Urinary excretion of catecholamines in healthy subjects in relation to body growth.
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Biomedical subjects
Publications and source records attributed to A Parra.
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The clinical characteristics and body composition of eight hypopituitary dwarfs (10.2-21.6 yr) were analyzed before and after 6 and 12 mo of growth hormone therapy. 2 IU 3 times/wk. Before treatment, growth rate was 1.8 +/- 0.7 cm/yr, height age was 2.0-12.8 yr less, and bone age 2.0-11.1 yr less than chronologic age. Total body water (TBW), lean body mass (LBM), extracellular water (ECW), and intracellular water (ICW) were below normal for chronologic age, but normal for height. Muscle mass (MM) was below normal for age and height. During HGH therapy, growth rate was 7.1 +/- 1.6 cm/yr in the first 6 mo and 7.8 +/- 1.4 cm/yr during the next 6 mo; the ratio of change in height age to change in chronologic age was greater than or equal to 1.0 in all patients and the ratio of change in bone age to change in height age was 1.2 in one patient and less than or equal to 1.0 in the others. TBW, LBM, ECW, and ICW increased according to height increments; however, MM increased at a faster rate than expected from the height gains. Also, a relative or absolute loss of total body fat was recorded during the first 6 mo of therapy. It is suggested (1) that among the body composition parameters studied, muscle mass is the tissue most closely reflecting the lack of HGH and also its therapeutic benefits and (2) evaluation of body composition in hypopituitary dwarfs in response to HGH therapy shows striking changes not reflected by the determination of stature or weight alone.
The prolactin concentration in human seminal plasma and in human epididymal cauda fluid was assessed by radioimmunoassay. The prolactin concentration in cauda plasma was found to be similar to that found in male blood serum (5.5 to 9.1 ng/ml) and significantly lower than the concentration of the hormone found in seminal plasma obtained either from euspermic (48 +/- 12 ng/ml) or from vasectomized volunteers (50 +/- 10.2 ng/ml) (P less than 0.001). Calcium binding and/or transport in ejaculated spermatozoa were found to be little (0.29 +/- 0.08 nmoles/10(8) cells) and dependent on a quickly saturable process. The addition of 200 ng of human prolactin/ml induced a 60% increase in this parameter, while 50 ng of prolactin/ml were ineffective. Epididymal human spermatozoa differ from ejaculated sperm cells in showing greater, time-dependent, calcium binding and/or transport under basal conditions (2.00 +/- 0.35 nmoles/10(8) cells/hour), and in being more susceptible to the stimulating action of prolactin (4.4 +/- 0.68 nmoles/10(8) cells/hour in the presence of 50 ng of prolactin/ml).
A radioimmunoassay to quantitate ethinylestradiol (EE-2) in both plasma and endometrium is described. In 29 women under sequential oral contraceptive therapy (chlormadinone acetate, 2 mg, plus mestranol, 80 microgram) for 6 to 84 months, a single blood sample and a single endometrial sample were simultaneously obtained on different days of the pseudomenstrual cycle. In 24 women under 40 years of age the mean plasma EE-2 concentrations were similar during the first (989 +/- 94 pg/ml) and the second half of the cycle (1053 +/- 186 pg/ml) (P greater than 0.05). A similar finding was observed with regard to mean endometrial EE-2 concentrations (3.55 +/- 2.1 and 5.89 +/- 1.7 microgram/gm of wet tissue, respectively). On the other hand, five women over 40 years of age had plasma EE-2 concentrations similar to those of the previous group, but the mean endometrial EE-2 concentrations was 0.9 +/- 0.6 microgram/gm of wet tissue (P less than 0.05). Although plasma follicle-stimulating hormone and luteinizing hormone did not show midcycle peak values, complete suppression of both gonadotropins was not observed. These results show that endometrium has a great ability to concentrate EE-2, and this ability seems to be greater in women below age 40 than above. Whether or not this observation might be related to the known higher incidence of endometrial cancer in women less than 40 years old who have been under chronic sequential oral contraceptive therapy cannot be disclosed from this limited number of determinations.
Five uremic (7.0 - 15.2 years), non-dialyzed children treated medically (group 1) had an intravenous glucose tolerance test (0.5 g/kg). Blood samples were obtained at frequent intervals and duplicate determinations of plasma glucose (glucose-oxidase method on Somogyi-Nelson protein-free filtrates), insulin and free fatty acids were performed. The same study was performed in eleven children (12.3 - 18.0 years) with chronic renal failure undergoing long-term hemodialysis (group 2), before and two hours after dialysis. Results were compared to a group (group 3) of eight healthy children (7.5 -- 17.5 years). In group 1 a "normal" insulin response was observed in the presence of hyperglycemia and the plasma glucose clearance was in the diabetic range. Twice weekly hemodialysis produced no beneficial acute effects on group 2, based on absolute glucose values or plasma glucose clearance rates, on groups as well as on individual basis; however, a clear hyperinsulinemia was present which was of even higher magnitude three and six months after the initial study. These results demonstrated that chronic hemodialysis had no beneficial acute effects on plasma glucose concentration or plasma glucose clearance rate. However, it may have obvious long term beneficial effects on glucose tolerance by enhancing pancreatic insulin release (to overcome peripheral insulin resistance) to such an extent as to maintain a normal carbohydrate tolerance.
Twelve women of normal weight (ages 17 to 36 years) with scanty menstrual bleeding were studied. They had no signs of virilization, gynecologic or endocrine pathology, or past history of hormonal treatment. Five women (group 1) experienced withdrawal bleeding after a 3-day course of chlormadinone acetate (2 mg/day) and the other seven did not (group 2). Daily venous blood samples were obtained 10 to 15 days afterward for 5 consecutive days of no treatment (control period) and during the next 5 days while the women received paramethasone acetate (PA), 2 mg/day (treatment period). In each plasma sample the concentrations of 17beta-estradiol (E2) and luteinizing hormone (LH; LER-907) were determined. The mean plasma E2 levels in group 1 were 35 +/- 8 and 86 +/- 10 pg/ml during the control and treatment periods, respectively (P less than 0.001), and the mean plasma LH levels were 28 +/- 6 and 94 +/- 34 ng/ml, respectively (P less than 0.001). No significant changes in plasma E2 and LH levels were observed in group 2 in either period. During the control period, the plasma E2 level in group 2 (14 +/- 2 pg/ml) was lower than that in group 1 (P less than 0.01); however, plasma LH levels were similar in both groups. The administration of PA for 5 months induced monthly ovulation in group 1 but not in group 2. These data suggest that the best results are obtained in women with optimal pretreatment levels of plasma E2.
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The neuroendocrine function of a 19 years old female dwarf with primary amenorrhoea and lack of sexual development (asexual ateleiosis) was studied. Undetectable fasting plasma levels of growth hormone (GH) and a lack of response to three different provocative stimuli was observed. Oestrogen administratin did not modify the GH response. Thyroid and adrenal function were within normal limits. Undetectable plasma levels of immunoreactive oestradiol and lack of oestrogenic activity in vaginal smears indicated absence of ovarian function. Low levels of circulating gonadotrophins with a significant rise after synthetic LH-RH administration was demonstrated, while clomiphene citrate failed to induce ovulation. Following 6 months of continuous GH administration a significant increase in the growth rate was evident, whereas no pubertal development was observed. These data are interpreted as demonstrating the suprahypophyseal origin of the sexual infantilism in a patient with inappropriate GH secretion. It is suggested that a combined deficiency of LH-RH and GH-RH may account for the aetiology of this disorder.
A total of 134 women were studied, 75 of whom were using cyclic steroid contraception (ethinyl estradiol, 0.05 mg plus norgestrel, 0.5 mg) and 59 of whom had normal ovaulatory cycles. By radioimmunoassay techniques simultaneous determinations were made of total estrogens (TE) and progesterone (P) in both plasma and endometrium and of FSH and LH in plasma, covering all days of the pseudomenstrual and true menstrual cycles. As expected, the ovulating women showed a midcycle peak of plasma TE and an increase in plasma P thereafter, while no cyclic variations were observed in the treated group. Correlations of endometrial concentrations of TE and P with plasma FSH and LH levels are discussed. In 13 of the 75 treated women elevations of endometrial P concentrations were present, presumably demonstrating the "escape phenomenon." The possible future value of endometrial hormone determinations is suggested.
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A 3-hr glucose tolerance test was performed in 12 thyrotoxic patients before and after propranolol treatment for 30 days (120 mg/day). Plasma glucose, free fatty acid, insulin, and growth hormone levels were determined on each test and compared to each other and against nine clinically healthy volunteers. In eight thyrotoxic patients (subgroup A) an improvement in carbohydrate tolerance was observed after propranolol treatment, along with a fall in the previously elevated fasting FFA; no change in plasma insulin levels was observed. Plasma growth hormone levels were higher than normal both before and after propranolol; however, a 46% glucose-induced suppression was seen in both instances. In the other four patients (subgroup B) (who had had a marked and rapid weight loss) a deterioration of the previously normal glucosnificant changes in insulin levels. Elevated fasting plasma free fatty acids remained so despite propranolol treatment. Plasma growth hormone was higher than normal before and after propranolol; a late suppression (at 120 min) and no suppression at all were seen, respectively. After propranolol treatment, subgroup B had higher plasma free fatty acid than subgroup A in the fasting state and at 30 and 180 min. It is proposed that the improvement or deterioration in carbohydrate tolerance after propranolol treatment might be related to whether or not a satisfactory propranolol-induced lipolytic blockade is achieved, leading to a decrease in plasma free fatty acid levels, improved insulin sensitivity, and better peripheral glucose utilization. Therefore, a uniform dose of propranolol will not always be sufficient to obtain adequate lipolytic blockade, particularly if the thyrotoxic patient has had a marked and rapid weight loss.
The in vitro biosynthesis of estrogens and androgens by gonadal tissues of the ovotestes was studied in three siblings with familial true hermaphrodism and correlated with daily steroid and gonadotropin plasma levels. The probands were 15, 13, and 11 years old with normal male phenotype and external genitalia, grade III hypospadias, bilateral scrotal ovotestes, gynecomastia, and no uterus or fallopian tubes. Their karyotypes were 46XX both in peripheral lymphocytes and in gonadal fibroblasts, and no Y chromosome fluorescence was observed. A fusiform biopsy of each gonad was obtained, and the testicular and ovarian structures were excised and incubated for five days at 37 C with 3.8 muCi of 7alpha3H dehydroepiandrosterone, in Eagle's growth media, 95% O2 and 5% CO2. After standard procedures, four extractions with methylene chloride were performed, and the residue was assayed using Sephadex LH no. 20 chromatography. Testosterone (T), delta4androstenedione (delta 4), 5alphadehydrotestosterone (5alphaDHT), estrone (E1), estradiol-17 beta (E2) and estriol (E3) were measured. Also, during 16 consecutive days daily venous samples were obtained, and FSH, LH, E2, progesterone (P), and testosterone (T) were determined. The predominant steroids formed in vitro were estrogens, mainly E1 by either the testicular or ovarian structures. In the 11-year-old subject, the ovotestes were less active than in his oldest siblings. The patterns of androgen production showed that T was the principal androgen formed, followed by delta4 and minimal amounts of 5alphaDHT. The daily plasma hormonal profile resembled more closely a female pattern, specially in the 15 and 13-year-old patients. It is suggested that the ovotestes of these siblings had the enzymatic mechanisms necessary for estrogen and androgen biosynthesis, mainly E1 and T using a preferential metabolic pathway via androstenedione. Furthermore, it seems that the testicular structures had a greater capability to synthesize estrogens than the ovary.
A 10-year-old boy with idiopathic epilepsy refractory to treatment from age 4 and with clinical signs of hyperandrogenism was treated with chlormadinone acetate (24 mg/day) during two alternate periods of 3 months. The administration of chlormadinone was associated with a marked clinical and electroencephalographic improvement as well as a concomitant decrease in the levels of plasma testosterone and delta4 androstenedione. No changes in plasma gonadotropins were observed. Placebo had no effect neither in seizures nor in the concentration of hormones in the plasma. Since chlormadinone acetate is not a very potent gonadotropin inhibitor in males, it is suggested that the clinical and electroencephalographic improvement associated with the use of this compound, might be the consequence of a decrease in the plasma levels of androgens, mainly testosterone.