Drug-induced hepatitis refers to liver inflammation caused by toxic amounts of certain medications. The liver's job is to break down medicines in the blood, but too much medication can damage the liver. Certain factors increase susceptibility to drug-induced hepatitis, including female gender, older age, liver disease, alcohol use, and nutritional deficiencies. Diagnostic tests for potential drug-induced hepatitis include liver function tests and liver biopsy. A case study describes a patient who developed fulminant hepatitis while on antituberculosis medication due to risk factors of smoking and drinking.
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What is hepatitis and drug-induced liver injury
1.
2. What is hepatitis?
◤ Hepatitis refers to an inflammatory condition
of the liver. It is commonly the result of a
viral infection, but there are other possible
causes of hepatitis.
3. What is drug induced hepatitis?
◤ Drug-induced hepatitis is also called drug-
induced liver injury. It is a redness and
swelling (inflammation) of the liver that is
caused by a harmful (toxic) amount of certain
medicines.
◤ The liver helps to break down certain
medicines in your blood. If there is too much
medicine in your blood for your liver to break
down, your liver can become badly damaged.
This can lead to drug-induced hepatitis.
MEDICINES
withdrawn:
Bromfenac
trioglitazone
16. • Drugs have different toxicities based on races due to the rate of metabolic
enzymes which varies from individual to individual.
• Example: blacks and Hispanics have more chances of isoniazid toxicity.
Elderly persons have increased risk of hepatic injury due to decreased drug clearance,
drug-drug interactions, reduced hepatic blood flow.
Drug induced hepatic reactions are more common in females.
RACE
AGE
Risk Factors For Drug-induced Liver Injury
GENDER
17. • Alcohol induces liver injury and cirrhotic changes that alter drug metabolism.
• Alcohol depletes glutathione (hepato-protective) stores making the person
more susceptible to drugs toxicity.
Persons with diseases like AIDS, malnourishment & fasting may be susceptible to
drug reactions because of low glutathione stores.
ALCOHOL
OTHER CO-
MORBIDITIES
• The dose modification in persons having liver disease should be made on the
knowledge of the specific enzyme involved in the metabolism of that drug.
• HIV patients co-infected with hepatitis B or C virus are at more risk for
hepatotoxic effects when treated with antiretroviral therapy.
• Patients with cirrhosis are at increased risk of decompensation by toxic drugs.
LIVER
DISEASES
18. Host Factors That May Enhance Susceptibility To Drugs, Possibly Inducing Hepatitis
Female - Halothane, nitrofurantoin, sulindac
Male - Amoxicillin-clavulanic acid (Augmentin)
Old age - Acetaminophen, halothane, INH, amoxicillin-clavulanic acid
Young age -Salicylates, valproic acid
Fasting or malnutrition - Acetaminophen
Large body mass index/obesity - Halothane
Diabetes mellitus - Methotrexate, niacin
Renal failure - Tetracycline, allopurinol
AIDS - Dapsone, trimethoprim-sulfamethoxazole
Hepatitis C - Ibuprofen, ritonavir, flutamide
Preexisting liver disease - Niacin, tetracycline, methotrexate
24. » malaise
» epigstric pain
» pale skin
Day
1
Day
2
Day
3
a 55-year old patient with a known case of TB meningoencephalitis was started on CAT I ATT (isoniazid
300mg, ethambutol 800mg, rifampicin 450mg) after which he experienced the following symptoms:
CASE STUDY:
» episodic vomiting
» scleral icterus
» anorexia
Patient factors
chainsmoker
alcoholic
Presenting complain
A. Altered senseorium
B. Grade IV breathlessness
C. Abdominal distention
» episodic vomiting
» epigstric discomfort
» malaise
25. Diagnostic test
A. LFT
B. CT scan
C. Blood and urine culture
D. viral serology
E. Liver biopsy
Results:
• Presence of candida albicans
• Hepatomegaly
• scleral icterus
• cerebral edema
LFT NORMAL DAY 5
AST (U/L) 15-17 1900
ALT (U/L) 30-65 1275
ALP (U/L) 50-136 120
T. BILIRUBIN
(µmol/l)
0.1-1.0 239
INR 2.0-3.0 4.1
CASE STUDY:
physical examination
A. unconscious
B. epigastric tenderness
C. opening of eyes to painful stimuli
D. drowsy
26. Treatment
initially the patient was treated with:
• Mannitol 25%
• Inj. dexamethasone 8mg IM
• IV fluids
• Hepatic diet
• Vit. K to prolong INR
• Heparin
• Lactulose syp.
The patient is diagnosed with fulminant
hepatitis due to ATT because there was:
• Elevation of PTT
• Hyperbilirubinemia
• Hyperammonemia
• Increased hepatic cells
• Discontinuation of isoniazid and rifampicin
and added streptomycin 500mg and
ethanbutol 800mg as a substitute for
meningoenchepalitis.
Pharmacist Role
• Educate pt. about the actions and side
effects of drugs.
• Withdraw ATT if DILI symptoms appear.
• Must analyze LFT reports before and after
therapy.
• Must analyze patient factors as smoking
and drinking alcohol exacerbate these
symptoms.
CASE STUDY:
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