gastrins and Adrenocortical-Hyperfunction

This study was undertaken to elucidate the impact of hypercortisolism in meal-related gastrointestinal hormone secretion and appetite in female endurance athletes. Thirteen elite runners and seven sedentary women participated on two occasions, either receiving intravenous injection of 250 micrograms synthetic adrenocorticotropic hormone (ACTH) 1-24 or saline. Blood samples were collected before and after the injection, and then in connection with a standardized meal. Serum concentrations of cortisol, cholecystokinin (CCK), gastrin, insulin and glucose were analyzed. Self-ratings of appetite were assessed by visual analog scales. Elevated basal levels of cortisol and glucose were found in the athletes. ACTH-induced cortisol response was comparable between groups, but a negative correlation between basal cortisol levels and the ACTH-induced response was found. In sedentary women, ACTH challenge enhanced meal-related CCK and gastrin responses, whereas athletes showed a blunted response of these hormones combined with decreased satiety and reduced levels of insulin. Blunted meal-related response of gastrointestinal hormones and decreased satiety in female runners after ACTH stimulation compared to sedentary women are probably due to difference in the effect of cortisol, which could be explained by cortisol insensitivity as a result of basal hypercortisolism in the athletes. Decreased CCK response and satiety in female athletes may reflect increased nutritional requirements.

Topics: Adrenocortical Hyperfunction; Adrenocorticotropic Hormone; Adult; Appetite; Blood Glucose; Cholecystokinin; Eating; Female; Gastrins; Gastrointestinal Hormones; Humans; Hydrocortisone; Insulin; Physical Endurance; Satiety Response

Topics: Adenoma; Adrenal Gland Neoplasms; Adrenocortical Hyperfunction; Aged; Carcinoma; Carcinoma, Papillary; Female; Gastrins; Humans; Hypercalcemia; Hypothyroidism; Multiple Endocrine Neoplasia; Pituitary Neoplasms; Thyroid Neoplasms

Prealbumin, one of the main thyroxine transport proteins, has recently been shown to be a valuable immunohistochemical marker of neuroendocrine tumours. We report the case of a multisecretory pancreatic endocrine tumour whose prealbumin secretion was so high that it produced a peak on routine serum protein electrophoresis and induced a euthyroid hyperthyroxinemia. The maximal binding capacity of prealbumin for thyroxine was indeed markedly increased, whereas its affinity for this hormone was normal. The tumour was associated with gastric hyperacidity and hypergastrinemia thereby evoking a Zollinger-Ellison syndrome. The secretin stimulation test and gastrin tumoural immunohistochemistry were, however, negative. We suggest that the concomitant tumoural production of gastrin-releasing peptide was responsible for the gastric hyperacidity and hypergastrinemia. This hormone probably also accounted for a moderate hypercorticism.

Topics: Adrenocortical Hyperfunction; Gastrins; Humans; Hyperthyroxinemia; Immunoenzyme Techniques; Male; Middle Aged; Multiple Endocrine Neoplasia; Pancreatic Neoplasms; Prealbumin; Thyroxine-Binding Proteins; Zollinger-Ellison Syndrome

The production of ACTH-like material by tumours arising in non-endocrine tissue may initiate severe adrenocortical hyperfunction. The pathogenesis and clinical and laboratory features of Cushing's syndrome associated with such tumours are characteristic. The autonomous production by the tumour of ACTH-like material cannot be suppressed by exogenous corticoids. The onset of clinical symptoms is rapid; muscle wasting, general weakness, thirst and peripheral edema predominate, and the classical signs of Cushing's syndrome may be absent. High levels of plasma 17-hydroxycorticosteroids and urinary 17-hydroxycorticosteroids and 17-ketosteroids, usually with normal levels of urinary aldosterone, commonly occur. Hypokalemic alkalosis unresponsive to replacement therapy may cause death. In the case reported herein, the intriguing possibility exists that two hormone-like substances were produced by the primary growth and its metastases: one, ACTH-like, to account for the adrenal hyperplasia and Cushing's syndrome; and another, gastrin-like, giving rise to the ulcerogenic diathesis.

Topics: 17-Hydroxycorticosteroids; 17-Ketosteroids; Adenoma, Islet Cell; Adrenalectomy; Adrenocortical Hyperfunction; Autopsy; Carcinoma, Islet Cell; Chloramphenicol; Cushing Syndrome; Drug Therapy; Gastrins; Humans; Hypokalemia; Neoplasm Metastasis; Neoplasms; Pancreatic Neoplasms; Pathology; Spironolactone; Zollinger-Ellison Syndrome