of cyclophosphamide;
avoidance of itraconazole, posaconazole and voriconazole advised by manufacturer
of lapatinib; avoidance of itraconazole and voriconazole advised by manufacturer
of nilotinib; posaconazole possibly inhibits metabolism of vinblastine and
vincristine (increased risk of neurotoxicity); itraconazole possibly inhibits
metabolism of vincristine (increased risk of neurotoxicity).
Diuretics: fluconazole increases plasma concentration of eplerenone (reduce dose
of eplerenone); itraconazole increases plasma concentration of eplerenone—avoid
concomitant use; plasma concentration of fluconazole increased by
hydrochlorothiazide
Ergot Alkaloids: increased risk of ergotism when triazoles given with ergotamine
and methysergide— avoid concomitant use.
5HT Agonists: itraconazole increases plasma concentration of eletriptan (risk of
toxicity)—avoid concomitant use.
Ivabradine: fluconazole increases plasma concentration of ivabradine—reduce
initial dose of ivabradine; itraconazole possibly increases plasma concentration of
ivabradine—avoid concomitant use.
Lipid-regulating Drugs: possible increased risk of myopathy when triazoles
given with atorvastatin or simvastatin; increased risk of myopathy when
itraconazole or posaconazole given with atorvastatin (avoid concomitant use);
fluconazole increases plasma concentration of fluvastatin; increased risk of
myopathy when itraconazole or posaconazole given with simvastatin (avoid
concomitant use).
Sirolimus: posaconazole possibly increases plasma concentration of sirolimus;
itraconazole and voriconazole increase plasma concentration of sirolimus— avoid
concomitant use.
8
9. Vardenafil: itraconazole possibly increases plasma concentration of vardenafil—
avoid concomitant use.
10.ANTI HISTAMINES
Anti-arrhythmics: increased risk of ventricular arrhythmias when mizolastine
given with .amiodarone, disopyramide, flecainide or propafenone—avoid conco
mitant use.
Antibacterials: manufacturer of loratadine advises plasma concentration possibly
increased by erythromycin; metabolism of mizolastine inhibited by erythromycin—
avoid concomitant use; increased risk of ventricular arrhythmias when mizolastine
given with moxifloxacin—avoid concomitant use; metabolism of mizolastine
possibly inhibited by macrolides (avoid concomitant use).
Antidiabetics: thrombocyte count depressed when ketotifen given with
metformin (manufacturer of ketotifen advises avoid concomitant use).
Antifungals: manufacturer of loratadine advises plasma concentration possibly
increased by ketoconazole; metabolism of mizolastine inhibited by itraconazole or
ketoconazole—avoid concomitant use; metabolism of mizolastine possibly inhibited
by imidazoles (avoid concomitant use).
Beta-blockers: increased risk of ventricular arrhythmias when mizolastine given
with sotalol—avoid concomitant use.
11.ANTIMUSCARICS
Antibacterials: manufacturer of fesoterodine advises dose reduction when
fesoterodine given with clarithromycin and telithromycin—consult fesoterodine
product literature; manufacturer of tolterodine advises avoid concomitant use with
clarithromycin and erythromycin; plasma concentration of darifenacin possibly
increased by erythromycin; plasma concentration of active metabolite of
esoterodine reduced by rifampicin.
Antifungals: antimuscarinics reduce absorption of ketoconazole; manufacturer of
fesoterodine advises dose reduction when fesoterodine given with itraconazole and
ketoconazole—consult fesoterodine. product literature; plasma concentration of
darifenacin increased by ketoconazole—avoid concomitant use; plasma
concentration of solifenacin increased by itraconazole and ketoconazole;
manufacturer of tolterodine advises avoid concomitant use with itraconazole and
ketoconazole; manufacturer of darifenacin advises avoid concomitant use with
itraconazole.
Calcium-channel Blockers: manufacturer of darifenacin advises avoid
concomitant use with verapamil.
Ciclosporin: manufacturer of darifenacin advises avoid concomitant use with
ciclosporin.
12.ANTI PSYCHOTICS
Analgesics: avoid concomitant use of clozapine with azapropazone (increased risk
of agranulocytosis); possible severe drowsiness when haloperidol given with
9
10. indometacin; increased risk of convulsions when antipsychotics given with
tramadol; enhanced hypotensive and sedative effects when antipsychotics given
with opioid analgesics.
Anti-arrhythmics: increased risk of ventricular arrhythmias when antipsychotics
that prolong the QT interval given with anti-arrhythmics that prolong the QT
interval; increased risk of ventricular arrhythmias when amisulpride, haloperidol,
phenothiazines, pimozide, sertindole or zuclopenthixol given with amiodarone—
avoid concomitant use; increased risk of ventricular arrhythmias when benperidol
given with amiodarone—manufacturer of benperidol advises avoid concomitant
use; increased risk of ventricular arrhythmias when sulpiride given with
amiodarone or disopyramide; increased risk of ventricular arrhythmias when
amisulpride, pimozide, sertindole or zuclopenthixol given with disopyramide—avoid
concomitant use; increased risk of ventricular arrhythmias when phenothiazines
given with disopyramide; increased risk of arrhythmias when clozapine given with
flecainide.
Antibacterials: increased risk of ventricular arrhythmias when pimozide given
with clarithromycin, moxifloxacin or telithromycin—avoid concomitant use;
increased risk of ventricular arrhythmias when sertindole given with erythromycin
or moxifloxacin—avoid concomitant use; increased risk of ventricular arrhythmias
when amisulpride or zuclopenthixol given with parenteral erythromycin—avoid
concomitant use; plasma concentration of clozapine possibly increased by
erythromycin (possible increased risk of convulsions); possible increased risk of
ventricular arrhythmias when pimozide given with erythromycin—avoid
concomitant use; increased risk of ventricular arrhythmias when sulpiride given
with parenteral erythromycin; plasma concentration of clozapine increased by
ciprofloxacin; plasma concentration of olanzapine possibly increased by
ciprofloxacin; increased risk of ventricular arrhythmias when haloperidol,
phenothiazines or zuclopenthixol given with moxifloxacin—avoid concomitant use;
increased risk of ventricular arrhythmias when benperidol given with moxifloxacin
— manufacturer of benperidol advises avoid concomitant use; plasma
concentration of aripiprazole possibly reduced by rifabutin and rifampicin—increase
dose of aripiprazole; plasma concentration of clozapine possibly reduced by
rifampicin; metabolism of haloperidol accelerated by rifampicin (reduced plasma
concentration); avoid concomitant use of clozapine with chloramphenicol or
sulphonamides (increased risk of agranulocytosis); plasma concentration of
quetiapine possibly increased by macrolides (reduce dose of quetiapine); possible
increased risk of ventricular arrhythmias when sertindole given with macrolides—
avoid concomitant use.
Antidepressants: plasma concentration of clozapine possibly increased by
citalopram (increased risk of toxicity); metabolism of aripiprazole possibly
inhibited by fluoxetine and paroxetine (reduce dose of aripiprazole); plasma
concentration of clozapine, haloperidol, risperidone, sertindole and zotepine
increased by fluoxetine; plasma concentration of clozapine and olanzapine
increased by fluvoxamine; plasma concentration of clozapine and sertindole
10
11. increased by paroxetine; plasma concentration of risperidone possibly increased by
paroxetine (increased risk of toxicity); metabolism of perphenazine inhibited by
paroxetine (reduce dose of perphenazine); plasma concentration of clozapine
increased by sertraline and venlafaxine; plasma concentration of haloperidol
increased by venlafaxine; clozapine possibly increases CNS effects of MAOIs;
plasma concentration of pimozide possibly increased by SSRIs (increased risk of
ventricular arrhythmias—avoid concomitant use); plasma concentration of
aripiprazole possibly reduced by St John’s wort—increase dose of aripiprazole;
antipsychotics increase plasma concentration of .tricyclics—possibly increased
risk of ventricular arrhythmias; increased risk of antimuscarinic side-effects when
phenothiazines given with tricyclics; increased risk of ventricular arrhythmias
when pimozide given with tricyclics—avoid concomitant use; possibly increased
antimuscarinic side-effects when clozapine given with tricyclics.
Antifungals: metabolism of aripiprazole inhibited by ketoconazole (reduce dose of
aripiprazole); increased risk of ventricular arrhythmias whensertindole given with
itraconazole or ketoconazole—avoid concomitant use; metabolism of aripiprazole
possibly inhibited by itraconazole (reduce dose of aripiprazole); possible increased
risk of ventricular arrhythmias when sertindole given with imidazoles or .triazoles
—avoid concomitant use; plasma concentration of quetiapine possibly increased by
imidazoles and triazoles (reduce dose of quetiapine); increased risk of ventricular
arrhythmias when pimozide given with imidazoles or triazoles—avoid concomitant
use .
Antimalarials: avoidance of antipsychotics advised by manufacturer of
artemether/lumefantrine; increased risk of ventricular arrhythmias when pimozide
given with mefloquine or quinine—avoid concomitant use.
Antipsychotics: avoid concomitant use of clozapine with depot formulation of
flupentixol, fluphenazine, haloperidol, pipotiazine, risperidone or zuclopenthixol as
cannot be withdrawn quickly if neutropenia occurs; increased risk of ventricular
arrhythmias when sulpiride given with haloperidol; increased risk of ventricular
arrhythmias when sertindole given with amisulpride—avoid concomitant use;
increased risk of ventricular arrhythmias when pimozide given with phenothiazines
— avoid concomitant use; increased risk of ventricular arrhythmias when pimozide
given with sulpiride.
Antivirals: plasma concentration of pimozide possibly increased by atazanavir—
avoid concomitant use; metabolism of aripiprazole possibly inhibited by
atazanavir, fosamprenavir, indinavir, lopinavir, nelfinavir, ritonavir and saquinavir
(reduce dose of aripiprazole); plasma concentration of pimozide possibly increased
by efavirenz, indinavir, nelfinavir and saquinavir (increased risk of ventricular
arrhythmias—avoid concomitant use); plasma concentration of aripiprazole
possibly reduced by efavirenz and nevirapine—increase dose of aripiprazole;
plasma concentration of pimozide and sertindole increased by fosamprenavir
(increased risk of ventricular arrhythmias—avoid concomitant use); plasma
concentration of clozapine possibly increased by fosamprenavir; plasma
concentration of sertindole increased by indinavir, lopinavir, nelfinavir, ritonavir
11
12. and saquinavir (increased risk of ventricular arrhythmias—avoid concomitant use);
plasma concentration of olanzapine reduced by ritonavir— consider increasing
dose of olanzapine; plasma concentration of clozapine increased by ritonavir
(increased risk of toxicity)—avoid concomitant use; plasma concentration of
antipsychotics possibly increased by ritonavir; plasma concentration of pimozide
increased by ritonavir (increased risk of ventricular arrhythmias—avoid
concomitant use).
Aprepitant: avoidance of pimozide advised by manufacturer of aprepitant.
Beta-blockers: enhanced hypotensive effect when phenothiazines given with
beta-blockers; plasma concentration of both drugs may increase when
chlorpromazine given with propranolol; increased risk of ventricular arrhythmias
when amisulpride, phenothiazines, pimozide, sertindole or sulpiride given with
sotalol; increased risk of ventricular arrhythmias when zuclopenthixol given with
sotalol—avoid concomitant use.
Cytotoxics: avoid concomitant use of clozapine with cytotoxics (increased risk of
agranulocytosis); avoidance of pimozide advised by manufacturer of lapatinib.
Desferrioxamine: manufacturer of levomepromazine (methotrimeprazine)
advises avoid concomitant use with desferrioxamine; avoidance of
prochlorperazine advised by manufacturer of desferrioxamine.
Diuretics: risk of ventricular arrhythmias with amisulpride or sertindole increased
by hypokalaemia caused by diuretics; risk of ventricular arrhythmias with pimozide
increased by hypokalaemia caused by diuretics (avoid concomitant use); enhanced
hypotensive effect when phenothiazines given with diuretics.
Ivabradine: increased risk of ventricular arrhythmias when pimozide or sertindole
given with ivabradine
Lithium: increased risk of ventricular arrhythmias when sertindole given with
lithium—avoid concomitant use; increased risk of extrapyramidal side-effects and
possibly neurotoxicity when clozapine, flupentixol, haloperidol, phenothiazines or
zuclopenthixol given with lithium; increased risk of extrapyramidal sideeffects
when sulpiride given with lithium.
Penicillamine: avoid concomitant use of clozapine with penicillamine (increased
risk of agranulocytosis)
Pentamidine Isetionate: increased risk of ventricular arrhythmias when
amisulpride given with pentamidine isetionate—avoid concomitant use; increased
risk of ventricular arrhythmias when phenothiazines given with pentamidine
isetionate
Sibutramine: increased risk of CNS toxicity when antipsychotics given with
sibutramine (manufacturer of sibutramine advises avoid concomitant use)
Ulcer-healing Drugs: effects of antipsychotics, chlorpromazine and clozapine
possibly enhanced by cimetidine; increased risk of ventricular arrhythmias when
sertindole given with cimetidine—avoid concomitant use; plasma concentration of
clozapine possibly reduced by omeprazole; absorption of sulpiride reduced by
sucralfate.
12
13. 13.ANXIOLYTICS AND HYPNOTICS
Antibacterials: metabolism of midazolam inhibited by clarithromycin,
erythromycin, quinupristin/ dalfopristin and .telithromycin (increased plasma
concentration with increased sedation); plasma concentration of buspirone
increased by erythromycin (reduce dose of buspirone); metabolism of zopiclone
inhibited by erythromycin and quinupristin/dalfopristin; metabolism of
benzodiazepines possibly accelerated by rifampicin (reduced plasma
concentration); metabolism of diazepam accelerated by rifampicin (reduced
plasma concentration); metabolism of buspirone and zaleplon possibly accelerated
by rifampicin; metabolism of zolpidem accelerated by rifampicin (reduced plasma
concentration and reduced effect); plasma concentration of zopiclone significantly
reduced by rifampicin; metabolism of diazepam inhibited by isoniazid.
Antidepressants: plasma concentration of melatonin increased by fluvoxamine—
avoid concomitant use; plasma concentration of some benzodiazepines increased
by fluvoxamine; sedative effects possibly increased when zolpidem given with
sertraline; manufacturer of buspirone advises avoid concomitant use with MAOIs;
plasma concentration of oral midazolam possibly reduced by St John’s wort;
increased sedative effect when anxiolytics and hypnotics given with mirtazapine,
tricyclic-related antidepressants or tricyclics.
Antifungals: plasma concentration of alprazolam increased by itraconazole and
ketoconazole; plasma concentration of midazolam increased by fluconazole,
itraconazole and ketoconazole (risk of prolonged sedation); plasma concentration
of buspirone increased by itraconazole (reduce dose of buspirone); plasma
concentration of midazolam increased by posaconazole.
Antipsychotics: increased sedative effect when anxiolytics and hypnotics given
with antipsychotics; buspirone increases plasma concentration of haloperidol;
increased risk of hypotension, bradycardia and respiratory depression when
parenteral benzodiazepines given with intramuscular olanzapine; diazepam
increases plasma concentration of zotepine.
Antivirals: plasma concentration of midazolam possibly increased by .atazanavir
—avoid concomitant use oforal midazolam; increased risk of prolonged
sedation when midazolam given with efavirenz— avoid concomitant use; increased
risk of prolonged sedation and respiratory depression when alprazolam,
clonazepam, diazepam, flurazepam or midazolam given with fosamprenavir;
plasma concentration of midazolam possibly increased by indinavir, nelfinavir and
ritonavir (risk of prolonged sedation—avoid concomitant use of oral midazolam);
increased risk of prolonged sedation when alprazolam given with .indinavir—avoid
concomitant use; plasma concentration of alprazolam, diazepam, flurazepam and
zolpidem possibly increased by ritonavir (risk of extreme sedation and respiratory
depression —avoid concomitant use); plasma concentration of anxiolytics and
hypnotics possibly increased by ritonavir; plasma concentration of buspirone
increased by ritonavir (increased risk of toxicity); plasma concentration of
midazolam increased by saquinavir (risk of prolonged sedation—avoid concomitant
use of oral midazolam).
13
14. Sodium Oxybate: benzodiazepines enhance effects of .sodium oxybate (avoid
concomitant use).
14.APRIPITANT
Antidepressants: manufacturer of aprepitant advises avoid concomitant use with
St John’s wort.
Antipsychotics: manufacturer of aprepitant advises avoid concomitant use with
pimozide.
Oestrogens: aprepitant possibly causes contraceptive failure of hormonal
contraceptives containing oestrogens (alternative contraception recommended)
Progestogens: aprepitant possibly causes contraceptive failure of hormonal
contraceptives containing progestogens (alternative contraception recommended).
15.ARTEMETHER WITH LUMIFANTINE
Anti-arrhythmics: manufacturer of artemether/lumefantrine advises avoid
concomitant use with .amiodarone, disopyramide or flecainide (risk of ventricular
arrhythmias).
Antibacterials: manufacturer of artemether/lumefantrine advises avoid
concomitant use with macrolides and quinolones.
Antidepressants: manufacturer of artemether/lumefantrine advises avoid
concomitant use with antidepressants
Antifungals: manufacturer of artemether/lumefantrine advises avoid concomitant
use with .imidazoles and triazoles
Antimalarials: manufacturer of artemether/lumefantrine advises avoid
concomitant use with .antimalarials; increased risk of ventricular arrhythmias
when artemether/lumefantrine given with quinine.
Antipsychotics: manufacturer of artemether/lumefantrine advises avoid
concomitant use with antipsychotics.
Beta-blockers: manufacturer of artemether/lumefantrine advises avoid
concomitant use with metoprolol and sotalol.
Grapefruit Juice: plasma concentration of artemether/ lumefantrine possibly
increased by grapefruit juice.
Ulcer-healing Drugs: manufacturer of artemether/ lumefantrine advises avoid
concomitant use withcimetidine.
Analgesics: avoid concomitant use of aspirin with NSAIDs (increased side-
effects); antiplatelet effect of aspirin possibly reduced by ibuprofen.
Antacids: excretion of aspirin increased by alkaline urine due to some antacids.
Anticoagulants: increased risk of bleeding when aspirin given with coumarins or
phenindione (due to antiplatelet effect); aspirin enhances anticoagulant effect of
heparins.
Antidepressants: increased risk of bleeding when aspirin given with SSRIs or
venlafaxine.
Antiepileptics: aspirin enhances effects of phenytoin and valproate.
14
15. Cytotoxics: aspirin reduces excretion of methotrexate (increased risk oftoxicity)
—but for concomitant use in rheumatic disease.
16.ATAZANAVIR
Anti-arrhythmics: atazanavir possibly increases plasma concentration of
amiodarone and .lidocaine (lignocaine).
Antibacterials: plasma concentration of both drugs increased when atazanavir
given with clarithromycin; atazanavir increases plasma concentration of rifabutin
(reduce dose of rifabutin); plasma concentration of atazanavir reduced by
rifampicin—avoid concomitant use; avoidance of concomitant atazanavir in severe
renal and hepatic impairment advised by manufacturer of telithromycin.
Antidepressants: plasma concentration of atazanavir reduced by St John’s wort
—avoid concomitant use .
Antifungals: plasma concentration of atazanavir increased by posaconazole
Antimalarials: caution with atazanavir advised by manufacturer of artemether/
lumefantrine.
Antimuscarinics: avoidance of atazanavir advised by manufactur of darifenacin;
manufacturer of fesoterodine advises dose reduction when atazanavir given with
fesoterodine—consult fesoterodine product literature .
Antipsychotics: atazanavir possibly inhibits metabolism of aripiprazole (reduce
dose of aripiprazole); atazanavir possibly increases plasma concentration of
.pimozide—avoid concomitant use.
Antivirals: manufacturer of atazanavir advises avoid concomitant use with
.efavirenz (plasma concentration of atazanavir reduced); avoid concomitant use of
atazanavir with indinavir; atazanavir increases plasma concentration of maraviroc
(consider reducing dose of maraviroc); plasma concentration of atazanavir
possibly reduced by nevirapine—avoid concomitant use; atazanavir increases
plasma concentration of saquinavir; plasma concentration of atazanavir reduced
by tenofovir, also plasma concentration of tenofovir possibly increased; atazanavir
increases plasma concentration of tipranavir (also plasma concentration of
atazanavir reduced).
Anxiolytics and Hypnotics: atazanavir possibly increases plasma concentration
of midazolam— avoid concomitant use of oral midazolam.
Calcium-channel Blockers: atazanavir increases plasma concentration of
diltiazem (reduce dose of diltiazem); atazanavir possibly increases plasma
concentration of verapamil.
Ciclosporin: atazanavir possibly increases plasma concentration of ciclosporin.
Cytotoxics: atazanavir possibly inhibits metabolism of .irinotecan (increased risk
of toxicity).
Ergot Alkaloids: atazanavir possibly increases plasma concentration of ergot
alkaloids—avoid concomitant use.
Lipid-regulating Drugs: possible increased risk of myopathy when atazanavir
given with atorvastatin; possible increased risk of myopathy when atazanavir
15
16. given with rosuvastatin—avoid concomitant use; increased risk of myopathy when
atazanavir given with simvastatin (avoid concomitant use).
Oestrogens: atazanavir increases plasma concentration of .ethinylestradiol—
avoid concomitant use.
Sildenafil: atazanavir possibly increases side-effects of sildenafil
Sirolimus: atazanavir possibly increases plasma concentration of sirolimus
Tacrolimus: atazanavir possibly increases plasma concentration of tacrolimus
Ulcer-healing Drugs: plasma concentration of atazanavir possibly reduced by
histamine H -antagonists; plasma concentration of atazanavir reduced by proton
pump inhibitors.
17.ATOMOXETINE
Analgesics: increased risk of ventricular arhythmias when atomoxetine given with
methadone; possible. increased risk of convulsions when atomoxetine given with
tramadol.
Anti-arrhythmics: increased risk of ventricular arrhythmias when atomoxetine
given with amiodarone or disopyramide
Antibacterials: increased risk of ventricular arrhythmias when atomoxetine given
with parenteral erythromycin; increased risk of ventricular arrhythmias when
atomoxetine given with moxifloxacin.
Antidepressants: metabolism of atomoxetine possibly inhibited by fluoxetine and
paroxetine; possible increased risk of convulsions when atomoxetine given with
antidepressants; atomoxetine should not be started until 2 weeks after stopping
MAOIs, also MAOIs should not be started until at least 2 weeks after stopping
atomoxetine; increased risk of ventricular arrhythmias when atomoxetine given
with .tricyclics.
Antimalarials: increased risk of ventricular arrhythmias when atomoxetine given
with mefloquine . Antipsychotics: increased risk of ventricular arrhythmias when
atomoxetine given with .antipsychotics that prolong the QT interval.
Beta-blockers: increased risk of ventricular arrhythmias when atomoxetine given
with sotalol.
Bupropion: possible increased risk of convulsions when atomoxetine given with
bupropion.
Diuretics: risk of ventricular arrhythmias with atomoxetine increased by
hypokalaemia caused by diuretics.
18.ATOVAQUONE
Antibacterials: plasma concentration of atovaquone reduced by .rifabutin and
.rifampicin (possible therapeutic failure of atovaquone); plasma concentration
of atovaquone reduced by tetracycline.
19.AZATHIOPRINE
16
17. Allopurinol: enhanced effects and increased toxicity of azathioprine when given
with allopurinol (reduce dose of azathioprine to one quarter of usual dose).
Aminosalicylates: possible increased risk of leucopenia when azathioprine given
with aminosalicylates.
Antibacterials: increased risk of haematological toxicity when azathioprine given
with sulfamethoxazole (as co-trimoxazole); increased risk of haematological
toxicity when azathioprine given with trimethoprim (also with co-trimoxazole).
Anticoagulants: azathioprine possibly reduces anticoagulant effect of coumarins
Antiepileptics: cytotoxics possibly reduce absorption of phenytoin.
Antipsychotics: avoid concomitant use of cytotoxics with clozapine (increased
risk of agranulocytosis).
20.AZTREONAM
Anticoagulants: aztreonam possibly enhances anticoagulant effect of coumarins.
20a.BARBITURATES
Antibacterials: barbiturates accelerate metabolism of chloramphenicol,
doxycycline and metronidazole (reduced plasma concentration); phenobarbital
possibly reduces plasma concentration of rifampicin; phenobarbital reduces plasma
concentration of telithromycin (avoid during and for 2 weeks after phenobarbital).
Anticoagulants: barbiturates accelerate metabolism of coumarins (reduced
anticoagulant effect).
Antidepressants: phenobarbital reduces plasma concentration of paroxetine;
phenobarbital accelerates metabolism of mianserin (reduced plasma
concentration); anticonvulsant effect of barbiturates possibly antagonised by
MAOIs and tricyclic-related antidepressants (convulsive threshold lowered);
anticonvulsant effect of barbiturates antagonised by SSRIs (convulsive threshold
lowered); avoid concomitant use of phenobarbital with .St John’s wort;
anticonvulsant effect of barbiturates antagonised by tricyclics (convulsive
threshold lowered), also metabolism of tricyclics possibly accelerated (reduced
plasma concentration).
Antifungals: phenobarbital possibly reduces plasma concentration of itraconazole
and .posaconazole; phenobarbital possibly reduces plasma concentration of
voriconazole—avoid concomitant use; Phenobarbital reduces absorption of
griseofulvin (reduced effect).
Antipsychotics: anticonvulsant effect of barbiturates antagonised by
antipsychotics (convulsive threshold lowered); phenobarbital accelerates
metabolism of haloperidol (reduced plasma concentration); plasma concentration
of both drugs reduced when Phenobarbital given with chlorpromazine;
Phenobarbital possibly reduces plasma concentration of aripiprazole—increase
dose of aripiprazole.
Antivirals: phenobarbital possibly reduces plasma concentration of abacavir,
darunavir, fosamprenavir and lopinavir; avoidance of Phenobarbital advised by
manufacturer of etravirine; barbiturates possibly reduce plasma concentration of
17
18. indinavir, nelfinavir and saquinavir; Phenobarbital possibly reduces plasma
concentration of indinavir, also plasma concentration of phenobarbital possibly
increased.
Calcium-channel Blockers: barbiturates reduce effects of .felodipine and
.isradipine; barbiturates probably reduce effects of .dihydropyridines, .diltiazem
and .verapamil.
Ciclosporin: barbiturates accelerate metabolism of .ciclosporin (reduced effect)
Corticosteroids: barbiturates accelerate metabolism of .corticosteroids (reduced
effect).
Cytotoxics: phenobarbital possibly reduces plasma concentration of etoposide;
phenobarbital reduces plasma concentration of irinotecan and its active Metabolite.
Diuretics: phenobarbital reduces plasma concentration of .eplerenone—avoid
concomitant use; increased risk of osteomalacia when phenobarbital given with
carbonic anhydrase inhibitors.
Oestrogens: barbiturates accelerate metabolism of .oestrogens (reduced
contraceptive effect.
Progestogens: barbiturates accelerate metabolism of .progestogens (reduced
contraceptive effect.
Sodium Oxybate: barbiturates enhance effects of sodium oxybate (avoid
concomitant use)
Sympathomimetics: plasma concentration of phenobarbital possibly increased by
methylphenidate.
Tacrolimus: phenobarbital reduces plasma concentration of .tacrolimus.
21.BETA BLOCKERS
Alpha-blockers: enhanced hypotensive effect when beta-blockers given with
.alpha-blockers, also increased risk of first-dose hypotension with postsynaptic
alpha-blockers such as prazosin.
Anaesthetics, Local: propranolol increases risk of .bupivacaine toxicity.
Anti-arrhythmics: increased myocardial depression when beta-blockers given
with .anti-arrhythmics; increased risk of ventricular arrhythmias when sotalol
given with .amiodarone or .disopyramide—avoid concomitant use; increased risk
of bradycardia, AV block and myocardial depression when beta-blockers given with
.amiodarone; increased risk of myocardial depression and bradycardia when beta-
blockers given with .flecainide; propranolol increases risk of .lidocaine (lignocaine)
toxicity; plasma concentration of metoprolol and propranolol increased by
propafenone.
Antibacterials: increased risk of ventricular arrhythmias when sotalol given
with .moxifloxacin—avoid concomitant use; metabolism of bisoprolol and
propranolol accelerated by rifampicin (plasma concentration significantly reduced);
plasma concentration of carvedilol, celiprolol and metoprolol reduced by rifampicin.
Antidepressants: plasma concentration of metoprolol increased by citalopram
and escitalopram; plasma concentration of propranolol increased by fluvoxamine;
18
19. plasma concentration of metoprolol possibly increased by paroxetine (enhanced
effect); labetalol and propranolol increase plasma concentration of imipramine;
enhanced hypotensive effect when beta-blockers given with MAOIs; increased risk
of ventricular arrhythmias when sotalol given with .tricyclics.
Antihistamines: increased risk of ventricular arrhythmias when sotalol given with
.mizolastine—avoid concomitant use.
Antimalarials: avoidance of metoprolol and sotalol advised by manufacturer of
.artemether/lumefantrine; increased risk of bradycardia when betablockers given
with mefloquine.
Antimuscarinics:increased risk of ventricular arrhythmias when sotalol givenwith
tolterodine.
Antipsychotics: plasma concentration of both drugs may increase when
propranolol given with chlorpromazine; increased risk of ventricular arrhythmias
when sotalol given with .zuclopenthixol— avoid concomitant use; increased risk of
ventricular arrhythmias when sotalol given with .amisulpride, .phenothiazines,
pimozide, .sertindole or .sulpiride; enhanced hypotensive effect when betablockers
given with phenothiazines.
Antivirals: avoidance of metoprolol for heart failure advised by manufacturer of
.tipranavir.
Anxiolytics and Hypnotics: enhanced hypotensive effect when beta-blockers
given with anxiolytics and hypnotics.
Atomoxetine: increased risk of ventricular arrhythmias when sotalol given with
.atomoxetine.
Barbiturates: plasma concentration of metoprolol and timolol reduced by barbi
turates;plasma concentration of propranolol possibly reduced bybarbiturates.
Calcium-channel Blockers: enhanced hypotensive effect when beta-blockers
given with calciumchannel blockers; possible severe hypotension and heart failure
when beta-blockers given with .nifedipine; increased risk of AV block and brady
cardia when beta-blockers given with .diltiazem; asystole, severe hypotension and
heart failure when betablockers given with .verapamil.
Ciclosporin: carvedilol increases plasma concentration of .ciclosporin
Clonidine: increased risk of withdrawal hypertension when beta-blockers given
with .clonidine (withdraw beta-blockers several days before slowly withdrawing
clonidine).
Diuretics: enhanced hypotensive effect when betablockers given with diuretics;
risk of ventricular arrhythmias with sotalol increased by hypokalaemia caused by
loop diuretics or .thiazides and related diuretics.
5HT Antagonists: increased risk of ventricular arrhythmias when sotalol given
with .dolasetron—avoid concomitant use.
Ivabradine: increased risk of ventricular arhythmias when sotalol with ivabradine.
Methyldopa: enhanced hypotensive effect when betablockers given with
methyldopa.
Moxisylyte (thymoxamine): possible severe postural hypotension when beta-
blockers given with .moxisylyte.
19
20. Sympathomimetics: increased risk of severe hypertension and bradycardia when
non-cardioselective beta-blockers given with .adrenaline (epinephrine), also
reponse to adrenaline (epinephrine) may be reduced; increased risk of severe
hypertension and bradycardia when non-cardioselective beta-blockers given
with .dobutamine; possible increased risk of severe hypertension and bradycardia
when noncardioselective beta-blockers given with .noradrenaline
(norepinephrine).
22.BEXAROTENE
Antipsychotics: avoid concomitant use of cytotoxics with .clozapine (increased
risk of agranulocytosis).
Cardiac Glycosides: cytotoxics reduce absorption of digoxin tablets.
Lipid-regulating Drugs: plasma concentration of bexarotene increased by
.gemfibrozil—avoid concomitant use.
23.BLEOMYCIN
Antipsychotics: avoid concomitant use of cytotoxics with .clozapine (increased
risk of agranulocytosis).
Cardiac Glycosides: cytotoxics reduce absorption of digoxin tablets
Cytotoxics: increased pulmonary toxicity when bleomycin given with .cisplatin.
24.BORTEZOMIB
Antipsychotics: avoid concomitant use of cytotoxics with .clozapine (increased
risk of agranulocytosis).
25.BOSENTAN
Antibacterials: plasma concentration of bosentan reduced by .rifampicin—avoid
concomitant use.
Anticoagulants: manufacturer of bosentan recommends monitoring anticoagulant
effect of coumarins.
Antidiabetics: increased risk of hepatotoxicity when bosentan given with
.glibenclamide—avoid concomitant use.
Antifungals: plasma concentration of bosentan increased by ketoconazole;
plasma concentration of bosentan possibly increased by .fluconazole—avoid
concomitant use; plasma concentration of bosentan possibly increased by
itraconazole.
Ciclosporin: plasma concentration of bosentan increased by .ciclosporin (also
plasma concentration of ciclosporin reduced—avoid concomitant use).
Oestrogens: bosentan possibly causes contraceptive failure of hormonal
contraceptives containing .oestrogens (alternative contraception recommended)
Progestogens: bosentan possibly causes contraceptive failure of hormonal
contraceptives containing.progestogens (alternative contraception recommended).
26.BROMOCRIPTINE
20
21. Sympathomimetics:risk of toxicity when bromocriptine given with isometheptene
or phenylpropanolamine.
27.BUPIVACAINE
Beta-blockers: increased risk of bupivacaine toxicity when given with .propranolol.
28.BUPROPION
Antidepressants: bupropion possibly increases plasma concentration of
citalopram; manufacturer of bupropion advises avoid for 2 weeks after stopping
.MAOIs; manufacturer of bupropion advises avoidconcomitant use with
.moclobemide.
Antiepileptics: plasma concentration of bupropion reduced by carbamazepine
and phenytoin; metabolism of bupropion inhibited by valproate.
Antivirals: plasma concentration of bupropion increased or decreased by
.ritonavir.
29.BUSULPHAN
Antibacterials: plasma concentration of busulfan increased by .metronidazole
(increased risk of toxicity).
Antipsychotics: avoid concomitant use of cytotoxics with .clozapine (increased
risk of agranulocytosis).
30.CALCIUM CHANNEL BLOCKERS
Alpha-blockers: enhanced hypotensive effect when calcium-channel blockers
given with .alpha-blockers, also increased risk of first-dose hypotension with
post-synaptic alpha-blockers such as prazosin.
Anaesthetics, General: enhanced hypotensive effect when calcium-channel
blockers given with general anaesthetics or isoflurane; hypotensive effect of
verapamil.
Anti-arrhythmics: increased risk of bradycardia, AV block and myocardial
depression when diltiazem or verapamil given with .amiodarone; increased risk of
myocardial depression and asystole when verapamil given with .disopyramide or
.flecainide.
Antibacterials: metabolism of verapamil possibly inhibited by .clarithromycin and
.erythromycin (increased risk of toxicity); metabolism of felodipine possibly
inhibited by erythromycin (increased plasma concentration); manufacturer of
lercanidipine advises avoid concomitant use with erythromycin; metabolism of
diltiazem, nifedipine, nimodipine and verapamil accelerated by .rifampicin (plasma
concentration significantly reduced); metabolism of isradipine and nicardipine
possibly accelerated by .rifampicin (possible significantly reduced plasma
concentration); plasma concentration of nifedipine increased by
.quinupristin/dalfopristin.
21
22. Antiepileptics: effects of dihydropyridines, nicardipine and nifedipine probably
reduced by carbamazepine; effects of felodipine and isradipine reduced by
carbamazepine; diltiazem and verapamil enhance effects of .carbamazepine;
effects of dihydropyridines, nicardipine and nifedipine probably reduced by
.phenytoin; effects of felodipine, isradipine and verapamil reduced by phenytoin;
diltiazem increases plasma concentration of .phenytoin but also effect of diltiazem
reduced; effects of felodipine and isradipine reduced by .primidone; effects of
dihydropyridines, diltiazem and verapamil probably reduced by .primidone.
Antifungals: metabolism of dihydropyridines possibly inhibited by itraconazole
and ketoconazole (increased plasma concentration); metabolism of felodipine
inhibited by .itraconazole and .ketoconazole (increased plasma concentration);
manufacturer of lercanidipine advises avoid concomitant use with itraconazole and
ketoconazole; negative inotropic effect possibly increased when calcium-channel
blockers given with itraconazole; plasma concentration of nifedipine increased by
micafungin.
Antivirals: plasma concentration of verapamil possibly increased by atazanavir;
plasma concentration of diltiazem increased by .atazanavir (reduce dose of
diltiazem); plasma concentration of diltiazem reduced by efavirenz; manufacturer
of lercanidipine advises avoid concomitant use with ritonavir; plasma
concentration of calcium-channel blockers possibly increased by .ritonavir.
Barbiturates: effects of dihydropyridines, diltiazem and verapamil probably
reduced by .barbiturates; effects of felodipine and isradipine reduced by
.barbiturates. calcium-channel blockers given with beta-blockers;
increased risk of AV block and bradycardia when diltiazem given with .beta-
blockers; asystole, severe hypotension and heart failure when verapamil given
with .beta-blockers; possible severe hypotension and heart failure when nifedipine
given with .beta-blockers.
Cardiac Glycosides: nifedipine possibly increases plasma concentration of
.digoxin; diltiazem, lercanidipine and nicardipine increase plasma concentration
of .digoxin; verapamil increases plasma concentration of .digoxin, also increased
risk of AV block and bradycardia.
Ciclosporin: diltiazem, nicardipine and verapamil increase plasma concentration
of .ciclosporin; combination of lercanidipine with .ciclosporin may increase plasma
concentration of either drug (or both)—avoid concomitant use; plasma
concentration of nifedipine possibly increased by ciclosporin (increased risk of
toxicity including gingival hyperplasia).
Cilostazol: diltiazem increases plasma concentration of cilostazol—avoid
concomitant use.
Ivabradine: diltiazem and verapamil increase plasma concentration ofivabradine
—avoid concomitant use
Lipid-regulating Drugs: diltiazem increases plasma concentration of atorvastatin
possible increased risk of myopathy when diltiazem given with simvastatin;
increased risk of myopathy when verapamil given with .simvastatin.
22
23. Magnesium (parenteral): profound hypotension reported with concomitant use
of nifedipine and .parenteral magnesium in pre-eclampsia.
Sirolimus: diltiazem increases plasma concentration of .sirolimus; plasma
concentration of both drugs increased when verapamil given with .sirolimus.
Tacrolimus: diltiazem and nifedipine increase plasma concentration of
.tacrolimus; felodipine, nicardipine and verapamil possibly increase plasma
concentration of tacrolimus.
Theophylline: calcium-channel blockers possibly increase plasma concentration of
theophylline (enhance effect);diltiazem increases plasma concentration of theophy
lline; verapamil increases lasma concentration of .theophylline (enhanced effect).
31.CARBAMAZEPINE
Analgesics: effects of carbamazepine enhanced by .dextropropoxyphene;
carbamazepine reduces plasma concentration of methadone; carbamazepine
reduces effects of tramadol; carbamazepine possibly accelerates metabolism of
paracetamol.
Antibacterials: plasma concentration of carbamazepine increased by
clarithromycin and erythromycin; plasma concentration of carbamazepine reduced
by .rifabutin; carbamazepine accelerates metabolism of doxycycline (reduced
effect); plasma concentration of carbamazepine increased by isoniazid (also
possibly increased isoniazid hepatotoxicity); carbamazepine reduces plasma
concentration of telithromycin (avoid during & for 2 weeks after carbamazepine).
Anticoagulants: carbamazepine accelerates metabolism of .coumarins (reduced
anticoagulant effect).
Antidepressants: plasma concentration of carbamazepine increased by
.fluoxetine and .fluvoxamine; carbamazepine reduces plasma concentration of
mianserin, mirtazapine and paroxetine; manufacturer of carbamazepine advises
avoid for 2 weeks after stopping .MAOIs, also antagonism of anticonvulsant effect;
anticonvulsant effect of antiepileptics possibly antagonised by MAOIs and tricyclic-
related antidepressants (convulsive threshold lowered); anticonvulsant effect of
antiepileptics antagonised by .SSRIs and .tricyclics (convulsive threshold lowered);
avoid concomitant use of antiepileptics with .St John’s wort; carbamazepine
accelerates metabolism of tricyclics (low plasma concentration & less effect).
Antifungals: plasma concentration of carbamazepine possibly increased by
fluconazole, ketoconazole and miconazole; carbamazepine possibly reduces
plasma concentration of itraconazole and .posaconazole; carbamazepine possibly
reduces plasma concentration of .voriconazole—avoid concomitant use;
carbamazepine possibly reduces plasma concentration of caspofungin—consider
increasing dose of caspofungin.
Antimalarials: possible increased risk of convulsions when antiepileptics given
with chloroquine and hydroxychloroquine; anticonvulsant effect of antiepileptics
antagonised by .mefloquine.
Antipsychotics: anticonvulsant effect of carbamazepine antagonised by
antipsychotics (convulsive threshold lowered); carbamazepine accelerates
23
24. metabolism of haloperidol, olanzapine, quetiapine, risperidone and sertindole
(reduced plasma concentration); carbamazepine reduces plasma concentration of
aripiprazole—increase dose of aripiprazole; carbamazepine accelerates metabolism
of .clozapine (reduced plasma concentration), also avoid concomitant use of drugs
with substantial potential for causing agranulocytosis; carbamazepine reduces
plasma concentration of paliperidone.
Antivirals: carbamazepine possibly reduces plasma concentration of darunavir,
fosamprenavir, lopinavir, nelfinavir, saquinavir and tipranavir; plasma
concentration of both drugs reduced when carbamazepine given with efavirenz;
avoidance of carbamazepine advised by manufacturer of etravirine;
carbamazepine possibly reduces plasma concentration of indinavir, also plasma
concentration of carbamazepine possibly increased; plasma concentration of
carbamazepine possibly increased by .ritonavir.
Calcium-channel Blockers: carbamazepine reduces effects of felodipine and
isradipine; carbamazepine. probably reduces effects of dihydropyridines,
nicardipine and nifedipine; effects of carbamazepine enhanced by .diltiazem and
.verapamil
Cardiac Glycosides: carbamazepine accelerates metabolism of digitoxin (reduced
effect)
Ciclosporin: carbamazepine accelerates metabolism of ciclosporin (reduced
plasma concentration) Corticosteroids: carbamazepine accelerates metabolism
of .corticosteroids (reduced effect).
Cytotoxics: carbamazepine reduces plasma concentration of .imatinib and
lapatinib—avoid concomitant use; carbamazepine reduces plasma concentration of
irinotecan and its active metabolite.
Diuretics: increased risk of hyponatraemia when carbamazepine given with
diuretics; plasma concentration of carbamazepine increased by acetazolamide;
carbamazepine reduce plasma concentration of eplerenone avoid concomitant use.
Hormone Antagonists: metabolism of carbamazepine inhibited by .danazol
(increased risk of toxicity); carbamazepine accelerates metabolism of gestrinone
(reduced plasma concentration); carbamazepine possibly accelerates metabolism
of toremifene (reduced plasma concentration).
Oestrogens: carbamazepine accelerates metabolism of oestrogens (reduced
contraceptive effect.
Progestogens: carbamazepine accelerates metabolism of .progestogens (reduced
contraceptive effect.
Ulcer-healing Drugs: metabolism of carbamazepine inhibited by .cimetidine
(increased plasma concentration).
32.CARDIAC GLYCOSIDES
Anti-arrhythmics: plasma concentration of digoxin increased by .amiodarone and
propafenone (halve dose of digoxin).
Antidepressants: plasma concentration of digoxin reduced by .St John’s wort—
avoid concomitant use.
24
25. Antifungals: increased cardiac toxicity with cardiac glycosides if hypokalaemia
occurs with amphotericin; plasma concentration of digoxin increased by
itraconazole.
Antimalarials: plasma concentration of digoxin possibly increased by .chloroquine
and hydroxychloroquine; possible increased risk of bradycardia when digoxin given
with mefloquine; plasma concentration of digoxin increased by .quinine.
Calcium-channel Blockers: plasma concentration of digoxin increased by
diltiazem, .lercanidipine and nicardipine; plasma concentration of digoxin possibly
increased by .nifedipine; plasma concentration of digoxin increased by .verapamil,
also increased risk of AV block and bradycardia.
Ciclosporin: plasma concentration of digoxin increased by .ciclosporin (increased
risk of toxicity).
Corticosteroids: increased risk of hypokalaemia when cardiac glycosides given
with corticosteroids.
Cytotoxics: absorption of digoxin tablets reduced by cytotoxics
Diuretics: increased cardiac toxicity with cardiac glycosides if hypokalaemia
occurs with acetazolamide, .loop diuretics or .thiazides and related diuretics;
plasma concentration of digoxin possibly increased by potassium canrenoate;
plasma concentration of digitoxin possibly affected by spironolactone; plasma
concentration of digoxin increased by .spironolactone.
33.CARMUSTINE
Antipsychotics: avoid concomitant use of cytotoxics with .clozapine (increased risk
of agranulocytosis).
34.CASPOFUNGIN
Ciclosporin: plasma concentration of caspofungin increased by .ciclosporin
(manufacturer of caspofungin recommends monitoring liver enzymes)
Corticosteroids: plasma concentration of caspofungin.
possibly reduced by dexamethasone—consider increasing dose of caspofungin
Tacrolimus: caspofungin reduces plasma concentration of .tacrolimus.
35.CEPHALOSPORINS
Anticoagulants: cephalosporins possibly enhance anticoagulant effect of
coumarins.
Anticoagulants: chloramphenicol enhances anticoagulant effect of .coumarins
Antidiabetics: chloramphenicol enhances effects of sulphonylureas.
Antiepileptics: chloramphenicol increases plasma concentration of .phenytoin
(increased risk of toxicity); metabolism of chloramphenicol accelerated by
.primidone (reduced plasma concentration).
Antipsychotics: avoid concomitant use of chloramphenicol with .clozapine
(increased risk of agranulocytosis).
Barbiturates: metabolism of chloramphenicol accelerated by .barbiturates
(reduced plasma concentration).
25
26. Ciclosporin: chloramphenicol possibly increases plasma concentration of
ciclosporin.
Tacrolimus: chloramphenicol possibly increases plasma concentration of
tacrolimus.
36.CHLOROQUINE AND HYDROXY CHLOROQUINE
Anti-arrhythmics: increased risk of ventricular arrhythmias when chloroquine
and hydroxychloroquine given with .amiodarone—avoid concomitant use.
Antibacterials: increased risk of ventricular arrhythmias when chloroquine and
hydroxychloroquine given with .moxifloxacin—avoid concomitant use.
Antimalarials: avoidance of antimalarials advised by manufacturer of
artemether/lumefantrine; increased risk of convulsions when chloroquine and
hydroxychloroquine given with .mefloquine
Cardiac Glycosides: chloroquine and hydroxychloroquine possibly increase
plasma concentration of digoxin.
Ciclosporin: chloroquine and hydroxychloroquine increase plasma concentration
of .ciclosporin (increased risk of toxicity).
37.CICLOSPORIN
ACE Inhibitors: increased risk of hyperkalaemia when ciclosporin given with .ACE
inhibitors.
Analgesics: increased risk of nephrotoxicity when ciclosporin given with .NSAIDs;
ciclosporin increases plasma concentration of .diclofenac (halve dose of
diclofenac). Angiotensin-II Receptor Antagonists: increased risk of hyperkalaemia
when ciclosporin given with .angiotensin- II receptor antagonists.
Antibacterials: metabolism of ciclosporin inhibited by clarithromycin and
erythromycin (increased plasma concentration); metabolism of ciclosporin
accelerated by .rifampicin (reduced plasma concentration); plasma concentration
of ciclosporin possibly reduced by .sulfadiazine; plasma concentration of
ciclosporin possibly increased by .chloramphenicol, doxycycline and .telithromycin;
increased risk of nephrotoxicity when ciclosporin given with aminoglycosides,
.polymyxins, .quinolones, sulphonamides or .vancomycin; increased risk of
myopathy when ciclosporin given with .daptomycin (preferably avoid concomitant
use); metabolism of ciclosporin possibly inhibited by .macrolides (increased
plasma concentration); plasma concentration of ciclosporin increased by
.quinupristin/ dalfopristin; increased risk of nephrotoxicity when ciclosporin given
with .trimethoprim, also plasma concentration of ciclosporin reduced by
intravenous trimethoprim.
Antidepressants: plasma concentration of ciclosporin reduced by .St John’s wort
—avoid concomitant use.
Antidiabetics: ciclosporin possibly enhances hypoglycaemic effect of repaglinide
Antiepileptics: metabolism of ciclosporin accelerated by .carbamazepine and
.phenytoin (reduced plasma concentration); plasma concentration of ciclosporin
26
27. possibly reduced by oxcarbazepine; metabolism of ciclosporin accelerated by
primidone (reduced effect).
Antifungals: metabolism of ciclosporin inhibited by fluconazole, .itraconazole,
.ketoconazole, posaconazole and .voriconazole (increased plasma concentration);
metabolism of ciclosporin possibly inhibited by .miconazole (increased plasma
concentration); increased risk of nephrotoxicity when ciclosporin given with
.amphotericin; ciclosporin increases plasma concentration of .caspofungin
(manufacturer of caspofungin recommends monitoring liver enzymes); plasma
concentration of ciclosporin possibly reduced by griseofulvin; plasma concentration
of ciclosporin possibly increased by micafungin.
Antimalarials: plasma concentration of ciclosporin increased by .chloroquine and
hydroxychloroquine (increased risk of toxicity).
Antimuscarinics: avoidance of ciclosporin advised by manufacturer of darifenacin
Antivirals: increased risk of nephrotoxicity when ciclosporin given with aciclovir;
plasma concentration of ciclosporin possibly increased by .atazanavir, nelfinavir
and .ritonavir; plasma concentration of ciclosporin increased by .indinavir; plasma
concentration of both drugs increased when ciclosporin given with .saquinavir.
Barbiturates: metabolism of ciclosporin accelerated by barbiturates (reduced
effect).
Beta-blockers: plasma concentration of ciclosporin increased by .carvedilol
Bile Acids: absorption of ciclosporin increased by ursodeoxycholic acid.
Bosentan: ciclosporin increases plasma concentration of .bosentan (also plasma
concentration of ciclosporin reduced—avoid concomitant use).
Calcium-channel Blockers: combination of ciclosporin with .lercanidipine may
increase plasma concentrationof either drug (or both)—avoid concomitant use;
plasma concentration of ciclosporin increased by diltiazem, .nicardipine and
verapamil; ciclosporin possibly increases plasma concentration of nifedipine
(increased risk of toxicity including gingival hyperplasia).
Cardiac Glycosides: ciclosporin increases plasma oncentration of .digoxin
(increased risk of toxicity).
Colchicine: possible increased risk of nephrotoxicity and myotoxicity when
ciclosporin given with colchicine (increased plasma concentration of ciclosporin).
Corticosteroids: plasma concentration of ciclosporin increased by high-dose
methylprednisolone (risk of convulsions); ciclosporin increases plasma
concentration of prednisolone.
Cytotoxics: increased risk of nephrotoxicity when ciclosporin given with
melphalan; increased risk of neurotoxicity when ciclosporin given with doxorubicin;
risk of toxicity when ciclosporin given with .methotrexate; plasma concentration of
ciclosporin possibly increased by imatinib; in vitro studies
suggest a possible interaction between ciclosporin and docetaxel (consult
docetaxel product literature); ciclosporin possibly increases plasma concentration
of etoposide (increased risk of toxicity).
27
28. Diuretics: increased risk of hyperkalaemia when ciclosporin given with potassium-
sparing diuretics and aldosterone antagonists; increased risk of nephrotoxicity and
possibly hypermagnesaemia when ciclosporin given with thiazides and related
Diuretics.
Grapefruit Juice: plasma concentration of ciclosporin increased by .grapefruit
juice (increased risk of toxicity).
Hormone Antagonists: metabolism of ciclosporin inhibited by danazol (increased
plasma concentration); plasma concentration of ciclosporin reduced by lanreotide
and .octreotide.
Lipid-regulating Drugs: increased risk of renal impairment when ciclosporin
given with bezafibrate or fenofibrate; increased risk of myopathy when ciclosporin
given with .rosuvastatin (avoid concomitant use); plasma concentration of both
drugs may increase when ciclosporin given with .ezetimibe; increased risk of
myopathy when ciclosporin given with .statins.
Metoclopramide: plasma concentration of ciclosporin increased by
metoclopramide.
Modafinil: plasma concentration of ciclosporin reduced by modafinil.
Oestrogens: plasma concentration of ciclosporin possibly increased by
oestrogens.
Orlistat: absorption of ciclosporin possibly reduced by orlistat Potassium Salts:
increased risk of hyperkalaemia when ciclosporin given with .potassium salts
Progestogens: metabolism of ciclosporin inhibited by progestogens (increased
plasma concentration).
Sevelamer: plasma concentration of ciclosporin possibly reduced by sevelamer
Sirolimus: ciclosporin increases plasma concentration of sirolimus.
Sitaxentan: ciclosporin increases plasma concentration of sitaxentan .Avoid
concomitant use.
Sulfinpyrazone: plasma concentration of ciclosporin reduced by .sulfinpyrazone
Tacrolimus: plasma concentration of ciclosporin increased by .tacrolimus
(increased risk of nephrotoxicity). Avoid concomitant use.
Ulcer-healing Drugs: plasma concentration of ciclosporin possibly increased by
cimetidine; plasma concentration of ciclosporin possibly affected by omeprazole.
38.CILOSTAZOL
Anagrelide: avoidance of cilostazol advised by manufacturer of .anagrelide.
Antibacterials: plasma concentration of cilostazol increased by .erythromycin
(also plasma concentration of erythromycin reduced)—avoid concomitant use.
Antifungals: plasma concentration of cilostazol possibly increased by
ketoconazole—avoid concomitant use.
Antivirals: plasma concentration of cilostazol possibly increased by
fosamprenavir, .indinavir, .lopinavir, nelfinavir, .ritonavir and .saquinavir—avoid
concomitant use.
Calcium-channel Blockers: plasma concentration of cilostazol increased by
diltiazem—avoid concomitant use.
28
29. Ulcer-healing Drugs: plasma concentration of cilostazol possibly increased by
cimetidine and lansoprazole—avoid concomitant use; plasma concentration of
cilostazol increased by .omeprazole (risk of toxicity)—avoid concomitant use.
Muscle Relaxants: clindamycin enhances effects of non-depolarising muscle
relaxants and .suxamethonium.
39.CLONIDINE
Antidepressants: enhanced hypotensive effect when clonidine given with MAOIs;
hypotensive effect of clonidine antagonised by .tricyclics, also increased risk of
hypertension on clonidine withdrawal.
Beta-blockers: increased risk of withdrawal hypertension when clonidine given
with .beta-blockers (withdraw beta-blockers several days before slowly
withdrawing clonidine).
Sympathomimetics: possible risk of hypertension when clonidine given with
adrenaline (epinephrine) or noradrenaline (norepinephrine); serious adverse
events reported with concomitant use of clonidine and .methylphenidate (causality
not established).
40.CLOPIDOGRIL
Anticoagulants: manufacturer advises avoid concomitant use with warfarin;
antiplatelet action of clopidogrel enhances anticoagulant effect of coumarins and
phenindione; increased risk of bleeding when clopidogrel given with heparins.
41.COLCHICINE
Antibacterials: increased risk of colchicine toxicity when given with
clarithromycin or .erythromycin.
Ciclosporin: possible increased risk of nephrotoxicity and myotoxicity when
colchicine given with ciclosporin (increased plasma concentration of ciclosporin).
Lipid-regulating Drugs: possible increased risk of myopathy when colchicine
given with .statins.
42.COLESTYRAMINE
Anticoagulants: colestyramine may enhance or reduce anticoagulant effect of
coumarins and phenindione.
43.CORTICOSTEROIDS
Antibacterials: plasma concentration of methylprednisolone possibly increased by
clarithromycin; metabolism of corticosteroids possibly inhibited by erythromycin;
metabolism of methylprednisolone inhibited by erythromycin; corticosteroids
possibly reduce plasma concentration of isoniazid; metabolism of corticosteroids
accelerated by rifamycins (reduced effect).
Anticoagulants: corticosteroids may enhance or reduce anticoagulant effect of
coumarins (high-dose corticosteroids enhance anticoagulant effect).
29
30. Antiepileptics: metabolism of corticosteroids accelerated by .carbamazepine,
phenytoin and .primidone (reduced effect).
Antifungals: metabolism of corticosteroids possibly inhibited by itraconazole and
ketoconazole; plasma concentration of active metabolite of ciclesonide increased
by ketoconazole; plasma concentration of inhaled mometasone increased by
ketoconazole; plasma concentration of inhaled and oral budesonide increased by
ketoconazole; metabolism of methylprednisolone inhibited by ketoconazole;
increased risk of hypokalaemia when corticosteroids given with amphotericin—
avoid concomitant use unless corticosteroids needed to control reactions; plasma
concentration of inhaled budesonide increased by itraconazole; metabolism of
methylprednisolone possibly inhibited by itraconazole; dexamethasone possibly
reduces plasma concentration of caspofungin— consider increasing dose of
caspofungin.
Antivirals: dexamethasone possibly reduces plasma concentration of indinavir,
lopinavir and saquinavir; plasma concentration of corticosteroids, dexamethasone
and prednisolone possibly increased by ritonavir; plasma concentration of inhaled
andintranasal budesonide and fluticasone increased by ritonavir.
Barbiturates: metabolism of corticosteroids accelerated by .barbiturates (reduced
effect).
Ciclosporin: high-dose methylprednisolone increases plasma concentration of
.ciclosporin (risk of convulsions); plasma concentration of prednisolone increased
by ciclosporin.
Clonidine: corticosteroids antagonise hypotensive effect of clonidine.
Cytotoxics: increased risk of haematological toxicity when corticosteroids given
with .methotrexate.
Diazoxide: corticosteroids antagonise hypotensive effect of diazoxide.
Vaccines: high doses of corticosteroids impair immune response to .vaccines,
avoid concomitant use with live vaccines.
44.COUMARINS
Alcohol: anticoagulant control with coumarins may be affected by major changes
in consumption of alcohol.
Anabolic Steroids: anticoagulant effect of coumarins nhanced by .anabolic
steroids.
Analgesics: anticoagulant effect of coumarins possibly nhanced by .NSAIDs,
celecoxib,dextropropoxyphene, .etodolac, .etoricoxib, flurbiprofen, .ibuprofen,
mefenamic acid, meloxicam, .parecoxib, .piroxicam and .sulindac; anticoagulant
effect of coumarins enhanced by azapropazone (avoid concomitant use); anticoagu
lant effect of coumarins possibly enhanced by diclofenac, also increased risk of
haemorrhage with intravenous diclofenac (avoid concomitant use); increased risk
of bleeding when coumarins given with ketorolac (avoid concomitant use); anticoa
guant effect of coumarins enhanced by .tramadol; increased risk of bleeding when
coumarins given with aspirin (due to antiplatelet effect); anticoagulant effect of
coumarins possibly enhanced by prolonged regular use of paracetamol.
30
31. Anti-arrhythmics: metabolism of coumarins inhibited by amiodarone (enhanced
anticoagulant effect); anticoagulant effect of coumarins enhanced by propafenone
Antibacterials: experience in anticoagulant clinics suggests that INR possibly
altered when coumarins are given with .neomycin (given for local action on
gut); anticoagulant effect of coumarins possibly enhanced by .azithromycin,
.aztreonam,cephalosporins, levofloxacin, .tetracyclines, tigecycline and
trimethoprim; anticoagulant effect of coumarins enhanced by .chloramphenicol,
ciprofloxacin, .clarithromycin, .erythromycin, metronidazole, .nalidixic acid,
norfloxacin, ofloxacin and .sulphonamides; studies have failed to demonstrate an
interaction with coumarins, but common experience in anticoagulant clinics is that
INR can be altered by a course of broad-spectrum penicillins such as ampicillin;
metabolism of coumarins accelerated by .rifamycins (reduced anticoagulant effect)
Antidepressants: anticoagulant effect of warfarin possibly enhanced by
venlafaxine; anticoagulant effect of coumarins possibly enhanced by SSRIs;
anticoagulant effect of coumarins reduced by .StJohn’s wort (avoid concomitant
use); anticoagulant effect of warfarin enhanced by mirtazapine; anticoagulant
effect of coumarins may be enhanced or reduced by .tricyclics.
Antidiabetics: anticoagulant effect of warfarin possibly enhanced by exenatide;
coumarins possibly enhance hypoglycaemic effect of .sulphonylureas, also possible
changes to anticoagulant effect.
Antiepileptics: metabolism of coumarins accelerated by .carbamazepine and
.primidone (reduced anticoagulant effect); metabolism of coumarins accelerated
by .phenytoin (possibility of reduced anticoagulant effect, but enhancement also
reported); anticoagulant effect of coumarins possibly enhanced by valproate.
Antifungals: anticoagulant effect of coumarins enhanced by .fluconazole,
itraconazole, ketoconazole and .voriconazole; anticoagulant effect of coumarins
enhanced by .miconazole (miconazole oral gel and possibly vaginal formulations
absorbed); anticoagulant effect of coumarins reduced by .griseofulvin.
Antimalarials: isolated reports that anticoagulant effect of warfarin may be
enhanced by proguanil.
Antivirals: anticoagulant effect of warfarin may be enhanced or reduced by
atazanavir, .nevirapine and ritonavir; anticoagulant effect of coumarins may be
enhanced or reduced by fosamprenavir; anticoagulant effect of coumarins possibly
enhanced by ritonavir; anticoagulant effect of warfarin possibly enhanced by
saquinavir.
Anxiolytics and Hypnotics: anticoagulant effect of coumarins may transiently be
enhanced by chloral and triclofos
Aprepitant: anticoagulant effect of warfarin possibly reduced by aprepitant
Barbiturates: metabolism of coumarins accelerated by barbiturates (reduced
anticoagulant effect).
Bosentan: monitoring anticoagulant effect of coumarins recommended by
manufacturer of bosentan Clopidogrel: anticoagulant effect of coumarins enhanced
due to antiplatelet action of .clopidogrel; avoidance of warfarin advised by
manufacturer of clopidogrel.
31
32. Corticosteroids: anticoagulant effect of coumarins may be enhanced or reduced
by .corticosteroids (highdose corticosteroids enhance anticoagulant effect)
Cranberry Juice: anticoagulant effect of coumarins possibly enhanced by
.cranberry juice—avoid concomitant use.
Cytotoxics: anticoagulant effect of coumarins possibly enhanced by .etoposide,
ifosfamide and .sorafenib; anticoagulant effect of coumarins enhanced by
fluorouracil; anticoagulant effect of coumarins possibly reduced by .azathioprine,
mercaptopurine and .mitotane; increased risk of bleeding when coumarins given
with .erlotinib; replacement of warfarin with a heparin advised by manufacturer of
imatinib (possibility of enhanced warfarin effect).
Dipyridamole: anticoagulant effect of coumarins enhanced due to antiplatelet
action of .dipyridamole.
Disulfiram: anticoagulant effect of coumarins enhanced by .disulfiram.
Dopaminergics: anticoagulant effect of warfarin enhanced by .entacapone.
Enteral Foods: anticoagulant effect of coumarins antagonised by vitamin K
(present in some .enteral feeds ).
Glucosamine: anticoagulant effect of warfarin enhanced by .glucosamine (avoid
concomitant use).
Hormone Antagonists: anticoagulant effect of coumarins possibly enhanced by
bicalutamide and toremifene; metabolism of coumarins inhibited by .danazol
(enhanced anticoagulant effect); anti-coagulant effect of coumarins enhanced by
flutamide and .tamoxifen.
Levamisole: anticoagulant effect of warfarin possibly enhanced by .levamisole
Lipid-regulating Drugs: anticoagulant effect of coumarinsmay be enhanced or
reduced by.colestyramine; anticoagulant effect of warfarin may be transiently
reduced by atorvastatin; anticoagulant effect of coumarins enhanced by .fibrates,
.fluvastatin and simvastatin; anticoagulant effect of coumarins possibly enhanced
by ezetimibe and .rosuvastatin.
Memantine: anticoagulant effect of warfarin possibly enhanced by memantine
Oestrogens: anticoagulant effect of coumarins may be enhanced or reduced by
oestrogens
Orlistat: monitoring anticoagulant effect of coumarins recommended by
manufacturer of orlistat.
Progestogens: anticoagulant effect of coumarins may be enhanced or reduced by
progestogens.
Raloxifene: anticoagulant effect of coumarins antagonized by raloxifene.
Retinoids: anticoagulant effect of coumarins possibly reduced by .acitretin.
Sibutramine: increased risk of bleeding when anticoagulants given with
sibutramine
Sitaxentan: anticoagulant effect of coumarins enhanced by .sitaxentan
Sulfinpyrazone: anticoagulant effect of coumarins enhanced by .sulfinpyrazone.
Sympathomimetics: anticoagulant effect of coumarins possibly enhanced by
.methylphenidate
32
33. Terpene Mixture: anticoagulant effect of coumarins possibly reduced by
Rowachol.
Testolactone: anticoagulant effect of coumarins enhanced by .testolactone
Testosterone: anticoagulant effect of coumarins enhanced by .testosterone
Thyroid Hormones: anticoagulant effect of coumarins enhanced by .thyroid
hormones.
Ubidecarenone: anticoagulant effect of warfarin may be enhanced or reduced by
ubidecarenone.
Ulcer-healing Drugs: metabolism of coumarins inhibited by .cimetidine
(enhanced anticoagulant effect); anticoagulant effect of coumarins possibly
enhanced by esomeprazole, .omeprazole and pantoprazole; absorption of
coumarins possibly reduced by sucralfate (reduced anticoagulant effect).
Vaccines: anticoagulant effect of warfarin possibly enhanced by influenza vaccine
Vitamins: anticoagulant effect of coumarins antagonized by .vitamin K.
45.CYCLOPHOSPHAMIDE
Antipsychotics: avoid concomitant use of cytotoxics with .clozapine (increased
risk of agranulocytosis).
Cytotoxics: increased toxicity when high-dose cyclophosphamide given with
pentostatin—avoid concomitant use.
46.CYCLOSERINE
Alcohol: increased risk of convulsions when cycloserine given with .alcohol.
47.CYTARABINE
Antipsychotics: avoid concomitant use of cytotoxics with .clozapine (increased
risk of agranulocytosis).
Analgesics: possible increased risk of bleeding when dabigatran etexilate given
with .NSAIDs.
Anti-arrhythmics: plasma concentration of dabigatran etexilate increased by
amiodarone (reduce dose of dabigatran etexilate).
48.DANAZOL
Anticoagulants: danazol inhibits metabolism of coumarins (enhanced
anticoagulant effect).
Antiepileptics: danazol inhibits metabolism of carbamazepine(increased toxicity).
Ciclosporin: danazol inhibits metabolism of ciclosporin (increased plasma
concentration).
Lipid-regulating Drugs: possible increased risk of myopathy when danazol given
with .simvastatin.
49.DAPTOMYCIN
Ciclosporin: increased risk of myopathy when daptomycin given with .ciclosporin
(preferably avoid concomitant use).
33
34. Lipid-regulating Drugs: increased risk of myopathy when daptomycin given with
fibrates or .statins (preferably avoid concomitant use).
50.DARUNAVIR
Antibacterials: darunavir increases plasma concentration of .rifabutin (reduce
dose of rifabutin); plasma concentration of darunavir significantly reduced by
rifampicin—avoid concomitant use.
Antidepressants: darunavir possibly reduces plasma concentration of paroxetine
and sertraline; plasma concentration of darunavir reduced by .St John’s wort—
avoid concomitant use.
Antivirals: plasma concentration of darunavir reduced by efavirenz and
saquinavir; plasma concentration of both drugs increased when darunavir given
with indinavir; plasma concentration of darunavir reduced by .lopinavir, also
plasma concentration of lopinavir increased (avoid concomitant use); darunavir
increases plasma concentration of .maraviroc (consider reducing dose of
maraviroc).
Lipid-regulating Drugs: darunavir possibly increases plasma concentration of
pravastatin; possible increased risk of myopathy when darunavir given with
.rosuvastatin—avoid concomitant use.
51.DASATINIB
Antibacterials: metabolism of dasatinib accelerated by rifampicin (reduced
plasma concentration—avoid concomitant use).
Antipsychotics: avoid concomitant use of cytotoxics with .clozapine (increased
risk of agranulocytosis).
Cardiac Glycosides: cytotoxics reduce absorption of digoxin tablets.
52.DIDANOSINE
Allopurinol: plasma concentration of didanosine increased by .allopurinol (risk of
toxicity)—avoid concomitant use.
Antivirals: plasma concentration of didanosine possibly increased by ganciclovir;
increased risk of side-effects when didanosine given with .ribavirin—avoid
concomitant use; increased risk of side-effects when didanosine given with
stavudine; plasma concentration of didanosine increased by .tenofovir (increased
risk of toxicity)—avoid concomitant use;. plasma concentration of didanosine
reduced by tipranavir.
Cytotoxics: increased risk of toxicity when didanosine given with hydroxy
carbamide—avoid concomitant use.
53.DIMERCAPROL
Iron: avoid concomitant use of dimercaprol with .iron.
54.DIMETHYL SULFOXIDE
Analgesics: avoid concomitant use of dimethyl sulfoxide with .sulindac.
34
35. 55.DIPYRIDAMOLE
Anti-arrhythmics: dipyridamole enhances and extends he effects of .adenosine
(important risk of toxicity).
Anticoagulants: antiplatelet action of dipyridamole enhances anticoagulant effect
of .coumarins and henindione; dipyridamole enhances anticoagulant effect of
heparins.
56.DISOPYRAMIDE
Anti-arrhythmics: increased myocardial depression when anti-arrhythmics given
with other .antiarrhythmics; increased risk of ventricular arrhythmias when
disopyramide given with .amiodarone—avoid concomitant use.
Antibacterials: plasma concentration of disopyramide possibly increased by
clarithromycin (increased risk of toxicity); plasma concentration of disopyramide
increased by .erythromycin (increased risk of toxicity); increased risk of
ventricular arrhythmias when disopyramide given with .moxifloxacin or
.quinupristin/ dalfopristin—avoid concomitant use; metabolism of disopyramide
accelerated by .rifamycins (reduced plasma concentration)
Antidepressants: increased risk of ventricular arrhythmias when disopyramide
given with .tricyclics.
Antifungals: increased risk of ventricular arrhythmias when disopyramide given
with .ketoconazole—avoid concomitant use; avoidance of disopyramide advised by
manufacturer of .itraconazole.
Antihistamines: increased risk of ventricular arrhythmias when disopyramide
given with .mizolastine— avoid concomitant use.
Antimalarials: avoidance of disopyramide advised by manufacturer
ofartemether /lumefantrine (risk of ventricular arrhythmias).
Antimuscarinics: increased risk of antimuscarinic sideeffects when disopyramide
given with antimuscarinics; increased risk of ventricular arrhythmias when
disopyramide given with .tolterodine.
Antipsychotics: increased risk of ventricular arrhythmias when anti-arrhythmics
that prolong the QT interval given with .antipsychotics that prolong the QT
interval; increased risk of ventricular arrhythmias when disopyramide given with
amisulpride, .pimozide, .sertindole or zuclopenthixol—avoid concomitant use;
increased risk of ventricular arrhythmias when disopyramide given with
phenothiazines or sulpiride.
Antivirals: plasma concentration of disopyramide possibly increased by .ritonavir
(increased risk of toxicity).
Atomoxetine: increased risk of ventricular arrhythmias when disopyramide given
with .atomoxetine.
Beta-blockers: increased myocardial depression when anti-arrhythmics given
with .beta-blockers; increased risk of ventricular arrhythmias when disopyramide
given with .sotalol—avoid concomitant use.
Calcium-channel Blockers: increased risk of myocardial depression and asystole
when disopyramide given with .verapamil.
35
36. Diuretics: increased cardiac toxicity with disopyramide if hypokalaemia occurs
with .acetazolamide, .loop diuretics or .thiazides and related diuretics.
5HT Antagonists: increased risk of ventricular arrhythmias when disopyramide
given with .dolasetron— avoid concomitant use.
Ivabradine: increased risk of ventricular arrhythmias when disopyramide given
with .ivabradine.
57.DISULFIRAM
Anticoagulants: disulfiram enhances anticoagulant effect of .coumarins.
Antiepileptics: disulfiram inhibits metabolism of phenytoin (increased risk of
toxicity).
Paraldehyde: risk of toxicity when disulfiram given with .paraldehyde.
58.DIURETICS
ACE Inhibitors: enhanced hypotensive effect when diuretics given with .ACE
inhibitors; increased risk of severe hyperkalaemia when potassium-sparing
diuretics and aldosterone antagonists given with .ACE inhibitors (monitor
potassium concentration with low-dose spironolactone in heart failure).
Alpha-blockers: enhanced hypotensive effect when diuretics given with .alpha-
blockers, also increased risk of first-dose hypotension with post-synaptic alpha-
blockers such as prazosin.
Analgesics: Diuretic effect of potassium canrenoate possibly antagonised by
NSAIDs; possibly increased risk of hyperkalaemia when potassium-sparing
diuretics and aldosterone antagonists given with NSAIDs; diuretics increase risk of
nephrotoxicity of NSAIDs, also antagonism of diuretic effect; effects of diuretics
antagonised by indometacin and ketorolac; increased risk of hyperkalaemia when
potassium-sparing diureticsand aldosterone antagonists given with indometacin;
occasional reports of reduced renal function when triamterene given with
.indometacin—avoid concomitant use; increased risk of toxicity when carbonic
anhydrase inhibitors given with high-dose aspirin; diuretic effect of spironolactone
antagonisedby aspirin. Angiotensin-II Receptor Antagonists: enhanced hypotensive
effect when diuretics given with angiotensin-II receptor antagonists; increased risk
of hyperkalaemia when potassium-sparing diuretics and aldosterone antagonists
given with .angiotensin-II receptor antagonists.
Anti-arrhythmics: plasma concentration of eplerenone increased by amiodarone
(reduce dose of eplerenone); hypokalaemia caused by acetazolamide, loop
diuretics or thiazides and related diuretics increases cardiac toxicity with
amiodarone; hypokalaemia caused by acetazolamide, loop diuretics or thiazides
and related diuretics increases cardiac toxicity with disopyramide; hypokalaemia
caused by acetazolamide, loop diuretics or thiazides and related diuretics increases
cardiac toxicity with .flecainide; hypokalaemia caused by acetazolamide, loop
diuretics or thiazides and related diuretics antagonizes action of .lidocaine
(lignocaine)
36
37. Antibacterials: plasma concentration of eplerenone increased by .clarithromycin
and .telithromycin— avoid concomitant use; plasma concentration of eplerenone
increased by erythromycin (reduce dose of eplerenone); plasma concentration of
eplerenone reduced by .rifampicin—avoid concomitant use; avoidance of diuretics
advised by manufacturer oflymecycline; increased risk of otoxicity when loop
diuretics given with .aminoglycosides, polymyxins or .vancomycin; acetazolamide
antagonizes effects of .methenamine; increased risk of hyperkalaemia when
eplerenone given with trimethoprim.
Antidepressants: possible increased risk of hypokalaemia when loop diuretics or
thiazides and related diuretics given with reboxetine; enhanced hypotensive effect
when diuretics given with MAOIs; plasma concentration of eplerenone reduced
by .St John’s wort—avoid concomitant use; increased risk of postural hypotension
when diuretics given with tricyclics.
Antiepileptics: plasma concentration of eplerenone reduced by .carbamazepine
and .phenytoin—avoid concomitant use; increased risk of hyponatraemia. when
diuretics given with carbamazepine; acetazolamide increases plasma concentration
of carbamazepine; effects of furosemide (frusemide) antagonised by phenytoin;
increased risk of osteomalacia when carbonic anhydrase inhibitors given with
phenytoin or primidone; acetazolamide possibly reduces plasma concentration of
Primidone.
Antifungals: plasma concentration of eplerenone increased by .itraconazole
and .ketoconazole— avoid concomitant use; increased risk of hypokalaemia when
loop diuretics or thiazides and related diuretics given with amphotericin;
hydrochlorothiazide increases plasma concentration of fluconazole; plasma
concentration of eplerenone increased by fluconazole (reduce dose of eplerenone)
Antipsychotics: hypokalaemia caused by diuretics increases risk of ventricular
arrhythmias with amisulpride or .sertindole; enhanced hypotensive effect when
diuretics given with phenothiazines; hypokalaemia caused by diuretics increases
risk of ventricular arrhythmias with .pimozide (avoid concomitant use).
Antivirals: plasma concentration of eplerenone increased by .nelfinavir and
ritonavir —avoid concomitant use; plasma concentration of eplerenone increased
by saquinavir (reduce dose of eplerenone).
Atomoxetine: hypokalaemia caused by diuretics increases risk of ventricular
arrhythmias with atomoxetine
Barbiturates: increased risk of osteomalacia when carbonic anhydrase inhibitors
given with phenobarbital; plasma concentration of eplerenone reduced by
phenobarbital—avoid concomitant use.
Beta-blockers: enhanced hypotensive effect whendiuretics given with beta-
blockers; hypokalaemia caused by loop diuretics or thiazides and related
diuretics increases risk of ventricular arrhythmias with .sotalol.
Cardiac Glycosides: hypokalaemia caused by acetazolamide, loop diuretics or
thiazides and related diuretics increases cardiac toxicity with .cardiac glycosides;
spironolactone possibly affects plasma concentration of digitoxin; spironolactone
37