A rare case of primary hyperparathyroidism associated with primary aldosteronism and breast cancer is reported. A 44-year-old woman was admitted to our hospital to undergo surgical removal of breast cancer. She had hypertension with low serum potassium, and slightly but significantly elevated serum calcium levels. Further studies demonstrated an enlarged left superior parathyroid gland and a left aldosterone-producing adrenocortical adenoma. Blood pressure was controlled with spironolactone and nifedipine, and left mastectomy was done for breast cancer. The pathological diagnosis was scirrhous breast carcinoma. Although the postoperative course was uneventful, her serum calcium gradually and progressively rose to higher levels. Left superior parathyroidectomy and left adrenalectomy were then performed simultaneously. The pathological diagnoses of the resected parathyroid gland and adrenal gland were parathyroid chief cell adenoma and adrenocortical adenoma with hyperplasia of zona glomerulosa, respectively. To clarify if the occurence of these tumors may be related to MEN1 gene mutations, we analyzed MEN1 gene in this patient, and found a loss of heterozygosity of the MEN1 locus in the parathyroid adenoma and breast cancer. Thus, we conclude that an alteration of the MEN1 gene and/or another tumor suppressor gene located at the MEN1 locus on chromosome 11q13 may be responsible for the development of parathyroid adenoma and breast cancer in our patient suggesting that the clinical spectrum of MEN1 might include breast cancer. In addition, serum calcium should be interpreted with caution in primary aldosteronism, because hypercalcemia may be masked in the presence of aldosterone excess. (Internal Medicine 43: 310-314, 2004)Key words: multiple endocrine neoplasia type 1 (MEN1), MEN1 gene, loss of heterozygosity, breast cancer, primary hyperparathyroidism, primary aldosteronism

We reported here an adult patient with vanishing bile duct syndrome due to chronic EBV infection. A 22-year-old male was admitted to a nearby hospital complaining of a sore throat and jaundice. He received a high dose of prednisolone for bile stasis of acute viral hepatitis. However, the hepatitis did not improve, and he was transferred to our hospital. He had exhibited jaundice for one year as well as hemophagocytic syndrome and intestinal perforation. Subtotal intestinal resection was successfully performed. Three follow-up biopsied liver specimens indicated vanishing bile duct syndrome. Positive results of EBV-DNA in his serum and mRNA of EBV by in situ hybridization of his liver indicated that massive doses of prednisolone caused chronic EBV infection and vanishing bile duct syndrome.

A gastric cancer with liver metastases was associated with low morning levels of plasma glucose (24 mg/dl), insulin (< 2.5 microU/ml) and growth hormone (0.23 ng/ml). Primary and metastatic tumour tissue stained positively with anti-insulin-like growth factor II (IGF-II) monoclonal antibody. Western immunoblot analysis revealed a high molecular weight IGF-II in the serum: 15 kDa (normal: 7.5 kDa). Postmortem reverse transcription polymerase chain reaction on mRNA from both sites revealed 471 base pairs size cDNA encoding prepro-IGF-II. These results suggest that the gastric carcinoma encoded, expressed, and secreted IGF-II, probably causing the extrapancreatic tumour hypoglycaemia.