We report an unusual case of granulomatous hypophysitis in which visual impairment, meningitis and hypopituitarism in a 76-year-old female were associated with radiological evidence of a pituitary mass. The sellar lesion was indistinguishable from pituitary tumor on neuroimaging studies, but the recovery of visual acuity and visual field abnormalities together with the improvement of pituitary function after steroid administration indicated that the mass lesion was due to an inflammatory disease of the pituitary gland. The pituitary tissue obtained by transsphenoidal hypophysectomy revealed granulomatous inflammatory cell infiltration with epithelioid cells and scattered multinucleated giant cells. Although a causal relationship with meningitis was not ascertained, possible exposure of the CSF space to the autoimmune inflammatory process of the pituitary gland was likely in view of the positive pituitary antibody reaction and radiological evidence of suprasellar extension. This entity should be considered when evaluating patients with a pituitary mass, hypopituitarism and meningitis.

Only a few reports have appeared which have attempted to determine whether the naturally occurring steroid, corticosterone, has the same site of action in the hypothalamus-pituitary-adrenal axis as the synthetic steroid, dexamethasone. The present studies help to define the site of inhibition of both corticosterone and dexamethasone on the hypothalamus-pituitary-adrenal axis. Infusion of 20 or 202 µg corticosterone over 6 h significantly reduced hypothalamic CRF (corticotropin-releasing factor) content, whereas it did not reduce plasma ACTH levels in normal rats. This finding indicates the possibility that the infusion of corticosterone may decrease the hypothalamic CRF content by reducing CRF production or enhancing intracel-lular and/or extracellular CRF degradation. On the other hand, infusion of 20 µg dexamethasone for 6 h to normal rats significantly decreased plasma ACTH levels, but did not alter the hypothalamic CRF content. This finding indicates that dexamethasone may inhibit the release or/and production of ACTH in the anterior pituitary. In addition, relatively large doses of corticosterone (504 µg/rat) and dexamethasone (202 µg/rat) may suppress CRF content and ACTH release at the level of both the hypothalamus and anterior pituitary.

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A 73-year-old womanwas diagnosed as primary hyperparathyroidism. Hypercalcemia recurred after parathyroidectomy, though serum calcium concentration temporarily resumed to normal. Hypercalcemiawas eventually shownto be due to multiple myeloma.In spite of the frequent association of hypercalcemia with malignant disease and the relative frequency of primary hyperparathyroidism as a cause ofhypercalcemia, primary hyperparathyroidism accompanied by multiple myelomahas been considered in only a limited number of reports. Here, the cases in the literature are reviewed and discussed. (Internal Medicine 34: 988-991, 1995)

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Abstract.We report a case of a 58-year-old man with adrenal medullary hyperplasia associated with cortisol producing adenoma. Preoperative examination showed both adrenocortical and adrenomedullary hyperfunction.No Cushingoid sign was present and pheochromocytoma-like symptoms were predominant. Abdominal computarized tomography revealed a left adrenal tumor stained by contrast medium.Histologically, the adrenal tumor was found to be a cortical adenoma, and medullary hyperplasia was observed in the remaining parenchyma.

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