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Biomedical subjects

P C Sizonenko

Publications and source records attributed to P C Sizonenko.

At least 127 records · Page 7Linked to original sources

FSH: II. Evidence for its mediating role on testosterone secretion in hypopituitarism.

Testicular responses to administration of human chorionic gonadotrophin (HCG) in 23 hypopituitary patients were compared to responses obtained in adequate control groups and correlated to basal plasma follicle stimulating hormone (FSH) and luteinizing hormone (LH) levels. Sixteen nonpubertal patients demonstrated a significantly diminished testosterone response (250 +/- 64 ng/100 ml, mean +/- SEM) along with low basal plasma FSH values (1.4 +/- 0.2 mU/ml) when compared to normal response (607 +/- 97 ng/100 ml) and normal FSH level (2.3 +/- 0.2 mU/ml), but with normal LH values. In 7 pubertal patients decreased testosterone responses to HCG (815 +/- 147 ng/100 ml) were observed with normal plasma FSH and LH values. Correlation between testosterone responses and FSH levels (r - 0.718, P less than 0.002) in the pre-pubertal hypopituitary patients was highly significant. No such correlation was observed between testosterone response and LH. The represent findings may a) give one explanation for the absence of response to HCG observed in some cases of hypopituitarism, b) give support to the hypothesis that FSH has a mediating role on LH-induced secretion of testosterone by the testis in human subjects.

Adolescent↗

[Changes in serum and urinary magnesium during and after extracorporeal circulation in cardiac surgery in children].

Magnesium plays an essential role in the processes of myocardial contraction and conduction. In cardiovascular surgery, extracorporeal circulation (ECC) in haemodilution results in various electrolyte distrubances, with invariably hypomagnesaemia. A group of 13 children undergoing open heart surgery was compared with a group of 17 children operated upon under the same conditions but with the addition of magnesium to the filling solution for the extracorporeal circulation. Changes in blood and urinary electrolytes during and after ECC were studied. Hypomagnesaemia was seen in both groups after surgery but the provision of magnesium supplements shortened the duration. In addition, blood phosphate levels remained significantly higher in the group receiving magnesium. The significance of these various findings is discussed and a technique for the provision of magnesium supplements is proposed.

Adolescent↗

Asymptomatic chronic hypomagnesemia and hypokalemia in a child: Cell membrane disease.

An 8-year-old boy was followed for four years because of chronic hypomagnesemia and hypokalemia. THe clinical manifestations were episodic and characterized by spontaneous carpopedal spasm. There were no other signs of magnesium or potassium deficiency. Metabolic studies revealed that the urinary exceretion of magnesium and potassium was elevated in relation to the serum level, but appropriate for a normal boy of that age. No abnormality was detected in the renin-angiotensin-aldosterone system, and the renal functions were normal. Various therapeutic attempts (oral magnesium and/or potassium supplements, spironolactone) failed to correct the abnormal serum concentrations of magnesium and potassium. This disease may represent a defect in the maintenance of a normal gradient between intra-and extracellular magnesium and potassium.

Aldosterone↗

Hormonal changes during puberty. IV. Longitudinal study of acrenal androgen secretions.

Longitudinal studies of plasma dehydroepiandrosterone sulfate (DHEA-S) and dehydroepiandrosterone (DHEA) were made in 13 girls aged 7 years and 14 aged 10 years, during 3 years, at 6-month intervals. Similarly, two groups of 12 boys aged 8 years and 11 years were followed. In addition, 3 girls with premature adrenarche and 4 male patients with Addison's disease were studied. In the normal girls a significant rise of plasma DHEA-S and DHEA occurred from 6 years of bone age (51.4 +/- 9.0 ng/ml and 50.5 +/-9.2 ng/100 ml, respectively) to 8 years (119. 7 +/- 19.1 ng/ml and 94.5 +/- 16.5 ng/100 ml). A further significant rise was apparent at 11 years (385.8 +/-60.9 ng/ml) and 329.0 +/- 78.4 ng/100 ml). In boys, a similar rise of DHEA-S and DHEA was observed between 6 years of bone age (75.8 %/- 12 ng/ml and 44.3 +/- 7.6 ng/100 ml) and 8 years (157.4 +/- 28.9 ng/ml and 76.1 +/- 8.9 ng/100 ml). Furhter significant rise of DHEA-S and DHEA were seen at 13 years of bone age (563.7 +/- 123.7 ng/ml and 267.9 +/- 50.0 ng/100 ml, respectively). Testosterone in both sexes rose 2-3 years later than DHEA-S and DHEA. In female patients with premature adrenarche, higher plasma levels of DHEA-S and DHEA were found when compared to normal levels at similar chronological and bone ages. Very low plasma concentrations of DHEA-S and DHEA were obsrved in the patients with Addison's disease.

Addison Disease↗

Human serum melatonin changes during the menstrual cycle.

Serum melatonin concentration in early morning during the menstrual cycle, studied in five healthy women, showed that melatonin was elevated at the time of menstrual bleeding and had its nadir at the time of the menstrual cycling in humans.

Adult↗

Plasma growth hormone, insulin, and glucagon responses to arginine infusion in children and adolescents with idiopathic short stature, isolated growth hormone deficiency, panhypopituitarism, and anorexia nervosa.

The effects of intravenous infusion of arginine (20 g/m2) after an overnight fast on plasma immunoreactive growth hormone (GH), insulin (IRI), and glucagon (IRG), and blood glucose were examined in five groups of children and adolescents: 10 normal individuals, 18 with idiopathic short stature, 6 with isolated growth hormone deficiency, 8 with panhypopituitarism, and 6 with anorexia nervosa. The mean fasting plasma GH concentration was significantly elevated in the group with anorexia nervosa (P less than 0.05), and similar to the value for the normal group in all other groups. After arginine infusion, four- to sixfold increases of plasma GH were observed in the normal children, and similar increases were seen in those with idiopathic short stature as well as in those with anorexia nervosa; whereas, in the children with isolated growth hormone deficiency or panhypopituitarism, there was no significant increase in plasma GH. Fasting blood glucose concentrations were significantly lower than normal in subjects with isolated growth hormone deficiency (P less than 0.05), panhypopituitarism (P less than 0.001), and anorexia nervosa (P less than 0.001), whereas fasting plasma IRI and IRG concentrations were similar to the values in the normal group. Plasma IRI increased eightfold at the end of the 30-min arginine infusion in the normal subjects; the increase was slightly but not significantly less in those with idiopathic short stature, and significantly less in those with isolated growth hormone deficiency (P less than 0.05), panhypopituitarism (P less than 0.001), and anorexia nervosa (P less than 0.05). Arginine infusion resulted in two- to threefold increases of plasma IRG in the normal group, and similar increases were observed in all of the other groups tested. These results suggest that whereas pancreatic beta cell responsiveness may be deficient in children and adolescents with isolated growth hormone deficiency, panhypopituitarism, or anorexia nervosa, pancreatic alpha cell responsiveness, to arginine at least, appears to be intact under these conditions.

Adolescent↗

Melatonin radioimmunoassay.

A radioimmunoassay for melatonin has been developed after the raising of anti-melatonin antibodies in rabbits. The radioimmunoassay is specific and the sensitivity range is greater than the tadpole bioassay.?Author

Adult↗

Hormonal changes in puberty III: Correlation of plasma dehydroepiandrosterone, testosterone, FSH, and LH with stages of puberty and bone age in normal boys and girls and in patients with Addison's disease or hypogonadism or with premature or late adrenarche.

In 104 normal boys, aged 7 to 14 years (bone ages 5 to 15 years), plasma dehydroepiandrosterone (DHEA) rose from 52.7 at 7 years, to 112.0 ng/100 ml at 10 years. A further rise occurred at 12 years (188 ng/100 ml). In relation to the bone age, DHEA increased from a mean plasma level of 31.1 at a bone age of 5 years to 77.1 ng/100 ml at one of 7 years. Further increases were observed with mean values of 163.2 at a bone age of 11 years, and of 221.2 at a bone age of 12 years, with a maximum of 333.4 ng/100 ml at bone ages of 14-15 years. The first significant increase of plasma testosterone (T) was noted at a bone age of 12 years (54.8 ng/100 ml). The major rise of T was preceded by the rise of plasma LH and was accompanied by the rise of plasma FSH. Plasma DHEA and T were also measured in 123 normal girls, ages 6 to 13 years (bone ages 5 to 15 years). DHEA rose significantly from a mean level of 44.7 at 6 years, to 80.9 ng/100 ml at 8 years, with further increases between 9 and 10 years and between 10 and 11 years. In relation to bone age, DHEA increased significantly from a mean plasma concentration of 30.9 at a bone age of 5 years, to that of 58.6 ng/100 ml at 7 years. Further increases were observed with values of 191.1 at a bone age of 10 years and 485.6 ng/100 ml at a bone age of 13 years. The first significant rise of testosterone (T) occurred at 10 years of both chronological and bone age. DHEA rose before the increase of gonadotropins. The major rise of T at a bone age of 10 years occurred concurrently with increases in plasma FSH and LH. Low levels of DHEA were observed in Addison's disease. In hypogonadotropin hypogonadism and in anorchia, DHEA levels were normal, suggesting that DHEA is produced primarily in the adrenal gland. In seven girls with early adrenarche, plasma concentrations of DHEA were in the upper range of normal values, whereas T levels were within the normal range. Conversely in girls with late adrenarche, plasms DHEA was lower than normal but T was within the normal limits. The elevation of DHEA prior to the first signs of puberty suggests that DHEA may play a role in the maturation of the hypothalamic-hypophysealgonadal axis. However, the mechanism that triggers the secretion of DHEA is not known.

Addison Disease↗

Hypophyso-gonadal function in humans during the first year of life. 1. Evidence for testicular activity in early infancy.

Total and unbound testosterone and Delta(4)-androstenedione have been determined in 104 cord blood samples. The same sexual steroids and pituitary gonadotropins have been measured in 46 normal male infants aged 27-348 days and 34 normal female infants aged 19-332 days. In cord blood of female neonates mean total and unbound testosterone was 29.6+/-7.5 and 0.89+/-0.4 ng/100 ml, respectively (mean+/-1 SD); Delta(4)-androstenedione was 93+/-38 ng/100 ml. In male neonates mean plasma total and unbound testosterone was 38.9+/-10.8 and 1.12+/-0.4 ng/100 ml; Delta(4)-androstenedione was 85+/-27 ng/100 ml. In female infants testosterone concentrations remained constant during the 1st yr of life with a mean concentration of 7+/-3 ng/100 ml. Mean unbound testosterone and Delta(4)-androstenedione concentrations were 0.05+/-0.03 and 16.7+/-8.3 ng/100 ml, respectively. Mean plasma levels of follicle-stimulating hormone and luteinizing hormone were 8.7+/-3.3 and 12.9+/-7.7 mU/ml. In male infants mean plasma total testosterone concentration increased to 208+/-68 ng/100 ml from birth to 1-3 mo of age, decreasing thereafter to 95+/-53 ng/100 ml at 3-5 mo, 23.2+/-18 ng/100 ml at 5-7 mo, and reached prepubertal levels (6.6+/-4.6 ng/100 ml) at 7-12 mo. Mean unbound testosterone concentration plateaued from birth to 1-3 mo of age (1.3+/-0.2 ng/100 ml) decreasing to prepubertal values very rapidly. Mean Delta(4)-androstenedione concentration, although progressively decreasing during the 1st yr of life to 11.7+/-4.5 ng/100 ml, was higher than in the female at 1-3 mo of life (34+/-11 ng/100 ml). Mean plasma level of follicle-stimulating hormone was 6.7+/-2.9 mU/ml, and that of luteinizing hormone was 19.7+/-13.5 mU/ml, significantly higher than in the female. There was no correlation between gonadotropin and age or testosterone. The present data demonstrate that the testes are active during the first natal period. It is tempting to correlate this phenomenon to a progressive maturation of the hypothalamo-pituitary-gonadal axis. It is possible that the surge in testosterone occurring the first 3 mo could play a role in the future life pattern of the male human being.

Age Factors↗