Case Presentation:
A 48‐year‐old man presented with two weeks of progressive fatigue, nausea, and malaise. He reported subjective fevers, as well as progressive yellowing of his skin. He had no previous medical problems or prescription drug use. There was no history of intravenous drug use, blood transfusions or heavy alcohol use.
He was an ill appearing gentleman who was afebrile and hemodynamically stable. He was alert and oriented, his sclerae were icteric and his skin diffusely jaundiced. His abdomen was distended without a fluid wave or shifting dullness and he had hepatomegaly with right upper quadrant tenderness.
His aspartate aminotransferase (AST) was 4680 U/L, alanine aminotransferase (ALT) 3640 U/L, alkaline phosphatase 212 U/L
total bilirubin 16 mg/dL, albumin 3.1 gm/dL and INR 1.3. The acetaminophen level was less than 10 mcg/mL. A positive hepatitis C antibody was corroborated by the presence of hepatitis C RNA. Two weeks prior, his hepatitis C antibody was negative and his AST and ALT values were in the 200‐300 U/L range. While fasting, he had elevated iron levels and an iron saturation of 102% as well as a ferritin level of 12,731 ng/mL. The diagnosis of hemochromatosis was later borne out by genetic testing which revealed the patient to be a compound heterozygote for C282Y/H63D.
Discussion:
Dramatic elevation in serum hepatic markers (generally AST or ALT >1000 U/L) is encountered by the internist with some frequency. The most common etiologies include acute viral hepatitis, acetaminophen toxicity, ischemic liver, autoimmune hepatitis, Budd‐Chiari, congestive hepatopathy and idiosyncratic drug reactions.
The initial work up should consist of a thorough history with particular focus on the past medical history, medication history, family history, sexual history, travel history and any history of intravenous drug use. On physical examination, attention should be paid to the body mass index as well as any stigmata of cirrhosis. Initial laboratory work‐up should include serum acetaminophen levels, a drug toxicity screen, a comprehensive metabolic panel and an acute viral hepatitis panel. In our patient, this work up revealed hepatitis C to be a cause of the acute hepatitis.
Acute viral hepatitis is generally punctuated by three phases: a prodromal phase, an icteric phase and a convalescent phase. While the acute viral hepatitides can cause profound elevations in liver enzymes, hepatitis C tends to be insidious and rarely leads to fulminant hepatitis in the United States. In our patient, the rather profound elevation of aminotransferases led to the exploration of additional causes of underlying liver disease.
We hypothesize that this patient had a previously undiagnosed chronic liver disease secondary to hemochromatosis. Super‐infection with hepatitis C virus caused the dramatic rise in liver enzymes.
Conclusions:
Hospitalists often encounter liver enzyme abnormalities as well as hepatitis C. In this setting, it is prudent to consider a multifactorial etiology of liver disease in patients presenting with severe acute hepatitis believed to be secondary to acute hepatitis C infection.