Drug-Induced Liver Injury in the Setting of Glycogenic Hepatopathy

Maharaj, Valmiki; Fitz, Matthew; Ding, Xianzdong

doi:10.1007/s11606-017-3996-z

Cited by 7 publications

(2 citation statements)

References 9 publications

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“…Should a diabetic patient be on additional medications and the course of management be complicated by continued elevations in transaminases despite fluid resuscitation and treatment with insulin, it would be wise to drug induced liver injury (DILI) along with associated GH. Maharaj et al[ 39 ] published the case of a patient who initially presented with DKA, hepatomegaly, and elevated transaminases but was later diagnosed with GH accompanied by DILI. He had a past medical history of T1DM and bipolar disorder that was being treated with the antipsychotic drugs paliperidone and asenapine.…”

Section: Nafldmentioning

confidence: 99%

Glycogenic hepatopathy: A narrative review

Sherigar

Castro

Yin

et al. 2018

WJH

112

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Glycogenic hepatopathy (GH) is a rare complication of the poorly controlled diabetes mellitus characterized by the transient liver dysfunction with elevated liver enzymes and associated hepatomegaly caused by the reversible accumulation of excess glycogen in the hepatocytes. It is predominantly seen in patients with longstanding type 1 diabetes mellitus and rarely reported in association with type 2 diabetes mellitus. Although it was first observed in the pediatric population, since then, it has been reported in adolescents and adults with or without ketoacidosis. The association of GH with hyperglycemia in diabetes has not been well established. One of the essential elements in the pathophysiology of development of GH is the wide fluctuation in both glucose and insulin levels. GH and non-alcoholic fatty liver disease (NAFLD) are clinically indistinguishable, and latter is more prevalent in diabetic patients and can progress to advanced liver disease and cirrhosis. Gradient dual-echo MRI can distinguish GH from NAFLD; however, GH can reliably be diagnosed only by liver biopsy. Adequate glycemic control can result in complete remission of clinical, laboratory and histological abnormalities. There has been a recent report of varying degree of liver fibrosis identified in patients with GH. Future studies are required to understand the biochemical defects underlying GH, noninvasive, rapid diagnostic tests for GH, and to assess the consequence of the fibrosis identified as severe fibrosis may progress to cirrhosis. Awareness of this entity in the medical community including specialists is low. Here we briefly reviewed the English literature on pathogenesis involved, recent progress in the evaluation, differential diagnosis, and management.

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Section: Nafldmentioning

confidence: 99%

Glycogenic hepatopathy: A narrative review

Sherigar

Castro

Yin

et al. 2018

WJH

112

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“…Glycogen granules were seen outside the hypertrophied cells with the appearance of pale areas that indicate the depletion, especially in the 30 days group. Antipsychotic drug treatment can give rise to hyperglycemia that in turn cause an increase in glycogen consumption, it is also believed that the reactive metabolites have a role in the depletion process (52). Detoxification can cause glycogen depletion (53) that happens after using materials that cause hepatotoxicity, linked completely with the formation of reactive metabolites that lead to glycogenolysis which protects against the toxic side effects of the drug (54).…”

Section: -Disscusionmentioning

confidence: 99%

Morphological and Histopathological Liver Abnormalities Caused by Carbamazepine-Induced Injury in Female Albino Mice

R. Jaber,

A. Al-Bakri

2024

JOBRC

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Background: The adverse effects of drugs can damage various organs, especially the liver, leading to a hepatic injury known as hepatotoxicity. Drug-induced liver injury (DILI) is challenging nowadays because of the large number of different drugs used, one of the offending medications that cause DILI is carbamazepine (CBZ), since the liver has an array of functions including detoxification, it will deal with several damages caused by exposure to the drugs. Objective: investigate the effect of (CBZ) 20mg/kg/day on female mice liver after 14 and 30 days of treatment on morphological and histopathological levels. Materials and methods: 20mg/kg/day of CBZ was administered orally for (14) days to (10) female mice, another (10) mice were taking the same concentration for 30 days, and control groups were administered tap water. Results: The findings showed that CBZ can cause liver enlargement, changes in liver appearance, distortion in Glisson’s capsule, cytologic alterations, hepatocyte hypertrophy, ballooning degeneration, pyknosis, karyolysis, karyomegaly, sinusoids dilation, increase in the number and sizes of Kupffer cells, fibrosis, glycogen depletion, and cirrhosis. Conclusion: These findings have shown that carbamazepine (CBZ) can cause hepatotoxicity that can manifest into morphological and histopathological changes.

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Hepatic Glucose Metabolism and Its Disorders in Fish

Han

Zheng³

et al. 2021

Advances in Experimental Medicine and Biology

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Drug-Induced Liver Injury in the Setting of Glycogenic Hepatopathy

Cited by 7 publications

References 9 publications

Glycogenic hepatopathy: A narrative review

Glycogenic hepatopathy: A narrative review

Morphological and Histopathological Liver Abnormalities Caused by Carbamazepine-Induced Injury in Female Albino Mice

Hepatic Glucose Metabolism and Its Disorders in Fish

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