Hypercorticism--a risk factor in arterial hypertension and atherosclerosis.

The present work has attempted an analysis of the role hypercorticism as a risk factor in arterial hypertension and atherosclerosis. Our series consisted of 149 male and female patients of various ages. The incidence of cardiovascular disorders in relation to age and the glucidic lipidic metabolic disorders were also investigated. The results showed that hypercorticism may trigger in very young patients as well arterial hypertension (AH) and glucidic-lipid metabolic disorders both incriminated as risk factors in including atherosclerosis. Hypercorticism was proved to be an aggravating factor of pre-existing cardiopathy. Efficient management of adrenocortical hormones excess brings complete resolution of arterial hypertension and glucidic lipid metabolic disorders in young patients and most adult patients who had no cardiovascular complaints prior to the endocrine syndrome.

Knowledge of the hormonal peculiarities of essential arterial hypertension may direct therapy and prevent errors.

The endocrine system becomes involved in the physiopathologic mechanisms of essential arterial hypertension (EAH) by the interference of hormones with the pressor and depressor substances. A "depressor" pharmacodynamic model with beta-blockers based on the variations of hormone-dependent data offers a series of characteristics for assessing the vasoconstrictive and volemic components, evolution (accelerated for instance) and treatment. Hormone data are also useful for avoiding errors and for increasing the efficiency and control of the therapy. It is not uncommon for EAH to become endocrine-dependent, for instance: increase in aldosterone secretion by activation of the renin-angiotensin (RA) system or of the hypophysis- corticoadrenal system and the adreno-sympathetic system, transforms the relatively "benign" evolution of EAH into an "accelerated" one. The incidence of hyperreactive corticoadrenal (with or without altered steroidogenesis), corticoadrenal hyperplasia or adenoma, is in reality higher than commonly diagnosed.

The effect of combined administration of L-proline and glycine on GH and IRI release in healthy prepuberal children.

Proline (100 mg/kg b.w.) was given per os and after 30 minutes 10% glycine was i.v. injected to 25 healthy children of both sexes. A positive response (an increase of over 5 ng/ml of serum level of GH) was found in 21 of the 25 children. The insulin test showed a positive response in 24 of the 25 children. It was concluded that the decrease in glycine dosage from 250 mg/kg b.w. (earlier reports by the same authors) to 100 mg/kg b.w. (present data) is generally compensated by l-proline priming. The IRI serum levels were almost unchanged. By l-proline priming, the glycine test can also be applied to subjects with body weight over 40 kg, in doses of 100 mg/kg b.w. for exploring the secretory reserve of the somatotropic axis.

Clinical use of glycine intravenous load for diagnosis of growth hormone deficiency.

Intravenous glycine injection (250 mg/kg of body weight) resulted in growth hormone release in normal children but not in those with growth hormone deficiency diagnosed by insulin-induced hypoglycaemia. In the latter significantly higher peak concentrations of serum alpha-amino nitrogen were also found. False negative responses to glycine (no GH release) were observed in two patients of short stature but normal pituitary function. In them the peak levels of serum alpha-amino nitrogen were lower than in those with hypopituitarism. We propose the clinical use of glycine as an inexpensive and innocuous procedure for the detection of GH deficiency in children. A post-glycine GH peak greater than 10-0 mu/l seems to be a good index of an intact GH reserve.