scholarly journals Amiodarone-Induced Acute Liver Injury

2020 ◽  
Vol 14 (1) ◽  
pp. 87-90
Author(s):  
Rajesh Essrani ◽  
Shehriyar Mehershahi ◽  
Rajesh Kumar Essrani ◽  
Shri Jai Kirshan Ravi ◽  
Sajeer Bhura ◽  
...  

Amiodarone is a lipophilic structure with a half-life of 25–100 days. Long-term oral amiodarone is associated with photosensitivity, thyroid dysfunction, and pulmonary and hepatic toxicity. Intravenous amiodarone can lead to sweating, heating sensation, nausea, phlebitis at the injection site, and rarely acute hepatitis. This is a compelling case of a 60-year-old male who developed acute liver injury 24–36 h after starting amiodarone. All the possible causes of acute liver injury were ruled out, and his liver enzymes improved after discontinuing amiodarone.

2011 ◽  
Vol 46 (11) ◽  
pp. 835-838
Author(s):  
Sinister Joel

The purpose of this feature is to heighten awareness of specific adverse drug reactions (ADRs), discuss methods of prevention, and promote reporting of ADRs to the US Food and Drug Administration's (FDA's) MEDWATCH program (800-FDA-1088). If you have reported an interesting, preventable ADR to MEDWATCH, please consider sharing the account with our readers.


2020 ◽  
Vol 2020 ◽  
pp. 1-4
Author(s):  
Lucas Ramer ◽  
Matthieu Tihy ◽  
Nicolas Goossens ◽  
Jean-Louis Frossard ◽  
Laura Rubbia-Brandt ◽  
...  

Disulfiram is a drug used to treat alcohol dependence since many years. It interferes with the metabolism of alcohol, may be associated with neurological and dermatological symptoms, and can be hepatotoxic. Due to the frequent coexistent liver test alterations due to alcohol, the true incidence of disulfiram-associated liver injury is unclear and severity of injury may vary from mildly elevated liver enzymes to fulminant hepatitis leading to death. There are several reported cases of disulfiram hepatitis in the literature. Liver histology, when available, demonstrates some degree of portal inflammation with eosinophils and hepatocyte necrosis. We present here a well-documented case of acute hepatitis due to disulfiram with typical histological lesions, favorable outcome following drug withdrawal, and a brief steroid course. The risk of hepatotoxicity should be kept in mind when prescribing disulfiram.


Hepatology ◽  
2015 ◽  
Vol 62 (4) ◽  
pp. 1070-1085 ◽  
Author(s):  
Binxia Chang ◽  
Ming-Jiang Xu ◽  
Zhou Zhou ◽  
Yan Cai ◽  
Man Li ◽  
...  

2011 ◽  
Vol 29 (7) ◽  
pp. 843.e5-843.e6 ◽  
Author(s):  
Andrea Verhovez ◽  
Fabrizio Elia ◽  
Alessandra Riva ◽  
Giovanni Ferrari ◽  
Franco Aprà

2014 ◽  
Vol 6 (2) ◽  
pp. 36-37
Author(s):  
Joseph P.M. Kane ◽  
Francis A. O'Neill

Clozapine, whilst associated commonly with a transient and benign increase in liver enzymes, has also been associated with varying presentations of hepatitis in existing case reports. This report describes what we believe to be the first documented case of acute liver injury and pleural effusion associated with clozapine, resolving after cessation of the agent. The case supports existing literature in advocating a high index of suspicion, particularly in the 4-5 weeks following clozapine initiation, when considering nonspecific clinical symptoms and signs.


PPAR Research ◽  
2018 ◽  
Vol 2018 ◽  
pp. 1-14 ◽  
Author(s):  
Wenwen Wang ◽  
Kan Chen ◽  
Yujing Xia ◽  
Wenhui Mo ◽  
Fan Wang ◽  
...  

Objective. Previous studies have characterized the hepatoprotective and anti-inflammatory properties of oleanolic acid (OA). This study aimed to investigate the molecular mechanisms of OA hepatoprotection in concanavalin A- (ConA-) induced acute liver injury.Materials and Methods. ConA (20 mg/kg) was intravenously injected to induce acute liver injury in Balb/C mice. OA pretreatment (20, 40, and 80 mg/kg) was administered subcutaneously once daily for 3 consecutive days prior to treatment with ConA; 2, 8, and 24 h after ConA injection, the levels of serum liver enzymes and the histopathology of major factors and inflammatory cytokines were determined.Results. OA reduced the release of serum liver enzymes and inflammatory factors and prevented ConA mediated damage to the liver. OA elevated the expression levels of peroxisome proliferator-activated receptor alpha (PPARα) and decreased the phosphorylation of c-Jun NH2-terminal kinase (JNK).Conclusion. OA exhibits anti-inflammatory properties during ConA-induced acute liver injury by attenuating apoptosis and autophagy through activation of PPARαand downregulation of JNK signaling.


2019 ◽  
Vol 116 (18) ◽  
pp. 9125-9134 ◽  
Author(s):  
Min-Jung Park ◽  
Louis G. D’Alecy ◽  
Michelle A. Anderson ◽  
Venkatesha Basrur ◽  
Yongjia Feng ◽  
...  

Carbamoyl phosphate synthetase-1 (CPS1) is the major mitochondrial urea cycle enzyme in hepatocytes. It is released into mouse and human blood during acute liver injury, where is has a short half-life. The function of CPS1 in blood and the reason for its short half-life in serum are unknown. We show that CPS1 is released normally into mouse and human bile, and pathologically into blood during acute liver injury. Other cytoplasmic and mitochondrial urea cycle enzymes are also found in normal mouse bile. Serum, bile, and purified CPS1 manifest sedimentation properties that overlap with extracellular vesicles, due to the propensity of CPS1 to aggregate despite being released primarily as a soluble protein. During liver injury, CPS1 in blood is rapidly sequestered by monocytes, leading to monocyte M2-polarization and homing to the liver independent of its enzyme activity. Recombinant CPS1 (rCPS1), but not control r-transferrin, increases hepatic macrophage numbers and phagocytic activity. Notably, rCPS1 does not activate hepatic macrophages directly; rather, it activates bone marrow and circulating monocytes that then home to the liver. rCPS1 administration prevents mouse liver damage induced by Fas ligand or acetaminophen, but this protection is absent in macrophage-deficient mice. Moreover, rCPS1 protects from acetaminophen-induced liver injury even when given therapeutically after injury induction. In summary, CPS1 is normally found in bile but is released by hepatocytes into blood upon liver damage. We demonstrate a nonenzymatic function of CPS1 as an antiinflammatory protective cytokine during acute liver injury.


2019 ◽  
Vol 17 (5) ◽  
pp. 1004-1006 ◽  
Author(s):  
Stefanie Quickert ◽  
Philipp A. Reuken ◽  
Michael Rose ◽  
Katharina Boden ◽  
Tony Bruns

2021 ◽  
Vol 14 (6) ◽  
pp. e242853
Author(s):  
Pierre-Clément Thiebaud ◽  
Christelle Hermand ◽  
Jennifer Sobotka ◽  
Pierre-Alexis Raynal

Patients with COVID-19 may be asymptomatic or present with extrarespiratory symptoms, such as liver injury. It has been reported that 22.5%–46.2% of patients have moderate elevation of liver enzymes. To our knowledge, acute hepatitis has never been described as an isolated symptom of COVID-19 in a previously healthy patient. We report the case of a 53-year-old patient with COVID-19 whose first clinical presentation was acute icteric hepatitis, several days before the development of others symptoms. During the pandemic, we suggest that patients with acute hepatitis be considered as COVID-19 suspects, tested and isolated.


2018 ◽  
Vol 12 (2) ◽  
pp. 230-233 ◽  
Author(s):  
Layth Al Attar ◽  
Wiliam Kilgore

Acute liver injury is an alarming condition, as it may lead to a devastating outcome. Of the many causes of acute liver injury, review of medications is crucial to identifying the cause of the injury. Some commonly used medications may unpredictably be the underlying cause of liver injury. We present a case of Peyronie’s disease treated with potassium para-aminobenzoate that developed acute liver injury. After starting the new treatment, the patient complained of right upper quadrant pain. He was found to have elevated liver enzymes. The condition resolved after stopping potassium para-aminobenzoate use. We report a potassium para-aminobenzoate side effect of liver injury that can be managed conservatively.


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