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Biomedical subjects

J Blankstein

Publications and source records attributed to J Blankstein.

At least 73 records · Page 4Linked to original sources
PubMed1980

Pituitary-adrenal function in women treated with low doses of prednisone.

In order to assess whether long-term low-dose glucocorticoid administration results in suppression of the hypothalamic-pituitary-adrenal (H-P-A) axis, we examined the response of plasma cortisol to insulin-induced hypoglycemia in 23 women treated with prednisone (5 mg/day) compared with that in 19 untreated women. Basal AM levels of plasma cortisol were unaffected (mean +/- SE, 11.6 +/- 0.9 versus 11.2 +/- 0.7 microgram/dl). The plasma cortisol increment at 609 minutes after insulin-induced hypoglycemia was significantly smaller in the treated group than in the untreated group (6.7 +/- 1.0 versus 11.6 +/- 1.2 microgram/dl, p less than 0.005). Thirteen of 23 women (56.5%) in the steroid-treated group compared to one of 19 (5.3%) in the untreated group, showed a rise in plasma cortisol of less than 6 microgram/dl at 60 minutes. Furthermore, a similar reduction in the increment of plasma cortisol was also found in a subset of 10 women tested both before and during prednisone treatment. These results indicate that the concept that low doses of glucocorticoids are free of suppressive effects on H-P-A function is not justified.

Adult↗
PubMed1980

Cortisol, 11-desoxycortisol, and 21-desoxycortisol concentrations in amniotic fluid during normal pregnancy.

Concentrations of unconjugated cortisol, 11-desoxycortisol, and 21-desoxycortisol were measured by radioimmunoassay in amniotic fluid throughout gestation. Cortisol levels rose from a median of 6.5 nanograms per milliliter prior to 20 weeks to 13.9 ng/ml at 28 to 37 weeks. Median levels of 11-desoxycortisol and 21-desoxycortisol were 2.6 ng/ml and 0.21 ng/ml, respectively, and did not change with advancing gestation. These normal values provide a basis for the application of assays of 11-desoxycortisol and 21-desoxycortisol in amniotic fluid in the prenatal diagnosis of congenital adrenal hyperplasia.

17-Hydroxycorticosteroids↗
PubMed1980

Adult-onset familial adrenal 21-hydroxylase deficiency.

Two sisters (28 and 30 years) were investigated for primary infertility and milk hirsutism. Both had normal puberty, were having regular menses and had normal female sexual characteristics. Studies revealed elevated urinary 17-ketosteroid levels (15.8, 18.8 mg/24 hours) and increased serum levels of 17-OH-progesterone (2,756, 1,121 ng/dl), 21-desoxycortisol (1,882, 1,090 ng/dl), progesterone (300, 346 ng/dl), dehydroepiandrosterone (DHA) (1,600, 1,700 ng/dl), and androstenedione (402, 366 ng/dl) and testosterone (100, 104 ng/dl), together with a slight increase in serum 11-desoxycortisol (1,180, 1,560 ng/dl). Blood pressure, serum sodium/potassium plasma renin and serum aldosterone, corticosterone, 11-desoxycorticosterone and cortisol levels were normal. The administration of ACTH caused a further increase in 21-hydroxylase precursors; the administration of dexamethasone normalized hormone levels and produced ovulatory cycles. Similar studies in two siblings were normal. The affected sisters were HLA identical and did not share any HLA antigens with their healthy siblings. The data suggest that these patients have a mild form of 21-hydroxylase deficiency which was insufficient to cause prenatal virilization. The gene for this disorder may be allelic with that for typical congenital adrenal hyperplasia.

Adrenal Cortex Hormones↗
PubMed1980

Aldosterone and corticosterone in amniotic fluid during various stages of pregnancy.

Concentrations of unconjugated aldosterone and corticosterone were measured in amniotic fluid (AF) at different stages of pregnancy. AT 9-20 weeks gestation the mean AF level of aldosterone was 14.4+/0.7 ng/dl, and of corticosterone 82.9 +/- 6.4 ng/dl. Both showed the same pattern during pregnancy, with a rise in AF levels in the last few weeks. At 28-40 weeks gestation the mean AF aldosterone level was 25.5 +/- 2.0 ng/dl and the mean AF corticosterone was 218.3 +/- 26.6 ng/dl.

Aldosterone↗
PubMed1979

Failure of naloxone to alter growth hormone and prolactin levels in acromegalic and in hyperprolactinaemic patients.

We examined the effects of high-dose intravenous naloxone administration in four acromegalic patients (mean serum growth hormone level 72 ng/ml) and in seven hyperprolactinaemic women (mean serum prolactin level 59 ng/ml), in order to assess whether this opiate antagonist would be effective in lowering growth hormone and prolactin levels. No effect was observed. This lack of effect suggests that an opioid pathway is not involved in the maintenance of elevated growth hormone or prolactin secretion in these patients. However, conclusions regarding the possible role of endogenous opioids in regulation of pituitary function in normal individuals cannot be drawn from this study.

Acromegaly↗
PubMed1977

A survey of amniocentesis in 925 patients at high risk of fetal genetic disorder.

Over a nine-year period, 925 pregnancies at an Israeli medical centre were selected for investigation by amniocentesis for genetic reasons. In only 30 pregnancies did failure of laboratory methods or difficulty with amniocentesis lead to a lack of results with which to assess the normality of the fetus. The information obtained by examination of the amniotic fluid in the other 895 pregnancies is presented and discussed.

Abortion, Therapeutic↗