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Antibody (HBsAb) was positive with a quantitative value of 0.53. Hepatitis B core immunoglobulin M (HBc IgM), HBcAb total, HBeAg, HBeAb were all negative with undetectable serum HBV DNA. The HBsAg was not confirmed as a true positive after repeat testing with an antibody neutralizing procedure involving a human antibody to HbsAg. Discussion: Accurate interpretation of laboratory tests is imperative in diagnosing hepatitis B. There was high suspicion that patient had false positive HBsAg. The patient's serological profile did not fit acute or chronic hepatitis B. The patient had no evidence of acute hepatitis B with negative HBc IgM, HBV DNA and no evidence of chronic hepatitis B with HBcAb total being negative. Furthermore, a positive HBsAb is not seen in acute and chronic hepatitis B. Transient HBsAg has been seen in patients for up to 2 weeks after HBV vaccination, however, our patient had not been vaccinated recently. The most common cause is the presence of heterophile antibodies. These naturally occurring human antibodies can bind to a variety of chemical structures including animal antibodies seen in immunochemistry assays. They can be neutralized by specific inactivating binders. Other viral infections such as Epstein-Barr Virus (EBV), transfusions, or systemic disease can cause false positives. A likely suspect was the patient's NSCLC causing a paraneoplastic syndrome which would be the first instance of such in the literature. There have been cases of parathyroid adenoma and basal cell carcinoma causing false positivity. Patients with false-positive HBsAg need further workup to prevent misdiagnosis and potentially harmful management.

The patient is a 69 year-old male with new onset jaundice of two weeks and a 6 month history of progressive hyperbilirubinemia with cholestasis who was admitted for evaluation. Physical examination revealed a well developed and well nourished, jaundiced male with scleral icterus, a II/VI systolic murmur at apex, mild abdominal discomfort over epigastrum on palpation without discernable hepatomegaly, normal distal pulses, no lower extremity edema, and no stigmata of chronic liver disease. Laboratory investigation revealed a total bilirubin of 19.3 mg/dL, alkaline phosphatase 693 U/L, and AST and ALT of 140 U/L and 117 U/L, respectively. CT scan of the abdomen and pelvis showed multiple foci of arterial enhancement, periportal edema without biliary dilatation, concerning for acute fulminant hepatitis. The patient had a dramatic and rapid decline the day following admission, developing cardiac arrhythmia and hypotension and subsequently died despite resuscitative efforts. Autopsy revealed amyloidosis AL, kappa light chain type involving the liver (Figures 1 and 2), heart (Figures 3 and 4), lungs and bone

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