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| | Nonalcoholic fatty liver disease (NAFLD) | Glycogenic hepatopathy (GH) |
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| Clinically | Symptoms: asymptomatic | Symptoms: mild epigastric pain, nausea, and vomiting. |
| Signs: nontender hepatomegaly | Signs: hepatomegaly ± tenderness. |
| Liver enzymes: mild to moderate (less than 5 times the upper normal limit), persistent elevated liver enzymes | Liver enzymes: severe flares of transaminases reaching up to 2000–4000 U/L |
| Liver function panel: depends on the degree of liver injury | Liver function panel: normal |
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| Radiological | Abdominal CT scan:
reduced hepatic CT attenuation due to fat deposition in the liver (low density) | Abdominal CT scan:
increased hepatic CT attenuation due to glycogen deposition in to liver (high density) |
| Gradient-dual-echo MRI can be considered a powerfully noninvasive tool for identification | Gradient-dual-echo MRI can be considered a powerfully noninvasive tool for identification |
| (i) High intensity on subtraction | (i) Low intensity on subtraction |
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| Histologically | Histological finding: (for a definitive diagnosis)
Ranges from
(i) steatosis alone
(ii) to nonalcoholic steatohepatitis (NASH) with varying risks of progression to cirrhosis | Histological finding: (for definitive diagnosis)
(i) swollen hepatocytes and pale cytoplasm
(ii) abundant cytoplasmic glycogen deposits are demonstrated by periodic acid-Schiff (PAS) staining and glycogen removal is demonstrated by diastase digestion
(iii) no evidence of necrosis, inflammation, steatosis, or fibrosis |
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| Pathogenesis | (i) Common in T2DM and T1DM, regardless of insulin therapy | (i) Common in T1DM and rare in T2DM with insulin therapy |
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| Treatment Prognosis | (i) Can progress to fibrosis and cirrhosis | (i) No progression to fibrosis or cirrhosis |
| (ii) Optimize treatment of risk factors and lifestyle modification | (ii) Reversible with adequate glycemic control |
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