Medication Bezoar with Extended-Release Nifedipine/Biliary Cirrhosis Caused by Erythromycin/Four Cases of Lactic Acidosis and Hepatic Steatosis Associated with Stavudine Therapy/Acute Myelopathy following Heroin Insufflation/Increased Lithium Concentrations with a “Safe” NSAID/Drug-Induced Stroke and Complications of Intravesical Bacillus Calmette-Guerin

2000 ◽  
Vol 35 (10) ◽  
pp. 1046-1050
Author(s):  
Joel Shuster
Keyword(s):  
Lactic Acidosis ◽  
Hepatic Steatosis ◽  
Extended Release ◽  
Biliary Cirrhosis ◽  
Bacillus Calmette Guerin ◽  
Drug Induced ◽  
Acute Myelopathy

scholarly journals Drug Induced Steatohepatitis: An Uncommon Culprit of a Common Disease

2015 ◽  
Vol 2015 ◽  
pp. 1-14 ◽  
Author(s):  
Liane Rabinowich ◽  
Oren Shibolet
Keyword(s):  
Metabolic Syndrome ◽  
Liver Disease ◽  
Liver Injury ◽  
Hepatic Steatosis ◽  
Early Recognition ◽  
Developed Countries ◽  
Common Disease ◽  
Drug Induced ◽  
Altered Expression ◽  
The Metabolic Syndrome

Nonalcoholic fatty liver disease (NAFLD) is a leading cause of liver disease in developed countries. Its frequency is increasing in the general population mostly due to the widespread occurrence of obesity and the metabolic syndrome. Although drugs and dietary supplements are viewed as a major cause of acute liver injury, drug induced steatosis and steatohepatitis are considered a rare form of drug induced liver injury (DILI). The complex mechanism leading to hepatic steatosis caused by commonly used drugs such as amiodarone, methotrexate, tamoxifen, valproic acid, glucocorticoids, and others is not fully understood. It relates not only to induction of the metabolic syndrome by some drugs but also to their impact on important molecular pathways including increased hepatocytes lipogenesis, decreased secretion of fatty acids, and interruption of mitochondrialβ-oxidation as well as altered expression of genes responsible for drug metabolism. Better familiarity with this type of liver injury is important for early recognition of drug hepatotoxicity and crucial for preventing severe forms of liver injury and cirrhosis. Moreover, understanding the mechanisms leading to drug induced hepatic steatosis may provide much needed clues to the mechanism and potential prevention of the more common form of metabolic steatohepatitis.

Zucker Lean Rats With Hepatic Steatosis Recapitulate Asymptomatic Metabolic Syndrome and Exhibit Greater Sensitivity to Drug-Induced Liver Injury Compared With Standard Nonclinical Sprague-Dawley Rat Model

2020 ◽  
Vol 48 (8) ◽  
pp. 994-1007
Author(s):  
Timothy P. LaBranche ◽  
Anna K. Kopec ◽  
Srinivasa R. Mantena ◽  
Brett D. Hollingshead ◽  
Andrew W. Harrington ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Pharmaceutical Industry ◽  
Liver Injury ◽  
Hepatic Steatosis ◽  
Sprague Dawley ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
Sd Rats ◽  
Normal Chow

Fatty liver disease is a potential risk factor for drug-induced liver injury (DILI). Despite advances in nonclinical in vitro and in vivo models to assess liver injury during drug development, the pharmaceutical industry is still plagued by idiosyncratic DILI. Here, we tested the hypothesis that certain features of asymptomatic metabolic syndrome (namely hepatic steatosis) increase the risk for DILI in certain phenotypes of the human population. Comparison of the Zucker Lean (ZL) and Zucker Fatty rats fed a high fat diet (HFD) revealed that HFD-fed ZL rats developed mild hepatic steatosis with compensatory hyperinsulinemia without increases in liver enzymes. We then challenged steatotic HFD-fed ZL rats and Sprague-Dawley (SD) rats fed normal chow, a nonclinical model widely used in the pharmaceutical industry, with acetaminophen overdose to induce liver injury. Observations in HFD-fed ZL rats included increased liver injury enzymes and greater incidence and severity of hepatic necrosis compared with similarly treated SD rats. The HFD-fed ZL rats also had disproportionately higher hepatic drug accumulation, which was linked with abnormal hepatocellular efflux transporter distribution. Here, we identify ZL rats with HFD-induced hepatic steatosis as a more sensitive nonclinical in vivo test system for modeling DILI compared with SD rats fed normal chow.

Thyrotoxic hepatitis

2017 ◽  
Vol 63 (1) ◽  
pp. 46-50
Author(s):  
Dmitrij V. Pikulev ◽  
Aleksej V. Klemenov
Keyword(s):  
Liver Injury ◽  
Clinical Symptoms ◽  
Correct Diagnosis ◽  
Clinical Signs ◽  
Rare Condition ◽  
Liver Function Tests ◽  
Biliary Cirrhosis ◽  
Liver Pathology ◽  
Drug Induced ◽  
Clinical Variants

In most cases, liver pathology in hyperthyroidism is confined to asymptomatic changes in laboratory indices, while clinical signs are much rarer. Three clinical variants of liver pathology in patients with hyperthyroidism can be differentiated: drug-induced hepatitis that develop in response to administration of thyrostatic agents (mainly propylthiouracil); concomitant autoimmune liver diseases (autoimmune hepatitis, primary biliary cirrhosis), and hepatopathies as a direct manifestation of thyrotoxicosis (thyrotoxic hepatitis). Thyrotoxic hepatitis is a rare condition difficult to diagnose. The variety of etiological factor of liver pathology in hyperthyroidism, universal clinical symptoms, and the lack of specific histological markers make it difficult to make a correct diagnosis. A clinical case of Graves’ disease complicated with severe thyrotoxic hepatitis, the edema-ascites syndrome and hyperbilirubinemia is reported. The patient was diagnosed with thyrotoxic hepatitis after all other reasons for liver pathology have been ruled out. The concomitant thyrogenic myocardiodystrophy, cardiomegaly and atrial fibrillation required ruling out the diagnosis of cardiogenic liver injury and made diagnosing more difficult. Normalization of the thyroid status in patients receiving mercazolyl therapy was accompanied by alleviation of clinical symptoms of hepatitis and the positive dynamics of the indices of liver function tests. A brief review of the data on clinical variants and mechanisms of liver injury in patients with thyrotoxicosis is presented.

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