scholarly journals CASE SERIES: ANTITUBERCULAR THERAPY-INDUCED HEPATITIS

Author(s):  
SIRISHA G

Drug-induced liver injury (DILI) accounts for 20–40% of cases of fulminant hepatic failure. Antitubercular therapy (ATT) may cause hepatotoxicity which can range from transient asymptomatic rise in liver enzymes to acute liver failure. The drugs in ATT responsible for hepatotoxicity include isoniazid, rifampicin, and pyrazinamide. Case series was done to present three different cases of ATT-induced hepatotoxicity which came to the Clinical Pharmacology and Therapeutics Department in NIMS for management.

2015 ◽  
Vol 8 (4) ◽  
pp. 190-192 ◽  
Author(s):  
Tabassum Firoz ◽  
Douglas Webber ◽  
Hilary Rowe

Liver disease in pregnancy can be classified as predating, co-incidental or unique to pregnancy. Medications are often overlooked as a significant cause of liver disease. We present the case of a 39-year-old patient who presented at 20 weeks with jaundice, elevated liver enzymes, and abnormal liver function progressing eventually to fulminant hepatic failure. The patient was on methyldopa and labetalol from 12 weeks’ gestational age. Liver biopsy was consistent with drug-induced liver injury. Both methyldopa and labetalol have been associated with hepatotoxicity including liver failure. This case highlights the importance of including medications as a cause of liver failure in pregnant patients.


2021 ◽  
Vol 17 (1) ◽  
pp. 5
Author(s):  
Sonal Singh ◽  
Anuj Singhal ◽  
ArunKumar Yadav ◽  
AmarTej Atal ◽  
Shubham Shukla

2000 ◽  
Vol 124 (12) ◽  
pp. 1800-1803 ◽  
Author(s):  
Marius J-M. Ilario ◽  
Jose E. Ruiz ◽  
Constantine A. Axiotis

Abstract Massive hepatic necrosis following exposure to phenytoin and trimethoprim-sulfamethoxazole is a rare occurrence and to the best of our knowledge has not been reported previously. Acute hepatic failure following administration of trimethoprim-sulfamethoxazole has rarely been seen, and only 4 cases have been well documented pathologically. We report a case of acute liver failure in a 60-year-old woman following ingestion of phenytoin and trimethoprim-sulfamethoxazole concomitantly over a 9-day period. Autopsy findings revealed acute fulminant hepatic failure. This case demonstrates the effects of chemical-chemical interactions in the potentiation of hepatotoxicity of single agents and specifically illustrates the need for discontinuing trimethoprim-sulfamethoxazole in the presence of early liver injury.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Christopher M. Karousatos ◽  
Justin K. Lee ◽  
David R. Braxton ◽  
Tse-Ling Fong

Abstract Background Complementary and alternative medicine use among Americans is prevalent. Originating in India, Ayurvedic medicine use in the United States has grown 57% since 2002. CAM accounts for a significant proportion of drug induced liver injury in India and China, but there have been only three reports of drug induced liver injury from Ayurvedic medications in the U.S. We report three cases of suspected Ayurvedic medication associated liver injury seen at a Southern California community hospital and review literature of Ayurvedic medication induced liver injury. Case presentations Three patients presented with acute hepatocellular injury and jaundice after taking Ayurvedic supplements for 90–120 days. First patient took Giloy Kwath consisting solely of Tinospora cordifolia. Second patient took Manjishthadi Kwatham and Aragwadhi Kwatham, which contained 52 and 10 individual plant extracts, respectively. Third patient took Kanchnar Guggulu, containing 10 individual plant extracts. Aminotransferase activities decreased 50% in < 30 days and all 3 patients made a full recovery. Roussel Uclaf Causality Assessment Method (RUCAM) scores were 7–8, indicating probable causality. These products all contained ingredients in other Ayurvedic and traditional Chinese medicines with previously reported associations with drug induced liver injury. Conclusions These patients highlight the risk of drug induced liver injury from Ayurvedic medications and the complexity of determining causality. There is a need for a platform like LiverTox.gov to catalog Ayurvedic ingredients causing liver damage.


2018 ◽  
Vol 113 (Supplement) ◽  
pp. S1350-S1351
Author(s):  
Majd Khasawneh ◽  
Zaid Imam ◽  
Fadi Odish ◽  
Mohamad Rasm Al Sibae

2017 ◽  
Vol 11 (3) ◽  
pp. 564-568 ◽  
Author(s):  
Qin Rao ◽  
Isaiah Schuster ◽  
Talal Seoud ◽  
Kevin Zarrabi ◽  
Nirvani Goolsarran

Nafcillin-induced acute liver injury is a rare and potentially fatal complication that has been known since the 1960s but inadequately studied. At this time, the only proven treatment is early discontinuation of the drug. Because of the high prevalence of nafcillin class antibiotic use in the United States, it is important for clinicians to have a high clinical suspicion for this diagnosis. We present a case of liver failure attributable to nafcillin use in a 68-year-old male with a history methicillin-sensitive Staphylococcus and L3/L4 osteomyelitis. After starting long-term antibiotic therapy, he presented with painless jaundice which necessitated discontinuation of the drug. At the time of presentation, the patient’s lab work exhibited a bilirubin/direct bilirubin of 9.4/8.2 mg/dL, alkaline phosphatase of 311 IU/L, and aspartate transaminase/alanine transaminase of 109/127 IU/L. The patient was switched to i.v. vancomycin given the concern for drug-induced liver injury. Imaging did not show obstruction of the hepatobiliary or pancreaticobiliary trees. Serology was unremarkable for viral etiology, autoimmune processes, Wilson disease, and hemochromatosis. A liver biopsy showed findings consistent with drug-induced liver injury. The patient’s liver function tests peaked at day 7 of admission and trended towards normal levels with cessation of nafcillin therapy. The patient was discharged with a diagnosis of nafcillin-induced acute liver injury. Our case highlights the importance of early recognition of the diagnosis and careful monitoring of liver function when nafcillin is employed in the clinical setting.


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