Endocrine Abstracts

Background

Hypoglycemia is a well-established as a serious paraneoplastic complication of hepatocellular carcinoma (HCC). However, hypoglycemia presenting the first presentation of HCC is not frequent. In this regard, we present the case of a patient who had hypoglycemia as first manifestation of HCC.

Observation

A 55yearold man presented to the Emergency Department with loss of consciousness preceded by dizziness, weakness and blurred vision due to severe hypoglycemia (20 mg/dl), from which he recovered after treatment with intravenous glucose. Then, he was admitted to our department. This symptomatology occurred for one month twice a week. He denied any recent alcohol consumption or the use of other drugs. Past medical history included only schizophrenia treated with Haloperidol and Trihexyphenidyl since 25 years. The patient was lethargic and his BMI was 18 kg/m². Clinical examination noted a hard and irregular hepatomegaly with collateral venous circulation. No splenomegaly was found. His cardiovascular and respiratory system findings were within normal limits. Laboratory testing revealed hypoglycemia as documented by a very low serum glucose 1.04 mmol/l, serum creatinine 52 µmol/l, serum glutamic oxaloacetic transaminase level of 243 IU/l and serum glutamic pyruvic transaminase level of 71 IU/l. The patient’s insulin level was < 0.1 IU/ml and the blood cortisol level was elevated, thus excluding respectively the diagnosis of insulinoma and adrenal insufficiency. The hepatitis B surface antigen level and the test for the hepatitis C virus antibody were negative. Abdominal ultrasound revealed enlarged dysmorphic liver, seat of multiple nodules saving no segment. Computed tomography revealed multiple hepatic lesions consistent with multifocal multicentric HCC and multiple pulmonary metastases. Subsequent investigations showed serum α-fetoprotein more than 4000 UI/ml (normal range < 4 UI/ml), IGF1 = 0.001 ng/ml, and IGF2 = 561 ng/ml. Therefore, the diagnosis of HCC and non-islet cell tumor hypoglycemia (NICTH) was considered. Initially, the patient was treated with continuous 10% dextrose infusion and due to the advanced disease stage, he was not a candidate for surgical or palliative cytoreductive therapies. He received only palliative treatment, including oral prednisolone 30 mg once daily in addition to frequent high complex carbohydrate meals with some improvement in the severity of hypoglycemia.

Conclusion

Hypoglycemia due to NICTH is an established paraneoplastic complication of HCC. The prognosis for metastatic or unresectable HCC is poor. The use of frequent, high complex carbohydrate meals and oral steroids are options for management of this condition.