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Old 09-11-2011
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Default Q. No.2 Git

A 37-year-old woman presents for evaluation of abnormal liver chemistries. She has long-standing obesity (current BMI 38) and has previously taken anorectic medications but not for the past several years. She takes no other medications and has not used parenteral drugs or had high-risk sexual exposure. On examination, her liver span is 13 cm; she has no spider angiomas or splenomegaly. Several sets of liver enzymes have shown transaminases two to three times normal. Bilirubin and alkaline phosphatase are normal. Hepatitis B surface antigen and hepatitis C antibody are normal, as are serum iron and total iron-binding capacity. Which of the following is the likely pathology on liver biopsy?

A)Macrovesicular fatty liver
B)Microvesicular fatty liver
C)Portal triaditis with piecemeal necrosis
D)Cirrhosis
E)Copper deposition
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Old 09-11-2011
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Default A

I'd go for A - macrovesicular changes in non-alcoholic steatohepatitis, seen in obese patients (gross macrovesicular fatty change with inflammation with or without Mallory bodies).
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Old 09-11-2011
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I go with C, I believe this is NASH.
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Old 09-11-2011
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The correct answer is A. Macrovesicular fatty liver.

This woman likely has nonalcoholic fatty liver (NAFL), which is associated with macrovesicular accumulation of fat in the liver. If hepatocellular necrosis is present, the condition is termed nonalcoholic steatohepatitis (NASH). This condition is histologically similar to alcoholic hepatitis, and increasing evidence suggests that it too is a precirrhotic condition. With the increasing incidence of obesity in Western societies, NASH may become the commonest cause of cirrhosis and end-stage liver disease.
Microvesicular fat is seen in the acute life-threatening conditions of acute fatty liver of pregnancy and Reye syndrome.
Portal triaditis and piecemeal necrosis of cells in the hepatic lobule are associated with several disorders, including autoimmune and chronic viral hepatitis.
Cirrhosis, characterized by bands of fibrous tissue, regenerating nodules, and disruption of the hepatic architecture, is the final common pathway of various chronic insults to the liver. Copper deposition is seen in Wilson disease.
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Old 09-11-2011
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Thanks for this really good Q. I have a question, how can we differentiate from the clinical scenario between NAFL & NASH ?.
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Old 09-11-2011
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Quote:
Originally Posted by ag2011n View Post
Thanks for this really good Q. I have a question, how can we differentiate from the clinical scenario between NAFL & NASH ?.
Good question, i think we cannot we need to do liver biopsy to differentiate the two. But generally NAFLD is more common.

I remember reading somewhere that the disease progression is like that

10% of cases of NAFLD progress to NASH in 10 yrs.
10% of cases of NASH progress to cirrhosis in 10 yrs.
10% of cases of cirrhosis progress to Ca in 10 yrs.
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