Biomedical subjects

S P Glickman

Publications and source records attributed to S P Glickman.

2 recordsLinked to original sources

PubMed1984

Androgen metabolism by isolated hairs from women with idiopathic hirsutism is usually normal.

We have tested the hypothesis that idiopathic hirsutism (IH) may be due to abnormality of androgen-responsive hair follicles. Because androgen metabolism within target cells is an important determinant of androgen action, we have analyzed the rates of formation and disposition of the major mediators of androgen action, testosterone (T) and dihydrotestosterone (DHT). In normal women, the pattern of androgen metabolism by growing hairs favors T predominance over DHT and inactivation of both these 17 beta-hydroxysteroids to 17-ketosteroids. This pattern results greatly from predominance of 17 beta-hydroxysteroid dehydrogenation. For example, in normal women's scalp hair, DHT disposition to 5 alpha-androstanedione proceeded at the rate of 8.6 +/- 2.0 (SEM) %/micrograms DNA/min, whereas DHT was formed from T at a rate of 0.14 +/- 0.02, and T was formed from androstenedione at a rate of 0.60 +/- 0.12, all significantly different from one another. Both the formation of 17-ketosteroids and the apparent 5 alpha-reductase activity were exaggerated in the pubic hair of men; whether these differences are site-, sex-, or androgen-related, remains to be determined. Pubic hairs tended to metabolize androgens at a greater rate than did scalp hair. This was related to the significantly greater DNA content of plucked pubic hairs, a difference unrelated to sex or androgen levels. Women with IH had heterogeneous pubic hair abnormalities. Only 1 of the 4 IH patients studied had abnormal pubic hair follicle androgen metabolism, with the greatest abnormality being an exaggerated rate of 17 beta-hydroxysteroid inactivation to 17-ketosteroids. Two of the other 3 IH cases had increased DNA content of plucked pubic hairs, a different kind of exaggeration of normal, which suggests an abnormality of hair follicle growth unrelated to androgen sensitivity. We favor the concept that IH is related to various distinct types of sexual hair abnormalities which reflect fundamental defects in the regulation of hair growth.

Adult↗

PubMed1982

Multiple androgenic abnormalities, including elevated free testosterone, in hyperprolactinemic women.

To investigate the basis of the hirsutism and elevated plasma dehydroepiandrosterone (DHA) and/or DHA sulfate (DHAS) in hyperprolactinemic women, we measured androgen binding parameters and an extensive profile of plasma androgens in normal (NL) and hyperprolactinemic women (HYPRL). ACTH tests and dexamethasone (dex) suppression tests were performed in subgroups. Free testosterone levels were higher in HYPRL (13.1 +/- 23.3 vs. 7.18 +/- 0.72 pg/ml; P less than 0.025), although total testosterone was comparable. This disparity was related to plasma testosterone-estradiol-binding globulin (TEBG) levels being one third lower in HYPRL (mean +/- SE, 27.4 +/- 4.0 nM) than in NL (41.2 +/- 3.7 nM; P less than 0.0125). Less striking elevations of plasma DHAS, androstenedione, and 11-deoxycortisol were found in HYPRL. Plasma total dihydrotestosterone [17 beta-hydroxy-5 alpha-androstan-3-one (tDHT)] was nearly 30% lower in HYPRL (11.2 +/- 2.6 ng/dl) than in NL (15.6 +/- 1.3 ng/dl; P less than 0.025), whereas free DHT was normal. Ratios of tDHT to precursors were lower in HYPRL (P less than 0.005). After ACTH stimulation, hyperresponsiveness of 17-hydroxyprogesterone and androstenedione were observed. Apparent adrenal enzyme efficiencies, judged from post-ACTH product to precursor ratios, were normal in HYPRL with one exception: the ratio of tDHT to total testosterone at 4 h was lower (P less than 0.05). Dex suppression normalized androgens and obliterated the abnormal tDHT to precursor ratios. These findings suggest an ACTH dependency of the abnormalities. In summary, we find that about 40% of HYPRL have an androgenic abnormality, and the most characteristic abnormality is an elevated free testosterone level (abnormal in 43%). Depressed TEBG and high DHAS levels were found with lesser frequency (19-21%). The plasma tDHT concentration was low, both in absolute terms and relative to its precursors. Dex suppressibility of the hyperandrogenemia was also observed. We postulate that PRL may exert multiple effects on steroid secretion and metabolism. Possibilities include the inhibition of the TEBG level.

Adolescent↗