Statin myopathy refers to muscle-related side effects caused by statin medications used to lower cholesterol. There are two main types: autoimmune statin myopathy and toxic statin myopathy. Autoimmune statin myopathy is rare but serious, involving muscle inflammation and weakness. Toxic statin myopathy is more common and involves temporary muscle pain and fatigue that resolves after stopping the statin. The document discusses the differences between the two conditions and reviews evidence on evaluating and managing statin intolerance. Non-statin lipid-lowering options are also summarized.
Rheumatoid arthritis is a chronic inflammatory disease that affects the joints and causes pain, swelling, stiffness and loss of function. It affects around 1% of the population worldwide. Recent advances in management include earlier diagnosis using classification criteria from ACR/EULAR and aggressive treatment with disease-modifying antirheumatic drugs alone or in combination with biological therapies that target cytokines like TNF-α. While DMARDs can control symptoms, biological therapies may induce remission and prevent further joint damage by acting faster than conventional treatments. Prompt diagnosis and management can now improve long-term outcomes for those suffering from rheumatoid arthritis.
The document discusses rheumatoid arthritis (RA), a chronic inflammatory disease that affects the joints and can damage heart tissue over time. It provides definitions of RA, discusses common symptoms like joint pain and stiffness, outlines diagnostic criteria and investigations used to diagnose the condition, such as checking for rheumatoid factor in the blood. The document also summarizes the pathological stages of RA and long term effects like joint deformity and disability.
This document provides guidelines for screening, treating, and managing lupus nephritis (LN). It defines LN and its classification system. For classes I and II LN, treatment focuses on extrarenal symptoms. Classes III and IV are treated aggressively with glucocorticoids and immunosuppressants. Maintenance therapy includes azathioprine or mycophenolate mofetil with low-dose steroids. Relapse is treated with the initial regimen. The guidelines recommend treatments and monitoring for various LN classes and complications.
Biological therapy in rheumatic diseasesSamar Tharwat
This document discusses biological therapies for rheumatic diseases. It provides a historical overview of biological therapies and reviews various cytokine inhibitors including tumor necrosis factor (TNF) inhibitors, interleukin inhibitors, T-cell and B-cell directed therapies. It summarizes several TNF inhibitors including infliximab, adalimumab, etanercept, golimumab, and certolizumab pegol. The document also reviews strategies for using biologics in rheumatoid arthritis and considerations for special patient populations.
Crystal arthropathies gout & pseudogoutShinjan Patra
Gout is one of the most dangerous underrated acute emergency in rheumatological diseases. CPPD disease is an another entity which is very much under-diagnosed in respect t OA
This document provides an overview of the approach to polyneuropathy. It begins by defining peripheral neuropathy and classifying it as mononeuropathy, multiple mononeuropathy, or polyneuropathy. It then discusses the anatomical classification and role of nerve fibers. The main etiologies of polyneuropathy are described including metabolic, toxic, vitamin deficiencies, inflammatory, infectious, hereditary, neoplastic, and idiopathic causes. The pathophysiology involves axonal degeneration, demyelination, and Wallerian degeneration. Key features that help differentiate axonal from demyelinating neuropathies are outlined. The document concludes by discussing investigations, treatment approaches, and references.
The document discusses aspirin resistance, which refers to a lack of inhibition of platelet aggregation despite regular aspirin intake at recommended doses. There are three main types of aspirin resistance - type I involves no inhibition of thromboxane synthesis, type II involves altered platelet functions both in vitro and in vivo, and type III involves inhibition of thromboxane synthesis but not platelet aggregation in response to collagen. The prevalence of aspirin resistance is estimated to be between 5-15% and is associated with a higher risk of death, heart attack or stroke. Potential causes include genetic factors, non-adherence to aspirin, use of enteric-coated aspirin or proton pump inhibitors. Laboratory testing can assess platelet function and thromboxane
Rheumatoid arthritis is a chronic inflammatory disease that affects the joints and causes pain, swelling, stiffness and loss of function. It affects around 1% of the population worldwide. Recent advances in management include earlier diagnosis using classification criteria from ACR/EULAR and aggressive treatment with disease-modifying antirheumatic drugs alone or in combination with biological therapies that target cytokines like TNF-α. While DMARDs can control symptoms, biological therapies may induce remission and prevent further joint damage by acting faster than conventional treatments. Prompt diagnosis and management can now improve long-term outcomes for those suffering from rheumatoid arthritis.
The document discusses rheumatoid arthritis (RA), a chronic inflammatory disease that affects the joints and can damage heart tissue over time. It provides definitions of RA, discusses common symptoms like joint pain and stiffness, outlines diagnostic criteria and investigations used to diagnose the condition, such as checking for rheumatoid factor in the blood. The document also summarizes the pathological stages of RA and long term effects like joint deformity and disability.
This document provides guidelines for screening, treating, and managing lupus nephritis (LN). It defines LN and its classification system. For classes I and II LN, treatment focuses on extrarenal symptoms. Classes III and IV are treated aggressively with glucocorticoids and immunosuppressants. Maintenance therapy includes azathioprine or mycophenolate mofetil with low-dose steroids. Relapse is treated with the initial regimen. The guidelines recommend treatments and monitoring for various LN classes and complications.
Biological therapy in rheumatic diseasesSamar Tharwat
This document discusses biological therapies for rheumatic diseases. It provides a historical overview of biological therapies and reviews various cytokine inhibitors including tumor necrosis factor (TNF) inhibitors, interleukin inhibitors, T-cell and B-cell directed therapies. It summarizes several TNF inhibitors including infliximab, adalimumab, etanercept, golimumab, and certolizumab pegol. The document also reviews strategies for using biologics in rheumatoid arthritis and considerations for special patient populations.
Crystal arthropathies gout & pseudogoutShinjan Patra
Gout is one of the most dangerous underrated acute emergency in rheumatological diseases. CPPD disease is an another entity which is very much under-diagnosed in respect t OA
This document provides an overview of the approach to polyneuropathy. It begins by defining peripheral neuropathy and classifying it as mononeuropathy, multiple mononeuropathy, or polyneuropathy. It then discusses the anatomical classification and role of nerve fibers. The main etiologies of polyneuropathy are described including metabolic, toxic, vitamin deficiencies, inflammatory, infectious, hereditary, neoplastic, and idiopathic causes. The pathophysiology involves axonal degeneration, demyelination, and Wallerian degeneration. Key features that help differentiate axonal from demyelinating neuropathies are outlined. The document concludes by discussing investigations, treatment approaches, and references.
The document discusses aspirin resistance, which refers to a lack of inhibition of platelet aggregation despite regular aspirin intake at recommended doses. There are three main types of aspirin resistance - type I involves no inhibition of thromboxane synthesis, type II involves altered platelet functions both in vitro and in vivo, and type III involves inhibition of thromboxane synthesis but not platelet aggregation in response to collagen. The prevalence of aspirin resistance is estimated to be between 5-15% and is associated with a higher risk of death, heart attack or stroke. Potential causes include genetic factors, non-adherence to aspirin, use of enteric-coated aspirin or proton pump inhibitors. Laboratory testing can assess platelet function and thromboxane
This document discusses the approach to evaluating musculoskeletal complaints. It notes that thorough history, physical examination, and targeted investigations are needed to differentiate between self-limited conditions and more serious issues. The assessment involves identifying patterns of joint involvement, associated symptoms, disease duration and characteristics, and examination of both local and systemic findings. Differential diagnoses are formulated based on factors like joint distribution, inflammatory markers, imaging features and disease chronology. A systematic approach is required to arrive at an accurate diagnosis and guide appropriate management.
The document discusses cerebellar ataxia and provides an outline for a lecture on the topic. It begins with definitions of ataxia and discusses the challenges in diagnosing cerebellar ataxia. It then presents a clinical scenario of a patient and outlines the topics to be covered in the lecture, including anatomy and physiology of the cerebellum, diagnostic approaches, classifications of ataxias, hereditary and acquired ataxias, treatment options, and conclusions.
This document provides guidance on evaluating patients presenting with arthritis. It discusses taking a rheumatologic history and performing a physical exam to determine if the arthritis is articular or non-articular, inflammatory or non-inflammatory, acute or chronic, and monoarticular or polyarticular. Key signs of inflammatory versus non-inflammatory arthritis are outlined. Common causes of mono/oligoarthritis like septic arthritis and gout are described. Approaches to polyarthritis and distinguishing rheumatoid arthritis from other conditions are also covered. Imaging and laboratory tests that can aid evaluation are mentioned.
Psoriatic arthritis is a chronic inflammatory disease that affects the joints and skin. It is characterized by osteolysis, bony proliferation, and can cause dactylitis, enthesitis, spondylitis, and various forms of arthritis. While it is classified as a type of spondyloarthritis, it is distinct from rheumatoid arthritis in that it is usually seronegative. The presentation and pattern of joint involvement in psoriatic arthritis can vary between patients and change over time, with the most common forms being asymmetrical oligoarthritis or symmetrical polyarthritis. Diagnosis is based on clinical features and classification criteria such as the CASPAR criteria.
This document summarizes statin-induced myopathies. It discusses statin mechanisms of action and predisposing factors. It describes different clinical phenotypes including rhabdomyolysis, myalgia with mild CK elevation, self-limited toxic myopathy, and immune-mediated necrotizing myopathy associated with anti-HMGCR antibodies. Immune-mediated necrotizing myopathy is characterized by muscle necrosis, regeneration, and scarce inflammation. Diagnosis involves detecting elevated CK, myopathic EMG findings, and anti-HMGCR antibodies. Treatment depends on severity but may include immunosuppression.
This document discusses idiopathic inflammatory myopathies (IIMs), including polymyositis, dermatomyositis, and inclusion body myositis. It reviews the clinical features, diagnostic criteria, pathology, and treatment strategies for these conditions. It also presents a case of a patient presenting with proximal muscle weakness who is diagnosed with polymyositis based on elevated CK, myopathic EMG findings, and muscle biopsy consistent with polymyositis. Treatment options discussed for IIMs include corticosteroids, immunosuppressants, rituximab, and intravenous immunoglobulin.
This document discusses antiplatelet drug resistance in Asian populations. It covers several topics:
- Aspirin and clopidogrel resistance, their types and mechanisms. Genetic polymorphisms can impact drug metabolism and effectiveness.
- Laboratory tests to identify resistance, including platelet function tests and genetic testing to identify variants affecting drug metabolism.
- Factors that can influence drug resistance, such as medication compliance, drug interactions, and genetic factors affecting metabolic pathways.
- Management strategies depending on the resistance type, such as increasing drug doses or trying alternative medications.
A 14-year-old male presented with pain and swelling in the upper back for 45 and 30 days respectively. Examination found a tender swelling at D5-D7 levels. Investigations showed elevated inflammatory markers. He was diagnosed with infective spondylodiscitis at D6-D7 without neurological deficits. He underwent pedicle screw fixation, decompression and biopsy. Intraoperative cultures grew MRSA sensitive to clindamycin. He was started on IV clindamycin and analgesics postoperatively.
This document provides information on rheumatoid arthritis (RA), including:
- RA is an autoimmune disease that results in chronic systemic inflammation, principally attacking synovial joints. It affects 1-3% of adults and is more common in women.
- Clinical manifestations include symmetrical joint pain, stiffness, and swelling typically in the hands, wrists and feet. This can lead to deformities like ulnar deviation.
- Extra-articular effects can include heart, lung, eye, nerve, and skin involvement.
- Diagnosis is based on criteria like joint symptoms lasting over 6 weeks and serological markers. Treatment aims to reduce inflammation and prevent joint damage.
This document discusses lupus nephritis, a form of kidney involvement that can occur in up to 70% of patients with systemic lupus erythematosus. It provides guidelines for diagnosing and classifying lupus nephritis based on the presence of proteinuria, cellular casts in urine, and renal biopsy findings. Renal biopsy is important for classifying the type of glomerular inflammation and scarring according to the ISN/RPS classification system and for guiding treatment decisions. Left untreated, lupus nephritis can lead to end-stage renal disease.
Mixed Connective Tissue Disease By Farshid MokhberiFarshid Mokhberi
Mixed connective tissue disease (MCTD) was first identified in 1972 and involves overlapping features of systemic lupus erythematosus, scleroderma, and myositis. The cause is unknown but likely involves autoimmunity against the U1-70 kD small nuclear ribonucleoprotein. Diagnosis requires high levels of anti-U1 RNP antibodies and a positive antinuclear antibody test. While prognosis can be poor if pulmonary hypertension develops, MCTD is generally very responsive to treatment with glucocorticoids.
Psoriatic arthritis is a form of inflammatory arthritis that affects approximately 7-42% of people with psoriasis. It most commonly presents between ages 35-50 as symmetric polyarthritis or asymmetric oligoarthritis of the hands and feet that can progress to involve more joints over time. Diagnosis is based on criteria such as evidence of psoriasis, nail changes, negative rheumatoid factor, dactylitis, and radiographic evidence of new bone formation. Treatment involves NSAIDs, local steroid injections, and disease-modifying antirheumatic drugs.
The document discusses definitions of remission for rheumatoid arthritis (RA) and the goals of treating RA. It provides context on the history of RA treatment goals moving from symptom relief to preventing joint damage and achieving remission. The key points are:
1) Definitions of remission have evolved from the original ACR criteria to the 2011 ACR-EULAR definition, which includes boolean and index-based definitions for use in clinical trials.
2) Achieving early remission through aggressive treatment is associated with better long-term outcomes for RA patients.
3) The 2011 definition was developed for clinical trials but needs validation for use in practice to guide treatment and measure remission.
A 38-year-old male presents with an extremely painful and swollen right foot that developed over the past 2 days. His history reveals recurrent pain in the right big toe joint over the past 5 years. On examination, he has a swollen tender first MTP joint with restricted movement. Laboratory tests show leukocytosis with neutrophilia and imaging reveals erosion of the first MTP joint. Gout is considered the most likely diagnosis, which is confirmed by joint aspiration demonstrating needle-shaped crystals. The patient is advised on lifestyle modifications and started on allopurinol to prevent recurrent gout attacks.
Anti coagulationin patient with ckd Prof.Basset El Essawy MD ph DFarragBahbah
1. The document discusses physiology and pathways of coagulation, as well as antiplatelet drugs, anticoagulants, and thrombolytics used to treat coagulation.
2. Standard heparin and low molecular weight heparins are compared, noting differences in molecular weight, bioavailability, monitoring needs, and clearance.
3. New oral anticoagulants are discussed as alternatives to warfarin, noting their benefits of fixed dosing, limited drug interactions and food effects, and lack of routine monitoring needs. However, concerns remain regarding a lack of monitoring methods and proven antidotes.
This document summarizes IgA nephropathy (IgAN), the most common primary glomerulonephritis globally. Key points include: IgAN is characterized by deposition of IgA in the mesangium. Clinical presentations range from asymptomatic hematuria to rapidly progressive glomerulonephritis. Prognosis depends on factors like proteinuria level and hypertension. Treatment involves renin-angiotensin system blockade, glucocorticoids, and immunosuppression. The Oxford classification uses pathological features to predict prognosis.
MYOPATHIES A SPECIAL AND SEPERATE ENTITY WITH SPECIFIC FEATURES IN EACH DISORDER MAKING US EASY FOR DIAGNOSIS,CONFIRMATION BY MUSCLE BIOPSY.THE SEMINAR WAS PRSENTED ON 06/07/2011...AT 09.00AM
HAVE A LOOK ..AND COMMENT..WITHOUT BIAS..
This document provides an overview of inflammatory arthritis, including:
1. It defines inflammatory arthritis and categorizes the different types. It discusses the history, physical exam findings, and initial lab/radiological evaluations used to diagnose suspected cases.
2. The document outlines the distinguishing features between inflammatory, mechanical, and non-inflammatory arthritis. It also discusses the patterns of joint involvement and distributions that can help differentiate diseases.
3. Laboratory tests that may be useful in the evaluation of inflammatory arthritis are described, including acute phase reactants, rheumatoid factor, and anti-CCP antibodies. The sensitivities and specificities of these tests are provided.
This document provides guidance on evaluating a patient presenting with arthritis. It describes how arthritis is defined and classified based on the number and duration of involved joints. Key components of the history include symptoms, physical exam findings, classification, differential diagnoses, and initial investigations for monoarthritis and polyarthritis. Initial workup may include blood tests, imaging, and synovial fluid analysis to help identify conditions like gout, pseudogout, septic arthritis, trauma, and rheumatic diseases.
Early Diabetes and Dyslipidaemia Treatment Optimisation.
Presentation by Dr Jeremy Chow
Cardiologist, Electrophysiologist
Asian Heart & Vascular Centre
www.ahvc.com.sg
This comprehensive exam discusses the management of Alzheimer's disease. It provides epidemiological data on AD, describes the pathophysiology involving beta-amyloid plaques and neurofibrillary tangles. It summarizes treatment guidelines from various organizations recommending acetylcholinesterase inhibitors for mild to moderate AD and memantine for moderate to severe AD. It also reviews several randomized controlled trials investigating the use of statins in AD treatment that did not show clear benefits in slowing progression. The health promotion model of Katharine Kolcaba's Comfort Theory is also critiqued, which focuses on strengthening patients by achieving relief, ease and transcendence in physical, psychospiritual, sociocultural and environmental contexts.
This document discusses the approach to evaluating musculoskeletal complaints. It notes that thorough history, physical examination, and targeted investigations are needed to differentiate between self-limited conditions and more serious issues. The assessment involves identifying patterns of joint involvement, associated symptoms, disease duration and characteristics, and examination of both local and systemic findings. Differential diagnoses are formulated based on factors like joint distribution, inflammatory markers, imaging features and disease chronology. A systematic approach is required to arrive at an accurate diagnosis and guide appropriate management.
The document discusses cerebellar ataxia and provides an outline for a lecture on the topic. It begins with definitions of ataxia and discusses the challenges in diagnosing cerebellar ataxia. It then presents a clinical scenario of a patient and outlines the topics to be covered in the lecture, including anatomy and physiology of the cerebellum, diagnostic approaches, classifications of ataxias, hereditary and acquired ataxias, treatment options, and conclusions.
This document provides guidance on evaluating patients presenting with arthritis. It discusses taking a rheumatologic history and performing a physical exam to determine if the arthritis is articular or non-articular, inflammatory or non-inflammatory, acute or chronic, and monoarticular or polyarticular. Key signs of inflammatory versus non-inflammatory arthritis are outlined. Common causes of mono/oligoarthritis like septic arthritis and gout are described. Approaches to polyarthritis and distinguishing rheumatoid arthritis from other conditions are also covered. Imaging and laboratory tests that can aid evaluation are mentioned.
Psoriatic arthritis is a chronic inflammatory disease that affects the joints and skin. It is characterized by osteolysis, bony proliferation, and can cause dactylitis, enthesitis, spondylitis, and various forms of arthritis. While it is classified as a type of spondyloarthritis, it is distinct from rheumatoid arthritis in that it is usually seronegative. The presentation and pattern of joint involvement in psoriatic arthritis can vary between patients and change over time, with the most common forms being asymmetrical oligoarthritis or symmetrical polyarthritis. Diagnosis is based on clinical features and classification criteria such as the CASPAR criteria.
This document summarizes statin-induced myopathies. It discusses statin mechanisms of action and predisposing factors. It describes different clinical phenotypes including rhabdomyolysis, myalgia with mild CK elevation, self-limited toxic myopathy, and immune-mediated necrotizing myopathy associated with anti-HMGCR antibodies. Immune-mediated necrotizing myopathy is characterized by muscle necrosis, regeneration, and scarce inflammation. Diagnosis involves detecting elevated CK, myopathic EMG findings, and anti-HMGCR antibodies. Treatment depends on severity but may include immunosuppression.
This document discusses idiopathic inflammatory myopathies (IIMs), including polymyositis, dermatomyositis, and inclusion body myositis. It reviews the clinical features, diagnostic criteria, pathology, and treatment strategies for these conditions. It also presents a case of a patient presenting with proximal muscle weakness who is diagnosed with polymyositis based on elevated CK, myopathic EMG findings, and muscle biopsy consistent with polymyositis. Treatment options discussed for IIMs include corticosteroids, immunosuppressants, rituximab, and intravenous immunoglobulin.
This document discusses antiplatelet drug resistance in Asian populations. It covers several topics:
- Aspirin and clopidogrel resistance, their types and mechanisms. Genetic polymorphisms can impact drug metabolism and effectiveness.
- Laboratory tests to identify resistance, including platelet function tests and genetic testing to identify variants affecting drug metabolism.
- Factors that can influence drug resistance, such as medication compliance, drug interactions, and genetic factors affecting metabolic pathways.
- Management strategies depending on the resistance type, such as increasing drug doses or trying alternative medications.
A 14-year-old male presented with pain and swelling in the upper back for 45 and 30 days respectively. Examination found a tender swelling at D5-D7 levels. Investigations showed elevated inflammatory markers. He was diagnosed with infective spondylodiscitis at D6-D7 without neurological deficits. He underwent pedicle screw fixation, decompression and biopsy. Intraoperative cultures grew MRSA sensitive to clindamycin. He was started on IV clindamycin and analgesics postoperatively.
This document provides information on rheumatoid arthritis (RA), including:
- RA is an autoimmune disease that results in chronic systemic inflammation, principally attacking synovial joints. It affects 1-3% of adults and is more common in women.
- Clinical manifestations include symmetrical joint pain, stiffness, and swelling typically in the hands, wrists and feet. This can lead to deformities like ulnar deviation.
- Extra-articular effects can include heart, lung, eye, nerve, and skin involvement.
- Diagnosis is based on criteria like joint symptoms lasting over 6 weeks and serological markers. Treatment aims to reduce inflammation and prevent joint damage.
This document discusses lupus nephritis, a form of kidney involvement that can occur in up to 70% of patients with systemic lupus erythematosus. It provides guidelines for diagnosing and classifying lupus nephritis based on the presence of proteinuria, cellular casts in urine, and renal biopsy findings. Renal biopsy is important for classifying the type of glomerular inflammation and scarring according to the ISN/RPS classification system and for guiding treatment decisions. Left untreated, lupus nephritis can lead to end-stage renal disease.
Mixed Connective Tissue Disease By Farshid MokhberiFarshid Mokhberi
Mixed connective tissue disease (MCTD) was first identified in 1972 and involves overlapping features of systemic lupus erythematosus, scleroderma, and myositis. The cause is unknown but likely involves autoimmunity against the U1-70 kD small nuclear ribonucleoprotein. Diagnosis requires high levels of anti-U1 RNP antibodies and a positive antinuclear antibody test. While prognosis can be poor if pulmonary hypertension develops, MCTD is generally very responsive to treatment with glucocorticoids.
Psoriatic arthritis is a form of inflammatory arthritis that affects approximately 7-42% of people with psoriasis. It most commonly presents between ages 35-50 as symmetric polyarthritis or asymmetric oligoarthritis of the hands and feet that can progress to involve more joints over time. Diagnosis is based on criteria such as evidence of psoriasis, nail changes, negative rheumatoid factor, dactylitis, and radiographic evidence of new bone formation. Treatment involves NSAIDs, local steroid injections, and disease-modifying antirheumatic drugs.
The document discusses definitions of remission for rheumatoid arthritis (RA) and the goals of treating RA. It provides context on the history of RA treatment goals moving from symptom relief to preventing joint damage and achieving remission. The key points are:
1) Definitions of remission have evolved from the original ACR criteria to the 2011 ACR-EULAR definition, which includes boolean and index-based definitions for use in clinical trials.
2) Achieving early remission through aggressive treatment is associated with better long-term outcomes for RA patients.
3) The 2011 definition was developed for clinical trials but needs validation for use in practice to guide treatment and measure remission.
A 38-year-old male presents with an extremely painful and swollen right foot that developed over the past 2 days. His history reveals recurrent pain in the right big toe joint over the past 5 years. On examination, he has a swollen tender first MTP joint with restricted movement. Laboratory tests show leukocytosis with neutrophilia and imaging reveals erosion of the first MTP joint. Gout is considered the most likely diagnosis, which is confirmed by joint aspiration demonstrating needle-shaped crystals. The patient is advised on lifestyle modifications and started on allopurinol to prevent recurrent gout attacks.
Anti coagulationin patient with ckd Prof.Basset El Essawy MD ph DFarragBahbah
1. The document discusses physiology and pathways of coagulation, as well as antiplatelet drugs, anticoagulants, and thrombolytics used to treat coagulation.
2. Standard heparin and low molecular weight heparins are compared, noting differences in molecular weight, bioavailability, monitoring needs, and clearance.
3. New oral anticoagulants are discussed as alternatives to warfarin, noting their benefits of fixed dosing, limited drug interactions and food effects, and lack of routine monitoring needs. However, concerns remain regarding a lack of monitoring methods and proven antidotes.
This document summarizes IgA nephropathy (IgAN), the most common primary glomerulonephritis globally. Key points include: IgAN is characterized by deposition of IgA in the mesangium. Clinical presentations range from asymptomatic hematuria to rapidly progressive glomerulonephritis. Prognosis depends on factors like proteinuria level and hypertension. Treatment involves renin-angiotensin system blockade, glucocorticoids, and immunosuppression. The Oxford classification uses pathological features to predict prognosis.
MYOPATHIES A SPECIAL AND SEPERATE ENTITY WITH SPECIFIC FEATURES IN EACH DISORDER MAKING US EASY FOR DIAGNOSIS,CONFIRMATION BY MUSCLE BIOPSY.THE SEMINAR WAS PRSENTED ON 06/07/2011...AT 09.00AM
HAVE A LOOK ..AND COMMENT..WITHOUT BIAS..
This document provides an overview of inflammatory arthritis, including:
1. It defines inflammatory arthritis and categorizes the different types. It discusses the history, physical exam findings, and initial lab/radiological evaluations used to diagnose suspected cases.
2. The document outlines the distinguishing features between inflammatory, mechanical, and non-inflammatory arthritis. It also discusses the patterns of joint involvement and distributions that can help differentiate diseases.
3. Laboratory tests that may be useful in the evaluation of inflammatory arthritis are described, including acute phase reactants, rheumatoid factor, and anti-CCP antibodies. The sensitivities and specificities of these tests are provided.
This document provides guidance on evaluating a patient presenting with arthritis. It describes how arthritis is defined and classified based on the number and duration of involved joints. Key components of the history include symptoms, physical exam findings, classification, differential diagnoses, and initial investigations for monoarthritis and polyarthritis. Initial workup may include blood tests, imaging, and synovial fluid analysis to help identify conditions like gout, pseudogout, septic arthritis, trauma, and rheumatic diseases.
Early Diabetes and Dyslipidaemia Treatment Optimisation.
Presentation by Dr Jeremy Chow
Cardiologist, Electrophysiologist
Asian Heart & Vascular Centre
www.ahvc.com.sg
This comprehensive exam discusses the management of Alzheimer's disease. It provides epidemiological data on AD, describes the pathophysiology involving beta-amyloid plaques and neurofibrillary tangles. It summarizes treatment guidelines from various organizations recommending acetylcholinesterase inhibitors for mild to moderate AD and memantine for moderate to severe AD. It also reviews several randomized controlled trials investigating the use of statins in AD treatment that did not show clear benefits in slowing progression. The health promotion model of Katharine Kolcaba's Comfort Theory is also critiqued, which focuses on strengthening patients by achieving relief, ease and transcendence in physical, psychospiritual, sociocultural and environmental contexts.
This document discusses guidelines for managing dyslipidemia with statins. It identifies 4 main groups that benefit from statin treatment based on their ASCVD risk: 1) those with clinical ASCVD, 2) those with LDL-C >190 mg/dL, 3) those with diabetes aged 40-75 with LDL-C 70-189 mg/dL, and 4) those aged 40-75 without clinical ASCVD or diabetes but with LDL-C 70-189 mg/dL and 10-year ASCVD risk >7.5%. The document reviews evidence that moderate- and high-intensity statin therapy lowers ASCVD risk across all baseline LDL-C levels above 70 mg/dL. It provides guidance on
Treating Cholesterol in Asian Patients: Balancing the Risk and Benefitsahvc0858
This document summarizes a presentation on treating cholesterol in Asians given by Dr. Jeremy Chow. It discusses the prevalence of hyperlipidemia in Singapore, challenges with statin usage in Asians including common myths, and new cholesterol targets for high-risk patients. It provides examples of managing different patient cases, including lifestyle modifications, medications such as statins and PCSK9 inhibitors, and balancing risks and benefits of treatment.
Treatment strategies in patients with statin intoleranceVishwanath Hesarur
Statins are among the most prescribed drugs in the world and are first-line therapy in the management of hyperlipidemia.
Their beneficial effects on cardiovascular morbidity and mortality have been demonstrated both in primary and in secondary prevention.
They are generally safe, but in some patients, statin therapy is stopped because of intolerance to the drug that may result in muscle aches and weakness, gastrointestinal symptoms, liver enzyme abnormalities, or other nonspecific discomforts.
The rate of reported statin-related events is about 5% to 10% in randomized, placebo controlled clinical trials.
This document summarizes treatment approaches for metastatic prostate cancer and castration-resistant prostate cancer (CRPC). It discusses how initial treatments aim to reduce androgen levels via surgical or medical castration. While initial responses are good, cancer typically becomes resistant to castration after 2-3 years. For CRPC, options discussed include secondary hormonal therapies, bone-targeted agents, chemotherapy, immunotherapy, radiotherapy, and novel targeted therapies. Key mechanisms of CRPC resistance and clinical considerations for treatment are also reviewed.
DrRic Using Food Choices to Control Inflammation (slide share edition)DrRic Saguil
1. The document discusses using food choices to control inflammation in the body and reduce the risk of chronic diseases like heart disease and cancer.
2. It recommends following an anti-inflammatory diet like the Mediterranean diet, which is high in vegetables, fruits, whole grains, fish and healthy fats.
3. Research studies have shown that following a Mediterranean diet is associated with reduced risk of death from all causes as well as specific diseases.
This randomized controlled trial evaluated the effectiveness of acetyl-L-carnitine (ALC) for treating diabetic neuropathy. Over 1,200 patients with type 1 or 2 diabetes and mild neuropathy were randomized to receive 500 mg or 1,000 mg ALC 3 times daily or placebo for 52 weeks. ALC treatment significantly improved vibration perception threshold and nerve fiber regeneration compared to placebo. Adverse effects were mild and similar between groups. While limited by a short trial period and some baseline differences, ALC appears to be a relatively safe and potentially effective treatment option for mild diabetic neuropathy.
This document discusses the history and treatment of gastrointestinal stromal tumors (GISTs). It notes that GISTs were originally misclassified until 1983 when they were identified as distinct tumors. Treatment progressed slowly until 1998 when the association between GISTs and c-KIT was discovered, leading to the development of imatinib in 2001. Imatinib was approved for metastatic/unresectable GIST in 2002 and as adjuvant therapy for high-risk GIST in 2008 and 2012. The document discusses risk assessment tools and provides guidelines for adjuvant imatinib therapy for intermediate-high risk GIST of 3 years duration. It also discusses neoadjuvant imatinib and subsequent treatment options including sunitinib
Weight diabetes and metabolic problems in patients taking atypical antipsycho...Alex J Mitchell
Free slide show on weight gain, diabetes and metabolic problems in those taking atypical antipsychotic medication in schizophrenia, bipolar disorder and related conditions. Image credits retained by original authors. Please give correct acknolwedgements if you present any material from here.
Cancer anorexia cachexia 23rd nov 2017 (1)Dr Mehak Aneja
Cancer cachexia is a multifactorial syndrome defined by loss of muscle mass and fat tissue. It is caused by chronic illness like cancer through increased inflammation, insulin resistance, and hypogonadism leading to weight loss, fatigue, and reduced muscle strength. Management includes treating the underlying cause, increasing nutrition, and pharmacological interventions. Progestagens like megestrol acetate are most effective in improving appetite and weight gain but have side effects. Corticosteroids also improve appetite but are not suitable long term. Emerging treatments target inflammation through omega-3 fatty acids, cannabinoids, and anti-cytokine drugs but results have been limited.
The African-American Heart Failure Trial (A-HeFT) studied the effects of adding a fixed dose of isosorbide dinitrate and hydralazine to standard heart failure therapies in Black patients with advanced heart failure. The trial found that combination therapy reduced all-cause mortality by 43%, reduced the risk of first hospitalization for heart failure by 33%, and improved patient quality of life compared to standard therapy alone in under 3 sentences.
This study compared outcomes of steroid withdrawal versus continued steroid therapy in kidney and heart transplant recipients. Over 1500 patients were enrolled from 1994-2002 and followed for 5-6 years on average. Results showed that steroid withdrawal led to superior patient and graft survival rates compared to controls continuing steroids. Steroid withdrawal also reduced risks of complications like osteoporosis and cataracts. However, it was associated with a small increased risk of acute rejection episodes. Overall, the study suggests that steroid withdrawal after 6 months is safe and effective for transplant recipients.
This document discusses dyslipidemia, including its epidemiology, classification, diagnosis, screening, and management. Some key points:
- Dyslipidemia is characterized by abnormal lipid levels and contributes to atherosclerosis. It can be primary or secondary.
- The prevalence of dyslipidemia in Saudi Arabia ranges from 20-44% according to studies.
- Diagnosis involves measuring lipid levels through a serum profile. Treatment involves lifestyle changes and lipid-lowering drugs like statins.
- Statins are beneficial for both primary and secondary prevention of cardiovascular disease according to clinical trials. Guidelines recommend statin use for those with specific risk factors.
This document provides guidance on evaluating and managing patients presenting with monoarthritis or polyarthritis. It discusses common causes of monoarthritis including septic, traumatic, and crystal deposition diseases. It also reviews key questions to ask patients and appropriate diagnostic tests. For polyarthritis, it distinguishes between acute and chronic presentations and lists associated diseases. The document then focuses on osteoarthritis, outlining risk factors, symptoms, diagnostic criteria, and pharmacological and non-pharmacological treatment approaches including exercise, weight loss, analgesics, and surgery.
This document presents the case of a 69-year-old Thai woman who presented with right hip pain for one month. Her physical examination revealed tenderness on hip rotation tests on the right side. Laboratory tests showed anemia, elevated creatinine, and presence of Bence Jones proteins in her urine, consistent with multiple myeloma. The document then provides background information on multiple myeloma, including its clinical presentation, diagnostic workup, criteria for diagnosis, and treatments for multiple myeloma and its complications.
The document discusses how paradigms and dogmas in critical care medicine are often promoted through guidelines even when evidence is poor or absent. It provides several examples of therapies that were once widely practiced as dogma but were later found to be ineffective or harmful when subjected to rigorous clinical trials. It warns that accepting poor evidence as truth and failing to embrace uncertainty can lead the field to practice as a "rational astrology" where beliefs are followed regardless of their factual accuracy. The document advocates for skepticism and embracing doubt to advance evidence-based practices in critical care.
The document discusses lipid-lowering therapy, particularly statin use, in patients with cardiovascular risk and liver disease. While statins are effective for cardiovascular risk reduction, patients with liver disease are often excluded from clinical trials. Physicians are also hesitant to prescribe statins to such patients due to concerns about liver and muscle toxicity. The document proposes a study to assess the efficacy and safety of combining statin therapy with ursodeoxycholic acid (UDCA) in patients with hyperlipidemia, cardiovascular risk and liver disease. The study would follow 262 patients across Russia for 6 months to evaluate clinical outcomes from co-administering statins and UDCA.
1. The document provides information on examining the shoulder, elbow, wrist, and hand, including anatomy, inspection, palpation, range of motion tests, and special tests.
2. Common causes of pain in these areas are described, including rotator cuff injuries, arthritis, tendinitis, bursitis, and neurological issues.
3. Examination techniques for each area include inspection for deformities, swelling, atrophy; palpation for temperature, tenderness, crepitus; and range of motion and special tests like impingement signs and drop arm test for shoulders.
F waves are produced when a supramaximal stimulus is applied to a motor nerve, causing antidromic impulses that travel to the spinal cord. Some motor neurons then backfire, producing the F wave. F wave latencies provide information about motor nerve conduction velocity and can help detect neuropathies. The H-reflex is produced when a weak stimulus excites muscle spindle Ia afferents, causing antidromic impulses in the spinal cord that excite alpha motor neurons. F wave and H-reflex latencies are used to evaluate spinal and peripheral nerve conduction.
The document provides an overview of the radiological anatomy of the spine. It describes the key anatomical structures of the cervical, thoracic, and lumbar regions of the spine, including the vertebral bodies, intervertebral discs, transverse processes, pedicles, lamina, spinous processes, ribs, and sacrum. Diagrams are included to illustrate these structures for each region.
Neuropathic arthropathy, also known as Charcot joint, is a condition characterized by progressive joint destruction and deformity caused by loss of sensation in the joints. It was first described in detail by Jean-Martin Charcot in 1868. The major theories for its pathophysiology are neurotrauma from repetitive micro-injuries without pain sensation, and neurovascular dysregulation leading to hyperemia and bone resorption. Diabetes is the most common cause. Imaging shows bone fragmentation, joint dislocation, and deformity. Treatment involves prolonged casting or bracing to immobilize joints during the acute inflammatory phase, followed by bracing and accommodative footwear. Later stages may require surgery.
power point presentation brucellosis.pptxazzaelnenaey
The document provides information about brucellosis, including its definition as a zoonotic disease caused by Brucella bacteria. It discusses the epidemiology, transmission, clinical presentation, diagnosis, and treatment of the disease. Brucellosis commonly involves the musculoskeletal system, with spondylitis, sacroiliitis, and peripheral arthritis being frequent manifestations. Diagnosis involves serological testing and culture of infected tissues. Treatment requires prolonged antibiotic therapy.
Case senario presentation...............azzaelnenaey
A 58-year-old postmenopausal woman presented with a left wrist fracture following a fall. Her medical history included asthma treated with corticosteroids, gastric ulcer, and a previous wrist fracture. Examination found a displaced, swollen wrist with no neurovascular compromise. X-ray revealed a Colles' fracture. Risk factors for osteoporosis from her history included advanced age, menopause, corticosteroid use, smoking, and lack of exercise. Further workup was needed to confirm the diagnosis and guide management, which may include bisphosphonates, parathyroid hormone, or calcium and vitamin D supplementation to prevent future fractures.
This document discusses rheumatoid arthritis and seronegative spondyloarthritis. It lists common hand deformities in rheumatoid arthritis such as swan neck and boutonniere deformities. It also lists criteria for arthritis including redness, swelling and tenderness. The sacroiliac joint is commonly affected in seronegative spondyloarthritis. Criteria for inflammatory back pain and members of the seronegative spondyloarthritis family are also enumerated.
1) The document describes several lysosomal storage disorders including Tay-Sachs disease, Sandhoff disease, and GM2 Activator deficiency. These disorders are caused by defects in genes encoding hexosaminidase enzymes, resulting in ganglioside accumulation.
2) The phenotypes range from infantile to juvenile to adult-onset, with infantile having the earliest onset of symptoms around 6 months and most severe progression leading to death by age 3-4. Juvenile and adult-onset phenotypes have later onset and slower progression.
3) Initial symptoms vary by phenotype but often involve developmental delay, loss of motor skills, weakness, and neurological decline. Disease progression results in loss of abilities and eventual death due to
Urate crystals can initiate and perpetuate acute inflammation by inducing cells like phagocytes and synovial cells to release inflammatory mediators. This leads to neutrophil infiltration into joints, causing synovitis. Colchicine inhibits this process by interfering with neutrophil migration, metabolism, and phagocytosis. It does this by disrupting microtubules involved in cell structure and movement, reducing neutrophil motility, chemotaxis, and the release of inflammatory factors. Colchicine is used to treat gout attacks and prevent recurrences by dampening the inflammatory response driven by neutrophils.
This document discusses psoriatic arthritis (PsA), including its clinical manifestations, patterns, imaging, diagnosis, and treatment. PsA is a chronic inflammatory arthritis occurring in 7-42% of psoriasis patients, typically presenting as painful, stiff joints. Five patterns are recognized: oligoarticular disease in 70% of cases affecting distal joints; asymmetric DIP involvement in 10% of cases; arthritis mutilans deforming fingers and toes in 5% of cases; symmetric polyarthritis resembling rheumatoid arthritis in 15% of cases; and psoriatic spondyloarthritis in 5% presenting with axial inflammation. Treatment involves NSAIDs, DMARDs like methotrexate, and biological agents
This document discusses the classification of vasculitis. It begins by defining vasculitis as a heterogeneous group of conditions where inflammation of blood vessels occurs independently or secondary to other diseases. It then describes how vasculitis typically presents depending on vessel size, such as limb claudication for large vessel vasculitis or palpable purpura for small vessel vasculitis. Specific types of vasculitis are then outlined according to vessel size and other characteristics, such as the diagnostic criteria for giant cell arteritis and Takayasu arteritis as examples of large vessel vasculitis.
Non steroid anti inflammatory drug.pptxazzaelnenaey
NSAIDs work by inhibiting cyclooxygenase enzymes (COX-1 and COX-2) which are involved in prostaglandin synthesis. This decreases inflammation but also inhibits platelet aggregation and increases risk of gastrointestinal ulcers/bleeds. Common side effects include gastrointestinal issues, renal toxicity, and cardiovascular effects. COX-2 inhibitors have fewer gastrointestinal side effects but increase risk of heart attack and thrombosis. Proper use and monitoring can help reduce risks.
Juvenile Idiopathic Arthritis (JIA) is defined as arthritis of unknown cause that begins before age 16 and lasts over 6 weeks. It is classified based on symptoms into subtypes including systemic onset JIA, oligoarticular JIA, and polyarticular JIA. Treatment involves a stepwise approach starting with NSAIDs and intra-articular steroids and escalating to DMARDs and biologicals. Complications can include chronic anterior uveitis, osteoporosis, and potentially life-threatening macrophage activation syndrome.
This document provides an overview of targeted disease-modifying antirheumatic drugs (DMARDs) for the treatment of rheumatoid arthritis (RA). It discusses the Janus kinase (JAK) signaling pathway and how JAK inhibitors block specific kinases to treat RA. The document reviews the timeline of RA treatments from early interventions like baths and injections to current first-line methotrexate and additions of targeted therapies like JAK inhibitors if treatment goals are not met. It profiles approved and investigational JAK inhibitors for RA including tofacitinib, baricitinib, upadacitinib, filgotinib, and peficitinib.
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...Donc Test
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A proprietary approach developed by bringing together the best of learning theories from Psychology, design principles from the world of visualization, and pedagogical methods from over a decade of training experience, that enables you to: Learn better, faster!
Does Over-Masturbation Contribute to Chronic Prostatitis.pptxwalterHu5
In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
1. Statin Myopathy
Lisa Christopher-Stine, MD, MPH
Professor of Medicine and Neurology
Director, Johns Hopkins Myositis Precision Medicine Center of Excellence
Johns Hopkins University School of Medicine
2. Disclosures
• I have the following relevant financial relationship(s) to disclose:
Consultant: , Janssen, Boehringer-Ingelheim, Mallinckrodt, EMD Serono,
Roivant/Priovant, Pfizer, ArgenX, Horizon Therapeutics, and Allogene.
• Grant/Research Support: Pfizer, Corbus and Kezar
• Royalties: Inova Diagnostics
• Intellectual Property/Patents: Inova Diagnostics (Anti-HMGCR autoantibody testing)
All of the relevant financial relationships listed for this individual have been
mitigated.
3. Evidence-Based Medicine (EBM)
Key References
• Albayda J, Christopher-Stine L. Identifying statin-associated autoimmune necrotizing myopathy.
Cleve Clin J Med. 2014 Dec;81(12):736-41.
• Christopher-Stine L, Basharat P. Statin-associated immune-mediated myopathy: biology and clinical
implications. Curr Opin Lipidol. 2017 Apr;28(2):186-192.
• Wood FA, Howard JP, Finegold JA, Nowbar AN, Thompson DM, Arnold AD, Rajkumar CA, Connolly
S, Cegla J, Stride C, Sever P, Norton C, Thom SAM, Shun-Shin MJ, Francis DP. N-of-1 Trial of a
Statin, Placebo, or No Treatment to Assess Side Effects. N Engl J Med. 2020 Nov 26;383(22):2182-
2184.
• Herrett E, Williamson E, Beaumont D, Prowse D, Youssouf N, Brack K, Armitage J, Goldacre B,
MacDonald T, Staa TV, Roberts I, Shakur-Still H, Smeeth L. Study protocol for statin web-based
investigation of side effects (StatinWISE): a series of randomised controlled N-of-1 trials comparing
atorvastatin and placebo in UK primary care. BMJ Open. 2017 Dec 1;7(12):e016604.
• Writing Committee, Lloyd-Jones DM, Morris PB, Ballantyne CM, Birtcher KK, Covington AM,
DePalma SM, Minissian MB, Orringer CE, Smith SC Jr, Waring AA, Wilkins JT. 2022 ACC Expert
Consensus Decision Pathway on the Role of Nonstatin Therapies for LDL-Cholesterol Lowering in
the Management of Atherosclerotic Cardiovascular Disease Risk: A Report of the American College
of Cardiology Solution Set Oversight Committee. J Am Coll Cardiol. 2022 Oct 4;80(14):1366-1418.
4. Broad Objectives
• Review clinical presentation, laboratory assessment, and
treatment plans for statin myopathy
• Outline alternative treatments for hyperlipidemia in those who
cannot tolerate statins
5. What we will cover today…
• What is the definition of “statin intolerance”, and how many statins does
a patient need to fail before meeting this definition?
• What is the definition of “statin myopathy”?
• What is the difference between autoimmune statin myopathy and
a statin myopathy where the drug acts as a direct myotoxin (“toxic” statin
myopathy”)?
• How common is statin intolerance in the “real world?”
• Are muscle enzymes (e.g., CK) routinely checked prior to starting
a statin for cholesterol reduction in routine clinical practice? What is the
implication?
• In statin clinical trials, do patients on placebo report the
same statin intolerance that those on statins do?
6. What we will cover today… (continued)
• Can statin myopathy occur with a normal CK?
• Should you ever do a muscle biopsy in acute rhabdomyolysis
related to statins?
• Can a patient with myositis (inflammatory myopathy like
dermatomyositis) safely take a statin?
• Do you need a muscle biopsy to diagnose autoimmune statin
myopathy?
• What is the evidence for CoQ10 supplementation (and other
supplements) in statin myopathy?
• What are some pharmacologic options for lipid reduction in
statin intolerance (including statin myopathy)?
7. A case... and a tale of two brothers
• ASM is a 71-year-old man with a history of ASCVD, hypertension,
hyperlipidemia, and type 2 diabetes mellitus
• The patient had been taking atorvastatin 80 mg daily for 37
months before it was stopped when the liver-associated enzymes
were found to be elevated initially.
• Sees his PCP for pre-procedural labs for a scheduled liver biopsy
to further evaluate persistently elevated liver-associated enzymes
(AST, ALT) for the past 4 months.
• The PCP realizes that a creatine kinase (CK) has never been
ascertained, so she also draws a CK which is markedly elevated.
• The patient wonders if he has “statin myopathy” like his brother.
8. • Patient History:
• Extreme fatigue and muscle soreness for the past 2 months;
reports difficulty climbing stairs, getting off low seated chairs,
and washing his hair in the shower.
• Denies frank dysphagia but has noticed occasionally having to
“double swallow” to swallow dry bread.
• Denies joint pain; no history of any autoimmune diseases
Exam: proximal weakness of deltoids and hip flexors
• CK: 5250 U/L ( normal range under 250 U/L)
• Anti-HMGCR testing is positive
• Family history- no known autoimmune diseases; brother (TSM)
had a diagnosis of self- limited (“toxic”) statin myopathy.
9. More about his brother (TSM)…
• Stopped atorvastatin 80 mg daily after 6 weeks of use because
his muscles were painful.
• Had calf and other diffuse muscle pain and fatigue but denied
true weakness
• Had a CK of 450 U/L; pre-statin CK was unknown.
• Anti-HMGCR testing is negative
• CK normalized after statin cessation but rose upon re-challenge
of atorvastatin at any dose and with rosuvastatin at higher doses
• Able to tolerate low-dose rosuvastatin with the addition of a
PCSK9 mAb inhibitor for excellent lipid control.
10. Do the two brothers (ASM and
TSM) have the same type of
statin myopathy?
ASM has autoimmume statin myopathy (a.k.a. statin- associated necrotizing autoimmune myopathy (SANAM) or anti-HMGCR associated IMNM)
TSM has toxic statin myopathy or self-limited statin myopathy
11. Statin Associated Autoimmune
Necrotizing Myopathy
Toxic (Self-Limited) Statin Myopathy
Incidence Rare (2-3 per 100K statin users) Common (13% of statin users
depending on definition)
Statin Atorvastatin overwhelmingly Any
Statin Duration Years (average 36 months) Days to weeks
Weakness Yes, almost always Varies
Myalgia Sometimes Often
Dysphagia Sometimes Never
CK range Usually >1000, rarely normal Varies
Clinical rhabdomyolysis Rare to Never Rare
New onset Raynaud’s Rare Never
HMGCR autoantibody Yes (sensitive and specific) No
Muscle Biopsy MHC class 1 upregulation;
degeneration, regeneration, necrosis
Degeneration, regeneration, Necrosis
Concomitant meds exacerbate it No Sometimes
Myopathy dissipates when statin
stopped
No Yes
Basharat PJ Am Coll Cardiol. 2016 Jul 12;68(2):234-5.
Albayda J. Cleve Clin J Med. 2014 Dec;81(12):736-41.
Christopher-Stine L, Arthritis Rheum. 2010 Sep;62(9):2757-66.
Mammen AL. Arthritis Rheum. 2011 Mar;63(3):713-21.
Christopher-Stine L,. Curr Opin Lipidol. 2017 Apr;28(2):186-192.
12. Statin Associated Autoimmune
Necrotizing Myopathy
Toxic (Self-Limited) Statin Myopathy
Incidence Rare (2-3 per 100K statin users) Common (13% of statin users
depending on definition)
Statin Atorvastatin overwhelmingly Any
Statin Duration Years (average 36 months) Days to weeks
Weakness Yes, almost always Varies
Myalgia Sometimes Often
Dysphagia Sometimes Never
CK range Usually >1000, rarely normal Varies
Clinical rhabdomyolysis Rare to Never Rare
Raynaud’s Rare Never
HMGCR autoantibody Yes (sensitive and specific) No
Muscle Biopsy MHC class 1 upregulation;
degeneration, regeneration, necrosis
Degeneration, regeneration, Necrosis
Concomitant meds exacerbate it No Sometimes
Myopathy dissipates when statin
stopped
No Yes
17. Lipophilic versus hydrophilic
• Meta-analysis: with the exception of the GAUSS-3* study, no
significant association between lipophilic or hydrophilic statins
and risk of skeletal muscle events.
• Another meta-analysis of statin randomized controlled trials
(RCTs) also found limited evidence that lipophilic statins were
associated with a greater risk of statin-associated muscle
symptoms (SAMS).
Irwin JCPharmacol Res. 2018 Feb;128:264-273.
Iwere R.B. Br. J. Clin. Pharmacol. 2015;80:363–371..
* Goal Achievement after Utilizing an anti-PCSK9 antibody in Statin Intolerant Subjects-3
18. Statin Compliance
• Evidence from RCTs :adverse cardiovascular event risk lowered by atherogenic
lipoprotein level reduction
• Benefit proportionate to degree of reduction and the length of time lower level is
maintained
• Despite benefits on cardiovascular outcomes, compliance to statin therapy often
inadequate
• Non-adherence to treatment up to 50% of patients
Gislason G.H., Eur. Heart J. 2006;27:1153–1158.
Blackburn D.F., Can. J. Cardiol. 2005;21:485–488.
19. Statin intolerance
• Statin-associated muscle symptoms (SAMS) are the most common side
effect (>80%) associated with statin discontinuation.
• Symptoms range from mild-to-moderate muscle pain, weakness, or
fatigue to rhabdomyolysis
• Reported by 10% to 25% of patients receiving statin therapy.
• Due to lack of “gold standard”, diagnostic test for SAMS is based on a
clinical index score (SAMS-CI), which is independent of creatine kinase
(CK) elevation.
20. Rosenson RS.Cardiovasc Drugs Ther Apr;31(2):2017;
31(2):179-186.
SAMS-CI
[from the Statin
Muscle
Safety Task Force
of the National
Lipid Association
(NLA)]
22. What about Exercise and Statins?
• Exercise together with statins can exacerbate /trigger SAMS
• After a training session, CK levels appear to increase more
in statin-treated athletes than in athletes not on therapy
• Association between high CK levels and age found only in
athletes on statin therapy
• Systematic review of the literature reports conflicting results on
the ability of statins to impair performance during exercise
Mendes P. Physiother. Can. 2014;66:124–132.
Parker B.A.. Exerc. Sport Sci. Rev. 2012;40:188–194.
Parker B.A. Am. J. Cardiol. 2012;109:282–287.
Noyes A.M. J. Clin. Lipidol. 2017;11:1134–1144.
23. CK in self-limited statin myopathy
• CK levels are frequently normal in symptomatic patients
taking statins, while also may be increased in asymptomatic
patients
• For these reasons, CK is a non-sensitive biomarker for statin-
induced myopathy, but is currently used in the evaluation of
SAMS due to the absence of other specific laboratory tests.
MRC/BHF Heart Protection Study Collaborative Group. BMC Clin. Pharmacol. 2009;9:6.
Downs J.R.,. Am. J. Cardiol. 2001;87:1074–1079.
25. Self-Assessment Method for Statin Side-
effects Or Nocebo (SAMSON) trial
• 12 month study of 60 UK patients with statin-associated
adverse events within 2 weeks of statin initiation (excl CK<5x
ULN+ of CK increase + myalgia)
• Double-blind, three-group, n-of-1 trial
• Test whether symptoms would be induced by a statin (atorva 20
mg) or placebo.
• 4 bottles contained statin tablets, 4 placebo tablets, and 4 empty
• Each bottle was to be used for a 1-month period ;random sequence.
• Smartphone application to report symptom intensity daily.
• Symptom scores ranged from 0 to 100
Wood FA. N Engl J Med 2020; 383:2182-2184
26. SAMSON trial (continued)
• Overall symptom severity scores:
• 8 for no-tablet months (95% CI, 4.7-11.3);
• 15.4 for placebo (95% CI, 12.1-18.7); and
• 16.3 for statin therapy (95% CI, 13-19.6).
• Difference in symptom severity reported for placebo compared with
statin therapy was not clinically significant (P < .388);
• Side effect severity was significant for both statin and placebo compared with
no- tablet months (P for both < .001).
• 90% developed the same symptoms on placebo using random monthly
crossover sequences over 12 months
• Half of the participants successfully re-started statins
• May reassure physicians and patients to pursue statin re-challenges
27. STATIN: Web-based Investigation of Side
Effects (STATINWISE)
• 151 of 200 randomized patients with statin intolerance from England and
Wales provided at least one VAS score on placebo and one on statin
active comparator
• A series of randomized, double blind, placebo controlled n-of-1 trials.
• Six two-month treatment periods
• three of active treatment (atorvastatin 20 mg)
• three of matching placebo
• randomly allocated order.
• Daily atorvastatin (20 mg) was compared with matching placebo
• Primary outcome measured daily by validated VAS 0-10 for last 7days of
each treatment period
• Secondary outcomes three months after the end of the final treatment
period:
• Restart statins?
• Trial useful in decision making? Herrett E. BMJ Open. 2017 Dec 1;7(12):e016604.
28. STATINWISE (continued)
• No evidence of difference in muscle symptom scores between statin and
placebo periods
• mean difference statin minus placebo -0.11, 95% confidence interval -0.36 to
0.14; p = 0.398).
• Withdrawals, adherence and missing data were similar during the statin
periods and the placebo periods.
• Few withdrew because of muscle symptoms
• Of the participants who completed six treatment periods and received their
results during an end of trial discussion, 3 months later:
• 88% said that the trial had been helpful
• 66% said that they had already resumed or intended to resume taking statins.
29. Statin therapy and underlying
neuromuscular disorders
• Statin therapy may exacerbate underlying neuromuscular
disorders
• myasthenia gravis
• dermato/polymyositis
• inclusion body myositis
• motor neuron disease,
• MELAS (mitochondrial encephalopathy, lactic acidosis, and stroke-like
episodes)
• Note : Regarding the inflammatory myopathies, the only absolute
contraindication to statins are patients with myositis who are HMGCR
ab+, (PCSK9 mAb inhibitors are safe in this population) Tay S.K. Pediatr. Neurol. 2008;39:426–428.
Alonso R.J. Atheroscler. Thromb. 2019;26:207–215.
Brunham L.R. Cardiovasc. Res. 2018;114:1073–1081
Thomas J.E. Eur. Neurol. 2007;57:232–235.
Tiniakou E. Arthritis Rheumatol. 2019 Oct;71(10):1723-1726.
30. Muscle Biopsy in Statin Myopathy
Statin Associated Necrotizing
Autoimmune Myopathy
• Muscle biopsy falling out of
favor with widely available
autoantibody testing in the
right clinical scenario
• HMGCR Ab testing positive
• High CK
• Proximal weakness
• +/- Myalgias
• Statin exposure (atorvastatin)
Self-limited Statin Myopathy
• No reason to biopsy when
rhabdomyolysis is acute.
• A clinical diagnosis
• HMGCR antibody testing
negative
• Acute increase in CK
• Urine myoglobin
• +/- Proximal Weakness
• Myalgias
• Statin exposure (any)
31. Are CKs checked at statin initiation?
What about when LFTS rise?
• No longer recommended to check CK at initiation of statin
therapy
• Routinely, PCPs and others never check CK after LFTS rise in
patients taking statins
32. Remember to check the CK if LFTS
are elevated! (Abstract #1283)
• Explored how frequently clinicians check CK in patients with elevated
transaminases to look for muscle injury
• Outpatient retrospective chart review May 2017 to May 2022
• 731 randomly selected patients taking statins
• Diagnosed with elevated transaminases (ICD code: R74.01)
• Records were reviewed to ascertain if subjects had a CK level checked
within one month of diagnosis of elevated transaminases
Only 169, (23%), had their CK checked within one month
• Of these 169 subjects, 26 (15%), had CK flagged as high
• 65 % had CK level >400 U/L and 19 % had CK level >1000 U/L
• 562 patients (77%) did not have their CK checked
Nidhaan A, Hastings A, Gonzalez D, Joshi R gilbert N, O'connor C. Frequency of Checking Creatine Kinase in Patients on Statins with Elevated Transaminase for Early
Detection of Statin Induced Myopathy [abstract]. Arthritis Rheumatol. 2022; 74 (suppl 9).
35. Strategies to increase statin tolerance
• Try “N of 1” personal trial off and on statin with symptom diary
• Switch brands
• Lower the dose
• Every other day or 3x/week dosing
• Lower dose of statin plus other non-statin
36. 2022 ACC Expert Consensus Decision
Pathway for Statin Intolerance
• Builds on the 2018 AHA/ACC/Multi-society cholesterol guideline
• Provides helpful guidance in several key areas on the use of
newer (approved since 2018) non-statin therapies for primary
and secondary prevention
• In patients with clinical ASCVD and partial or
complete statin intolerance;
• ezetimibe or a PCSK9 mAb inhibitor (evolocumab, alirocumab)
first-line non-statin therapy.
• bempedoic acid and inclisiran second line non-statin therapy
J Am Coll Cardiol. 2022 Oct 4;80(14):1366-1418.
37. What about CoQ10?
• Several studies have shown that statins reduce CoQ10 plasma levels in skeletal muscle tissue
(humans and rodents)
• A deficit of CoQ10 does not seem to be associated with:
-statin type
-intensity
-treatment duration
• Statins may interfere with mitochondrial function, causing an impaired muscle performance,
resulting in muscle damage.
• Structural abnormalities were detected in muscle biopsies of patients treated with statins, even
when they did not experience any symptoms
• 60 Patient RCT: The addition of CoQ10 (100 mg/day) x 3 months with
half dosage statin in patients with previous intolerance to statins improves
the perception of clinical symptoms such as asthenia, myalgia or pain.
Vladutiu G.D., Muscle Nerve. 2006;34:153–162.
Marcoff L. J. Am. Coll. Cardiol. 2007;49:2231–2237.
Mohaupt M.G. CMAJ. 2009;181:E11–E18.
Derosa G, Drug Des Devel Ther. 2019 Oct 21;13:3647-3655.
38. What about supplements?
The SPORT study
• ¾ of US citizens take a supplement ; 20 % for “heart health” or “cholesterol
health”
• Daily rosuvastatin (5 mg) lowered LDL, total cholesterol and serum
triglycerides significantly more than placebo and 6 common supplements
• No supplement lowered LDL more than placebo
• Over-the-counter dietary supplements
• Fish oil
• Cinnamon
• Garlic
• Turmeric
• Plant sterols
• Red yeast rice*
28 day 8-arm randomized, double-blind trial; 190 adults aged 40 to 75 years
who had LDL between 70 and 189 mg/dL, no history of atherosclerotic CVD and
an increased 10-year risk of ASCVD Laffin LJ, et al. J Am Coll Cardiol. 2022;doi:10.1016/j.jacc.2022.10.013.
39.
40. References (I)
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and 100-kd proteins is associated with an immune-mediated necrotizing myopathy. Arthritis Rheum. 2010 Sep;62(9):2757-66.
• Mammen AL, Chung T, Christopher-Stine L, Rosen P, Rosen A, Doering KR, Casciola-Rosen LA. Autoantibodies against 3-
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• Stroes ES, Thompson PD, Corsini A, et al. Statin-associated muscle symptoms: impact on statin therapy-European
Atherosclerosis Society Consensus Panel Statement on Assessment, Aetiology and Management. Eur Heart J. 2015 May
1;36(17):1012-22.
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PB, Brinton EA, Pollak A, Braun LT, Welty FK; American Heart Association Clinical Lipidology, Lipoprotein, Metabolism and
Thrombosis Committee, a Joint Committee of the Council on Atherosclerosis, Thrombosis and Vascular Biology and Council on
Lifestyle and Cardiometabolic Health; Council on Cardiovascular Disease in the Young; Council on Clinical Cardiology; and
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41. References (II)
• Newman CB. Safety of Statins and Nonstatins for Treatment of Dyslipidemia. Endocrinol Metab Clin North Am. 2022
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▪ Gislason G.H., Rasmussen J.N., Abildstrøm S.Z., Gadsbøll N., Buch P., Friberg J., Rasmussen S., Køber L., Stender S., Madsen
M., et al. Long-term compliance with beta-blockers, angiotensin-converting enzyme inhibitors, and statins after acute myocardial
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▪ Blackburn D.F., Dobson R.T., Blackburn J.L., Wilson T.W., Stang M.R., Semchuk W. Adherence to statins, beta-blockers and
angiotensin-converting enzyme inhibitors following a first cardiovascular event: A retrospective cohort study. Can. J. Cardiol.
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