Objective: To examine further the dynamics of adrenal steroidogenesis in selected groups of patients with polycystic ovary syndrome (PCOS) compared to normal ovulatory women of the same age. Materials and Methods: Serum cortisol, testosterone, dehydroepiandrosterone sulphate (DHEAS), androstenedione (A), luteinizing hormone (LH), follicle-stimulating hormone, prolactin, 17-hydroxyprogesterone (17-OHP) and sex hormone-binding globulin (SHBG) were measured in the early follicular phase of the period. In addition, 2-day dexamethasone suppression and short adrenotropic hormone (ACTH) stimulation tests were performed for the study group and controls. Results: Serum testosterone (4.3 ± 1.8 nmol/l), LH (7.6 ± 1.9 IU/l), and 17-OHP (4.7 ± 2.3 nmol/l) were higher while SHBG (24.7 ± 14.2 nmol/l) was lower in patients than the control. Testosterone was significantly suppressed after dexamethasone suppression test while the level of 17-OHP increased significantly in patients more than the control after 60 min of ACTH stimulation. In the PCOS, the ratio of 17-OHP/A showed a significant increase after ACTH stimulation while that of DHEAS/A decreased when compared to controls. Conclusion: The study suggests a contribution of adrenal cytochrome P-450C dysregulation in PCOS. This suggestion could lead to another method of treating some PCOS patients when the usual anti-androgens might not be fully effective in controlling most of the symptoms.

Congenital adrenal hyperplasia (CAH) is a family of inherited disorders of adrenal steroidogenesis, most commonly due to deficiency of P-450 21-hydroxylase (21-OH). There are two genes for 21-OH on the short arm of chromosome 6, the A gene which is thought to be inactive, and the B gene. These genes appear as 3.2 and 3.7 kb TaqI fragments on Southern blots. In a study of DNA from 60 normal controls with TaqI and a 21-OH cDNA probe, 12% exhibited a homozygous deletion of the A gene, and 22 and 8% heterozygous deletions of A and B genes respectively. TaqI analysis of eight patients with CAH revealed four without A or B gene deletions, three with heterozygous deletions of the B gene and one with a homozygous deletion of the B gene. On further analysis with KpnI, EcoRI, PvuII and BglII, however, these genotypes were amended to two with heterozygous deletions of the B gene and two with possible B to A gene conversions. The genotypes of the four patients without deletions remained unchanged. RNA from CAH and Cushing's adrenal tissue was also analysed using A and B gene-specific oligodeoxynucleotide probes. B gene transcripts were detected in both CAH and Cushing's adrenals, while no A gene transcripts could be detected in either tissue. The level of B gene-derived mRNA was greater in the Cushing's adrenal than in the CAH adrenal, which in turn was greater than that in the adrenal from a normal individual.(ABSTRACT TRUNCATED AT 250 WORDS)

Background: Even though vitamin A (Vit A) is one of the essential vitamins required for bone growth and development, it is still uncertain whether its effect on bone mineral density (BMD) is beneficial or harmful. Aim: To assess Vit A’s effect and its derivatives on BMD and the risk of developing osteoporosis. Data sources: PubMed, Cochrane Library, Science Direct, Embase, and Google Scholar were searched in February 2019 and updated in November 2020. Methods: Conducted following the preferred reporting items for systematic reviews and meta-analyses (PRISMA) guidelines. Results: A total of 13 studies were included in this report out of 9,124 citations. Five of them were cross-sectional studies, and nine were cohort studies. Three out of five cross-sectional studies showed an increase in BMD, while two showed a decrease in BMD. Four out of eight cohort studies found an increase in BMD; two studies found no association between vitamin A level and BMD; one showed an inverse U-shape association of vitamin A with BMD, suggesting that both the increase or decrease levels of vitamin A affect BMD, while only one study showed a decrease in BMD. Conclusion: Although most of the included studies showed a favorable effect of Vit A on BMD, Vit A’s role or its derivatives on BMD change remains unclear.

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