[Radioimmunological determination of plasma ACTH and beta-MSH in congenital adrenal gland hyperplasia].
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The function of atrial natriuretic peptide (ANP) is claimed to be control of salt and water homeostasis, and thus, the hormone may be involved in the pathogenesis of certain diseases with impaired volume regulation. We, therefore, studied plasma ANP concentration in dogs with chronic renal failure, congestive heart failure, and hyperadrenocorticism. Dogs with chronic renal failure had twofold higher plasma ANP concentration (16.2 +/- 5.8 fmol/ml), compared with healthy dogs (8.3 +/- 3.5 fmol/ml). An even more distinct increase (sixfold) of plasma ANP concentration was found in dogs with congestive heart failure (52.9 +/- 29.7 fmol/ml). In contrast, dogs with hyperadrenocorticism did not have high ANP plasma concentration (5.5 +/- 2.0 fmol/ml). High-performance liquid chromatographic analysis of plasma from dogs with congestive heart failure indicated that, in addition to the normal circulating form of ANP (99-126), the unprocessed precursor ANP (1-126) is detectable in the circulation. These qualitative and quantitative alterations of plasma ANP concentration in dogs further suggest involvement of this peptide in the development and/or maintenance of diseases associated with impaired volume regulation.
Differential diagnosis of the causes of intrauterine fetal death was carried out in 84 women; in 57 of them it was due to hyperandrogenism of various origins. 63.2% of patients suffered from mixed (combined ++ovario-adrenal) androgen hypersecretion, 33.3% from the adrenal and only 3.5% of women from the ovarian form of hyperandrogenism. Relationship between the frequency of intrauterine fetal death, the pregnancy term and the form of hyperandrogenism was revealed. Differential diagnosis of hyperandrogenism forms and preparatory pathogenetic therapy helped preserve the pregnancy and resulted in delivery of a viable healthy child in 77.4% of the examined women.
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Glucose-6-phosphatase (G-6-Phase) activity in the rat liver is established to correlate directly with the content of corticosteroids in blood: it lowers with hypocorticoidism (adrenalectomy) and rises with hypercorticoidism (stress). The highest G-6-Phase activity in the liver of the intact animals is observed in autumn, the lowest one in spring, i.e. in the periods when the adrenals function has minimal and maximal values, respectively. Thiamin (0.4 g/kg) is shown to cause a decrease in the G-6-Phase activity in the liver of the intact rats and adrenalectomized or hypophysectomized animals. An assumption is advanced that the found in the experiment a pronounced insulin-like effect of vitamin B with respect to the G-6-Phase activity is connected with an intensified synthesis of the corresponding hormone in the pancreas.
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Erythrocyte insulin receptor binding measurements were evaluated in 8 dogs with spontaneous hyperadrenocorticism. These dogs had normal serum glucose concentration, with normal to high serum insulin concentration (range, 45 to 1,400 pmol/L; normal, 40 to 170 pmol/L). Dogs with hyperadrenocorticism had significant (P less than 0.01) decrease in mean +/- SEM percentage of maximal binding for erythrocyte insulin receptors (2.25 +/- 0.21%), compared with results in 11 clinically normal pet dogs (4.29 +/- 0.42%). The decrease in erythrocyte receptor binding was attributed to significant (P less than 0.01) decrease in high-affinity receptor sites in dogs with hyperadrenocorticism (14.5 +/- 2.8), compared with clinically normal dogs (31.2 +/- 4.3). Significant differences in receptor affinity were not apparent between the 2 groups. Percentage of maximal binding for erythrocyte insulin receptors for dogs with hyperadrenocorticism was inversely correlated with serum insulin concentration (r = -0.85, P less than 0.01). Results indicate that the observed decrease in erythrocyte insulin receptor binding could contribute to insulin resistance and hyperinsulinemia associated with hyperadrenocorticism. Alternatively, decreased binding of insulin receptors in animals with hyperadrenocorticism may result from down-regulation secondary to hyperinsulinemia itself caused by insulin resistance at a postreceptor site (decreased responsiveness).
It has been found that in hypercorticism induced by a prolonged ACTH administration when protein synthesis is inhibited in the skeletal muscles the incorporation of Na2HP32O4 into muscle RNA intensifies by 30% and the RNA-polymerase activity of muscle nuclei is approximately twice as high. In the adrenalectomized rats 3 hours after a single hydrocortisone administration a sharp rise in the RNA-polymerase activity of the skeletal muscle nuclei is observed as well. Such an increase in RNA synthesis is suggested to be a response to the inhibition of protein synthesis through feedback mechanisms.
It is fairly frequent to encounter hyperlipemia on a rheumatic unit. Firstly the symptoms of certain idiopathic hyperlipemias sometimes include rheumatic changes. The latter include firstly, arthritis and tendinitis, above all observed in Type II hyperlipoproteinemia but also mentionned in Type IV, and secondly, exceptional bony lesions (generally of xanthoma type) which seem to occur exclusively in severe hyperglyceridemia. A few bone and joint diseases, such as gout or aseptic necrosis, frequently coexist with dyslipemia. Furthermore, various diseases may be simultaneously responsible for secondary hyperlipemia and involvement of the locomotor apparatus. Finally, the iatrogenic manifestations of the locomotor system appear mainly due to hypolipemic drugs, e.g. the muscle disorders seen in a few patients treated with clofibrate.
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In the light of seven cases of adrenal hypercorticalism associated with tumoral secretion of ACTH, the syndrome of inappropriate ACTH secretion is reviewed. This entity, which is related primarily to anaplastic bronchial carcinoma is characterized by paucity of clinical signs of hypercorticalism, rapidity of evolution and typical biological modifications. Other important criteria are hypokalemic alkalosis, high plasma levels of ACTH and 17-OHCS and failure of dexamethasome to suppress endogenous steroid secretion. However, the diagnosis can be proven only by extraction of a significant quantity of tumoral ACTH.
Daily, for 14 days, rabbits of one group were injected with corticotropin, i.e. ACTH-zinc-phosphate (10 units/kg), whereas rabbits of another group were given (in addition) sodium ribonucleate (40 mg/kg) through a tube into the stomach. Formation of lysyl-tRNA, leucyl-tRNA, and alanyl-tRNA in the liver and the skeletal muscles proved to be significantly greater in the animals which received ACTH together with sodium ribonucleate, as compared to that in the animals given the hormone alone. Hyperglycemia, hepatomegaly, and emaciation were less pronounced in the animals given both the preparations.
Hypercortisolism induces a functional suppression of the hypothalamus-pituitary-adrenal axis which is expected to subside within a year following either the removal of the cortisol producing adrenal adenoma or the withdrawal of glucocorticoid therapy. We report 3 women (35, 40 and 43 years old) with Cushing's syndrome due to cortisol producing adrenal adenoma. All had typical clinical and biochemical features of the syndrome dating from up to 4 years before surgery. Cortisol supplementation was given during the postoperative period (20 mg/day po at 9 AM, reduced to 10 mg/day after 6 months). Cortisol was withdrawn 16, 20 and 39 months after surgery, when 9 AM plasma concentration raised over 10 ug/dl [corrected]. An ACTH stimulatory test was performed until a normal response was obtained. Patients showed and abnormal response up to 16, 17 and 30 months after surgery, respectively. Complete recovery took place at 21, 36, and 55 months after the operation. We concluded that risk of hypocortisolism may persist up to 30 months after surgery for cortisol producing adenomas, due to complete or partial suppression of the hypothalamus-pituitary-adrenal axis.
In administration to quinea pigs of ethyl-p-chlorophenoxyisobutyrate daily in a dose of 0.2 g/kg per os for 15-26 days decreased the 17-OHCS concentration in the peripheral blood plasma. A fall of the urinary excretion of individual 17-OHCS occurred chiefly at the expense of free unchanged cortisol, tetrahydrocortisol and tetrahydro-11-desoxycortisol. The zona fasciculate displays the abundance of the sudanophilic material. A test with ACTH demonstrated that the present functional reserves of the adrenal cortex failed to change under the effect of the preparation. The content of NEFA decreased in the blood serum; as to cholesterol level - it reamined unchanged. Possible mechanisms of the action of the preparation and prospects of its use for the treatment of hypercorticism are discussed.
Adrenal responsiveness to ACTH stimulation (1 mg, i.m.) was assessed by measuring cortisol (Cort) and 17-hydroxyprogesterone (17OHP) at 0, 30, 60, and 90 minutes and progesterone (P), dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEA-S), delta 4-androstenedione (delta 4A), and testosterone (T) at 0, 60, and 90 minutes post-ACTH in 30 women with polycystic ovary syndrome (PCO). The results were compared with those from 12 normally menstruating women. Three distinct patterns of responses of the adrenal steroids were observed in PCO patients, while cortisol response was similar to that of normal controls: (a) normal responders (n = 9, 30% of PCO patients), in whom a delta max response similar to that of normals was observed, although basal delta 4A and T levels were found to be elevated; (b) 21-OH dysfunction group (n = 6, 16.6%), in whom delta max 17OHP levels and delta max 17OHP to delta max Cort ratio were significantly higher than those of normals and the other PCO groups, indicating a dysfunction at the 21-hydroxylase level; (c) adrenarchal type of response group (n = 16, 53%), in whom statistically significant (P less than .0001) hyperresponsiveness of DHEA and, in 11 of them, of delta 4A, with high delta max delta 4A to delta max DHEA to delta max Cort ratios were found, indicative of a selective overproduction of the steroids during steroidogenesis. Moreover, the significantly higher delta max delta 4A to delta max 17OHP ratio found in group c is a further indication of increased 17,20-lyase efficiency, as is encountered during adrenarche.(ABSTRACT TRUNCATED AT 250 WORDS)
In male rats with a high and low blood levels of corticosterone, the activity of serotonin-, dopamine-, noradrenaline-, glycine, GABA-, and cholinergic processes was shown to depend on the glycocorticoid content in the organism and receptor binding of 3H-corticosterone in different brain structures. The formation of adequate processes of neurotransmitter adaptation to a short-term vibration is only possible at a fairly high level of glycocorticoids in the organism.