scholarly journals Drug-induced fulminant hepatic failure in pregnancy

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.

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.


2021 ◽  
Vol 5 (4) ◽  
pp. 279-286
Author(s):  
Rodrigo Dorelo ◽  
Samantha T.A. Barcelos ◽  
Magela Barros ◽  
Valeria Elustondo ◽  
Ysela Y.P. Pérez ◽  
...  

Introduction and aim: Drug-induced liver injury (DILI) manifests as a spectrum of clinical presentations that carries morbidity and mortality. Patients with chronic liver disease (CLD), particularly hospitalized, are at high risk for developing DILI. We aimed to investigate the use of potentially hepatotoxic drugs (PHD) in patients with CLD in a tertiary university hospital. Materials and methods: Adult (≥ 18 years-old) with CLD admitted to the hospital from January 2016 to December 2018 were evaluated regarding PHD, assessing the risk of DILI and liver enzymes behavior after exposure. Results: From 931 hospitalized patients with CLD, 291 (31.3%) were exposed to hepatotoxic drugs during their hospitalization. Of those, 244 (83.8%) were cirrhotic. The most frequent causes of liver disease were hepatitis C (41.2%), followed by alcohol (13.2%), hepatitis C/alcohol (11.7%) and non-alcoholic fatty liver disease (5.8%). Decompensated cirrhosis (46.7%) was the main reason for hospital admission. The most often prescribed PHD were antibiotics (67.7%), cardiovascular drugs (34.4%), neuromodulators (26.1%) and anesthetics (19.9%). After exposure, 113 patients (38.8%) presented significant elevated liver enzymes. Surprisingly, PHD were more often prescribed in GI/Liver unit (48.8%) followed by emergency/intensive care unit (28.5%). A total of 65 patients (22%) died, however in neither case was it possible to safely infer causal relationship among PHD, liver enzymes and death. Conclusion: PHD prescription is frequent in patients with CLD even in a tertiary university hospital and in the gastroenterology and hepatology department, exposing these patients to an additional risk.


2019 ◽  
Vol 12 (11) ◽  
pp. e231741 ◽  
Author(s):  
Chencheng Xie ◽  
Hafez Mohammad Ammar Abdullah ◽  
Mohamed Abdallah ◽  
Erin Quist ◽  
Mumtaz Niazi

Anastrozole is an aromatase inhibitor that has been used more frequently over the last decade especially for oestrogen receptor-positive breast cancer. It has a relatively safe side effect profile. However, occasionally it has been associated with serious adverse events. Here, we present the case of a 58-year-old woman who presented with significantly elevated liver enzymes 4 years after starting anastrozole. She was not taking any other medications and an extensive workup did not reveal any other cause for her liver injury. The patient’s liver enzymes normalised after discounting the anastrozole. She scored 4 on the updated Roussel Uclaf Causality Assessment Method grading system which was possible for drug-induced liver injury. A review of the literature revealed six prior cases of anastrozole-related liver injury. Anastrozole should be considered as a possible culprit in patients who develop an unexplained acute liver injury.


2010 ◽  
Vol 29 (7) ◽  
pp. 615-622 ◽  
Author(s):  
Cătălina Lionte

Chloroform is a potent central nervous system and respiratory depressant. The toxicities associated with chloroform frequently occur after inhalation. Hepatotoxicity is secondary to production of a toxic metabolite, with a peak elevation of liver enzymes 72 hours after exposure. Acute liver failure after chloroform inhalation is rarely described, this syndrome being produced mainly by viral hepatitis, idiosyncratic drug-induced liver injury, and acetaminophen ingestion. This report describes the case of a 46-year-old woman who presented to emergency department with coma, signs of respiratory failure, and solvent odor of her breath after chloroform inhalation and binge drinking. In evolution appeared lethal acute liver failure and rhabdomyolysis, despite maximum supportive care. Necroptic examination revealed microvesicular steatosis and tubular renal necrosis, specific for chloroform toxicity. This case illustrates the dramatic impact on liver of two well-recognized hepatotoxins. Mechanisms of chloroform and alcohol-induced liver toxicity are reviewed.


2017 ◽  
Vol 10 ◽  
pp. 117954761773137 ◽  
Author(s):  
Silje Bergland Ellingsen ◽  
Elisabet Nordmo ◽  
Knut Tore Lappegård

Severe hepatotoxicity is a rare but well-known adverse reaction to statins. However, despite the widespread use of statins, only a few cases describing statin reexposure or switch to another statin after liver injury have been published. The literature on hepatotoxicity with ezetimibe alone or in combination with statins is also scarce. We report a case where a patient with a history of elevated liver enzymes while using atorvastatin, but prior and subsequent good tolerance to simvastatin and pravastatin, developed drug-induced liver injury on reexposure to a combination of atorvastatin and ezetimibe. The hepatotoxicity in our patient was most likely caused by reexposure to atorvastatin, although we cannot exclude ezetimibe as a contributing factor. This case highlights the risk of hepatotoxicity recurrence on rechallenge with the same statin. The tolerance to other statins in this case also strengthens the suspicion that statin-induced liver injury may not be a class effect, although the current data are too scarce to draw any definite conclusions.


2021 ◽  
Vol 8 (8) ◽  
pp. 1239
Author(s):  
Anant Parasher ◽  
Vandana Mohan

Fulminant hepatic failure is defined as a sudden, severe impairment of hepatic function leading to an encephalopathy, which occurs within eight weeks of appearance of first symptoms in the absence of pre-existing liver disease. The spectrum of liver disease in pregnancy may range from mild asymptomatic transaminitis to fatal and irreversible deterioration in liver function leading to significant morbidity and even mortality. Hepatic dysfunction in pregnancy may be categorized into Pre-eclampsia-associated liver diseases such as pre-eclampsia/eclampsia, the HELLP syndrome and Acute fatty liver of pregnancy (AFLP), and other causes of hepatic dysfunction namely Hyperemesis gravidarum (HG) and Intrahepatic cholestasis of pregnancy (IHCP). For this review, a search was conducted for published articles, case reports and clinical trials in MEDLINE/Pubmed from 1970 to 2020 with the keyword’s fulminant hepatic failure, acute liver failure in pregnancy, pre-eclampsia, HELLP and AFLP. We concluded that fulminant hepatic failure is one of the most dreaded complications in pregnancy in obstetrical units worldwide. Mandatory screening for etiology, early diagnosis and initiation of supportive management as soon as possible are absolutely essential to ensure better maternal and fetal outcomes. Effective communication with the obstetrician regarding timely delivery/termination of pregnancy ensures a favourable prognosis in the majority of cases. Liver transplant is a definitive life-saving option for cases of severe fulminant hepatic failure in pregnancy, and management has to be suited to each patient individually, keeping in mind the well-being of both the mother, and the child.


Pathogens ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 430 ◽  
Author(s):  
Katie Morgan ◽  
Kay Samuel ◽  
Martin Vandeputte ◽  
Peter C. Hayes ◽  
John N. Plevris

A novel strain of coronoviridae (SARS-CoV-2) was reported in Wuhan China in December 2019. Initially, infection presented with a broad spectrum of symptoms which typically included muscle aches, fever, dry cough, and shortness of breath. SARS-CoV-2 enters cells via ACE2 receptors which are abundant throughout the respiratory tract. However, there is evidence that these receptors are abundant throughout the body, and just as abundant in cholangiocytes as alveolar cells, posing the question of possible direct liver injury. While liver enzymes and function tests do seem to be deranged in some patients, it is questionable if the injury is due to direct viral damage, drug-induced liver injury, hypoxia, or microthromboses. Likely, the injury is multifactoral, and management of infected patients with pre-existing liver disease should be taken into consideration. Ultimately, a vaccine is needed to aid in reducing cases of SARS-CoV-2 and providing immunity to the general population. However, while considering the types of vaccines available, safety concerns, particularly of RNA- or DNA-based vaccines, need to be addressed.


2020 ◽  
Vol 8 ◽  
pp. 2050313X2091782
Author(s):  
Ginny Varghese ◽  
Lama Madi ◽  
Muna Ghannam ◽  
Rafaat Saad

Amlodipine is a commonly prescribed antihypertensive drug, well tolerated and has rarely been attributed as a cause for elevated liver enzymes. Here, we present a 47-year-old male patient known to be hypertensive and admitted to our rehabilitation facility after an acute stroke. During his stay, amlodipine was started in addition to other antihypertensive medications to control his blood pressure. His liver transaminases after 4 days (notably alanine aminotransferase) were found to be markedly elevated. After reviewing the medications and investigating probable causes, amlodipine was suspended. After 5 days of suspending amlodipine, the transaminases started to trend downward. The Naranjo Adverse Drug Reaction Probability Scale and the Roussel Uclaf Causality Assessment Method were performed to assess causality in this suspected idiosyncratic drug-induced liver injury case. Both the scores denoted a probable amlodipine-induced liver injury. Previous case reports related to amlodipine-induced liver injury are mentioned and presented in the table below. In conclusion, amlodipine, though not well known to be hepatotoxic, can induce liver enzyme elevations in an idiosyncratic manner.


2020 ◽  
Vol 8 ◽  
pp. 232470962095132
Author(s):  
Simcha Weissman ◽  
Nishan G. Rajaratnam ◽  
Nabeel Qureshi ◽  
Faisal Inayat ◽  
Sameh Elias

Antithyroid drug-induced severe liver injury is an uncommon but serious complication. We hereby delineate the case of a 38-year-old female who presented to the emergency department for an impending thyroid storm. After initiation of a single dose of propylthiouracil, her liver enzymes went into the thousands. She was subsequently admitted to the intensive care unit. Propylthiouracil was discontinued and corticosteroids were initiated with the resolution of her elevated liver enzymes. On follow-up, her liver function was at its baseline and thyroid hormone levels were under control. We hope this report will encourage clinicians to cast a broad differential diagnosis in patients presenting with liver injury in the acute setting. Furthermore, it is imperative to raise awareness regarding the ever-increasing list of pharmacologic agents that can perpetuate drug-induced hepatotoxicity.


2018 ◽  
Author(s):  
Pamela L Valentino ◽  
Udeme D Ekong

The approach to elevated liver transaminases presented here includes an understanding of the biochemical testing, as well as a sequential pathway of investigations. In the pediatric patient who is not in acute liver failure, we discuss the differential diagnoses that should be considered, categorized in a systems-based approach. Infectious, autoimmune, genetic/metabolic, and cholestatic disease; drug-induced liver injury; and nonalcoholic fatty liver disease are among the categories that should be considered. Following a thorough history and physical examination, the patient should be referred to a pediatric specialist with expertise in the diagnosis and treatment of liver disease. Appropriate investigations by a pediatric gastroenterologist/hepatologist initially include blood tests and abdominal Doppler ultrasonography.   This review contains 4 figures, 3 tables and 42 references Key words: acute liver failure, alanine aminotransferase, aspartate aminotransferase, cholestasis, chronic hepatitis, cirrhosis, elevated liver enzymes, end-stage liver disease, γ-glutamyl transaminase, portal hypertension


Sign in / Sign up

Export Citation Format

Share Document