Hepatomegaly Following Short‐Term High‐Dose Steroid Therapy

  title={Hepatomegaly Following Short‐Term High‐Dose Steroid Therapy},
  author={Theodore C. Iancu and Hanna Shiloh and Leon H. Dembo},
  journal={Journal of Pediatric Gastroenterology and Nutrition},
Summary Children treated with large doses of corticosteroids were found to develop hepatomegaly within a few days. No relationship could be established between the condition for which steroids were given and the liver enlargement. Liver biopsy was thought to be indicated, and thus was performed in three children because of diagnostic uncertainty. The light and electron microscopic examinations revealed normal liver architecture, without edema, sinusoid engorgement, or inflammatory changes. The… 
Glycogenic hepatopathy: A narrative review
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, which has been a recent report of varying degree of liver fibrosisidentified in patients with GH.
A case of glycogenic hepatopathy developed in a patient with new-onset fulminant type 1 diabetes: the role of image modalities in diagnosing hepatic glycogen deposition including gradient-dual-echo MRI.
A 21-year-old male patient with new-onset fulminant T1D complicated with diabetic ketoacidosis who subsequently developed GH just after the initiation of insulin treatment is demonstrated.
Hepatocellular Glycogen Accumulation in the Setting of Poorly Controlled Type 1 Diabetes Mellitus: Case Report and Review of the Literature
A case of a 23-year-old woman with a medical history of poorly controlled type 1 DM and gastroesophageal reflux disease who presented with progressively worsening right-sided abdominal pain and an aggressive glucose control regimen was implemented leading to resolution of symptoms and improvement in AST, ALT, and ALP.
Dumping Syndrome, a Cause of Acquired Glycogenic Hepatopathy
  • J. Resnick, I. Zador, D. Fish
  • Medicine
    Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
  • 2011
Dumping syndrome is proposed to be a cause of hepatocellular glycogenosis, the latter representing a form of acquired glycogenic hepatopathy.
Focal Hepatic Glycogenosis in a Patient With Uncontrolled Diabetes Mellitus Type 1.
This is the first reported case of abnormal focal glycogen deposition in a patient with diabetes mellitus type 1 with imaging and pathologic correlation and awareness of the imaging appearance of focal glycogens deposition can help to distinguish it from other pathologic conditions.
Four cases of type 1 diabetes mellitus showing sharp serum transaminase increases and hepatomegaly due to glycogenic hepatopathy
Clinicians should be aware of and recognize GH when dealing with uncontrolled DM patients and extremely high serum elevations of transaminases are important to identify clinically.
Glycogenic Hepatopathy in Type 1 Diabetes Mellitus
A 19-year-old male case, diagnosed with glycogenic hepatopathy, was put on glycemic control which led to significant decline in hepatomegaly and liver enzymes, and it was emphasized that, in type 1 diabetes mellitus cases, hepatopathy should also be considered in the differential diagnoses of elevated liver enzyme and hepatitis.
Differential Diagnosis of a Patient with Lysosomal Acid Lipase Deficiency: A Case Report
Although it occurs rarely, lysosomal acid lipase deficiency (LAL-D) should be considered in the differential diagnosis of microvesicular steatosis for a timely diagnosis in an obese 12-year-old boy of Mexican origin.
Glycogenic Hepatopathy
A 19-year-old woman with a history of poorly controlled diabetes mellitus and frequent admissions for diabetic ketoacidosis, who presented with abdominal pain, nausea, vomiting, and hepatomegaly, underwent a liver biopsy, which showed excessive intracytoplasmic glycogen accumulation consistent with glycogenic hepatopathy.
The present study suggests that drug interactions observed during corticosteroid therapy may be mediated, at least in part, through increased biliary, and also renal, excretion of P‐gp substrates, with primary periportal zonation with differential changes during induction.