Biomedical subjects
Publications and source records attributed to S L Asa.
We report the third case of renal hemangiopericytoma associated with spontaneous hypoglycemia. The clinical and pathological features suggest that excessive glucose storage by the tumor is an important factor in the pathogenesis of the hypoglycemia. Other possible mechanisms producing hypoglycemia associated with mesenchymal tumors are reviewed.
Two patients presented with abnormalities suggestive of pituitary adenoma; one during pregnancy and one in the postpartum period. However, pathologic examination of the pituitary showed extensive destruction by a lymphoplasmacytic infiltrate; no tumor was identified. Both patients developed hypopituitarism. We know of eight additional cases of lymphocytic hypophysitis, seven of which have been reported in the literature. In only three cases, including the two reported here, the diagnosis was established by biopsy. In each of those cases, the entity mimicked a pituitary tumor. This is the first report of electron microscopy of this lesion and the ultrastructural features support the previously suggested autoimmune etiology. The lesion has been described only in women and seven of ten patients were pregnant or postpartum at the onset. This fact and previously reported experimental evidence, including the identification of anti-prolactin cell antibodies, support our suggestion that lymphocytic hypophysitis associated with pregnancy represents a distinct clinicopathologic entity.
A hypothalamic neuronal hamartoma associated with a sparsely granulated growth hormone cell adenoma of the pituitary and acromegaly is reported. It is suggested that the patient had a primary neuronal tumor, whose neurosecretory activity promoted the development of the growth hormone secreting pituitary adenoma causing acromegaly.
An islet cell carcinoma of the pancreas is described in a 68-year old woman which clinically produced Zollinger-Ellison syndrome and, later in its course, Cushing syndrome. The tumor was found to contain gastrin, ACTH, alpha-endorphin, somatostatin and calcitonin, by the immunoperoxidase technic. Electron microscopy revealed a single tumor cell type containing secretory granules of variable size, morphology and electron density. It appears that a single tumor cell population produced all five hormones and caused a transition in clinical symptomatology, while undergoing no change in morphology.
The effects of growth hormone-releasing hormone (GHRH) were studied on densely granulated somatotroph adenoma cells and sparsely granulated somatotroph adenoma cells in culture by measuring release of growth hormone (GH) as well as ultrastructural morphometrical parameters and comparing them with those of control adenoma cells. Both types of adenoma cells cultured with GHRH showed similar increases of GH release into culture media and exhibited similar increases in cytoplasmic volume densities (CVD) of endoplasmic reticulum and Golgi apparatus and decreases in CVD of secretory granules and secretory granule diameter. These results indicate that (1) both types of somatotroph adenoma cells react similarly to GHRH stimulation, despite their morphologic differences, and (2) GHRH stimulates GH synthesis as well as GH release by somatotroph adenoma cells.
Report of the case of a 21-year-old man who presented with gynecomastia and was found to have a testicular embryonal carcinoma producing human chorionic gonadotropin (HCG), associated with massive hyperplasia of Leydig cells. While the morphologic features of Leydig cell hyperplasia have been documented with excess endogenous luteinizing hormone (LH), as in Klinefelter's syndrome, and following administration of exogenous HCG, to our knowledge, this is the first description of the histologic and ultrastructural changes in Leydig cells associated with increased secretion of endogenous HCG. The Leydig cell stimulation which results from excess endogenous HCG is unusual in that it causes an elevation of estrogens which may be greater than the rise in androgens. It is concluded that embryonal cell carcinoma of the testis, producing HCG, may lead to Leydig cell hyperplasia with morphologic features similar to those seen in other conditions with such hyperplasia, and that there is no correlation between those morphologic features and testosterone production.