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Insulin-induced hypoglycemias are a sign of non-sufficient counterregulation, in which different contra-insulinary hormones participate. The aim of the study was to investigate, whether there exists a difference between IDD and non-diabetics regarding secretion of glucagon, cortisol, and growth hormone during an insulin-induced hypoglycemia and further on pointing out, expecially, the importance of glucagon. Insulin-induced hypoglycemias are counterregulated in non-diabetics, not in IDD. The missing glucagon secretion during insulin-induced hypoglycemia in IDD seems to be independent from an autonomic neuropathy. Only after high doses of exogenous glucagon can one see a counterregulating increase of glucose. The STH secretion is similar in non-diabetics and IDD during an insulin-induced hypoglycemia and has evidently only a secondary effect in hypoglycemic counterregulation. The STH secretion may be the expression of a diencephal-triggered stress situation. The cortisol secretion is the same in both groups. The gluconeogenetic effect of cortisol is not sufficient to accomplish a fast compensation of hypoglycemia. This does not exclude long-term effects. When inhibiting the secretion of insulin and different contra-insulinary hormones with somatostatin, one is able to demonstrate that glucagon alone is a sufficiently counterregulatory hormone in insulin-induced hypoglycemias.

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A case report is given of severe extraintestinal hepatic amebiasis without diarrhea. Formation of an hepatic abscess could be avoided by early institution of appropriate antiamebic treatment, following the diagnosis using sonography and specific serological methods.

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A functional diagnosis of the diencephalohypophyseal system was carried out in patients with Sheehan syndrome, chromophobic adenoma, craniopharyngioma, prolactin-producing pituitary tumours, acromegaly, hypothalamo-pituitary dwarfism and constitutional retardation. A combined insulin hypoglycaemia/LH-RH/TSH test was performed to define frequency and extent of anterior pituitary insufficiency. With these illnesses, almost generally, a somatotropic insufficiency (except in acromegaly) was found. An impairment of gonadotropic function was often present, in general a pathologic LH-RH test correlating with a more or less developed androgen deficiency. An adrenocorticotropic insufficiency was found in most patients with sheehan syndrome, chromophobic adenoma and craniopharyngioma while in acromegaly and hypothalamo-pituitary dwarfism it was present less frequently, necessitating a substitution with corticoids. The TRH test reflects only incompletely a secondary hypothyroidism, and can be normal with organic processes of the diencephalo-hypophyseal region, making a T3 and T4 estimation in the blood decisive for a thyroid hormone substitution. A clear-cut separation of the hypothalamic from the pituitary cause of the insufficiency is neither possible with the LH-RH nor with the TRH test.

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Alteration of the metabolism of calcium and phosphate may be associated with symmetric cerebral calcification. Detailed investigations of the function of parathyroid glands including computer tomography of the brain are so far missing. In 6 patients with clinical and biochemical signs of altered function of the parathyroid glands symmetric cerebral calcification could be demonstrated by computer tomography. They are also visible by X-ray examination in one patient. Consequently, functional disturbances of the brain, cerebellum and of the extrapyramidal system may occur. Moreover, the combination of hypoparathyroidism and hypothyroidism also appears to result in the development of symmetric cerebral calcification. The pathogenesis of the calcification as well as therapeutic approaches will be discussed.

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Growth hormone (GH) release was measured in 17 patients with active acromegaly following the administration of insulin, LH-RH and TRH given intravenously either combined or each separately. The simultaneous application of insulin and the hypothalamic releasing hormones resulted in a striking increase of plasma GH in 15 out of 17 patients. Inappropriate stimulation of GH release was found in 9 out of the 17 patients with acromegaly, when TRH was given as the only hormone; conversely this phenomenon due to LH-RH application was observed in 4 cases. In insulin-induced hypoglycemia GH release could be stimulated in 5 patients. After selective, transsphenoidal hypophysectomy, 4 of 13 patients still showed a definite stimulation of GH release after the combined use of test substances. Two of these also exhibited a comparable stimulation of GH after TRH, indicating adenoma cells remaining active after operation. The combined insulin-induced hypoglycemia/LH-RH/TRH-test is therefore advisable for patients with acromegaly, since GH release as well as other hypophyseal partial functions can be tested. The performance of individual tests is essential for evaluating selective stimulation of GH release.

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As rare complication of post-pancreatitic pseudocyst in a 43-year-old patient, an obstruction of large vessels, situated retroperitoneally, is described. The partial thrombosis lead to a recurrent embolism of pulmonary artery with terminal right cardiac failure.

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PIP: The effect of luteinizing hormone-releasing hormone (LHRH) analogue after subcutaneous application over a 12-day period was evaluated in 15 normal males to determine whether gonadotropin secretion is influenced by longterm application. After 1.25 mcg/day, LH increases were measurable 3 hours after daily receipt of the analogue. After 2.5 mcg/day, the release of LH secretion was even greater, although this stimulation was markedly reduced in the 2nd week. After 5 mcg in 2-day intervals, a clearly induced LH increase was observed on the day of administration and was maintained for 10 hours. Similar results were noted for follicle-stimulating hormone (FSH). There was a response of FSH after 1.25 mcg and 2.5 mcg, but this response decreased in the 2nd week. After application of 5 mcg every other day, there was a consistent FSH increase that subsided on the treatment-free day and continued into the 2nd week of treatment. These findings suggest that LHRH analogues should be administered in low doses subcutaneously or intranasally at daily intervals to enable a longterm effect on gonadotropin release.^ieng

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Treatment of chronic insulin resistance in 3 adipose diabetics is reported. The clinical course shows that the actual success of the treatment of resistance depends less on weight reduction than on a short interruption of the insulin therapy and withdrawal of nutriment at the same time. After breaking off nourishment and insulin supply, the efficacy of the insulin therapy could be regained, at least partially, in all patients, and the diabetic metabolic state improved. In addition to the reduction in hyperinsulinism, physical activity and specific effects of diet are also probably important for the success of the treatment.

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Urinary excretion of hydroxyproline was examined with the Hypronosticon test in 25 patients with acromegaly (13 men, 12 women) and 15 healthy persons. At the same time, plasma levels and urinary excretion of phosphorus and calcium were also measured. Patients with active acromegaly had a significantly higher urinary hydroxyproline output (32.55 +/- 8.68 mg/24 h m2) than healthy persons (12.12 +/- 2.33 mg/24 h-m2). They also excreted considerably more hydroxyproline than patients with successfully treated acromegaly. Effective treatment was proved by STH levels and good suppressibility by 100 mg glucose. Unsucessfully treated patients, on the contrary, had a raised urinary excretion of hydroxyproline (31.23 +/- 16.61 mg/24 h-m2) and high fasting plasma levels of somatotropic hormone. Hydroxyprolinuria proved, therefore, of value in assessing the development and treatment of acromegaly.

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oestrone, oestradiol-17beta and testosterone in serum were measured during a LH-RH infusion test and a Leydig cell function test with HCG in healthy men and in patients with primary or secondary hypogonadism. Following infusion of LH-RH increases of LH (+112%), oestradiol (+62%) and testosterone (+51%) were observed in normal men, while oestrone remained unchanged. Of the patients only those with Klinefelter's syndrome showed a significant increase in testosterone and oestradiol after LH-RH infusion. During the Leydig cell function test oestradiol and testosterone exhibited a largely parallel pattern under normal and pathological conditions as well as in subjects with experimental hypogonadism. Augmentations of plasma oestrone were usually smaller than those for oestradiol.

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Alterations of sexual hormones in plasma of ageing males occur between the 50th and 60th year of life with individual variations: 1. Decreased values of testosterone in plasma and a poor response to gonadotrophins demonstrate a diminished synthesizing capacity of the testes in old men. 2. The decreased testosterone plasma values are followed by an increase in LH. The response of the anterior pituitary gland to LH-RH stimulation in old men is normal. 3. Under basal conditions estrone as well as estradiol plasma concentrations increase significantly with age because of increased conversion from androgens. 4. Parallel to estrogen plasma values an increased concentration of the sexual hormone binding globulin (SHBG) is found, resulting in a steep decrease of the free (= active) testosterone fraction. 5. Decreased testosterone, which is more strongly bound to SHBG and increased estrone and estradiol plasma values result in an androgen/estrogen imbalance in old men.

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