Steroid conversion ratio

As of this writing, there is only one published study on the use of hMG together with hCG anabolic steroid-induced azoospermia (no sperm count) that was persistent 1 year after cessation from steroid use.[47] This case report was a married couple with primary subfertility secondary to azoospermia and male hypogonadotropic hypogonadism. The husband was a bodybuilder who admitted to have used the anabolic steroids testosterone cypionate, methandrostenolone, oxandrolone, testosterone propionate, oxymetholone, nandrolone decanoate, and methenolone enanthate.[47] He was given twice-weekly injections of 10,000 IU of hCG (Profasi; Serono) and daily injections of 75 IU of hMG (Humegon; Organon) for 3 months. Results showed that semen parameters returned to normal after 3 months of treatment and the couple conceived spontaneously 7 months later.[47] It was concluded that anabolic steroid-induced azoospermia that is persistent after cessation of steroid use may be treated successfully with hCG and hMG.[47]

Cells of the zona fasciculata and zona reticularis lack aldosterone synthase (CYP11B2) that converts corticosterone to aldosterone, and thus these tissues produce only the weak mineralocorticoid corticosterone. However, both these zones do contain the CYP17A1 missing in zona glomerulosa and thus produce the major glucocorticoid, cortisol. Zona fasciculata and zona reticularis cells also contain CYP17A1, whose 17,20-lyase activity is responsible for producing the androgens, dehydroepiandrosterone (DHEA) and androstenedione. Thus, fasciculata and reticularis cells can make corticosteroids and the adrenal androgens, but not aldosterone.

Can et al. (1998) studied the molecular genetics of a large isolated inbred Turkish kindred with male pseudohermaphroditism (PPSH; 264600 ) due to either 5-alpha-reductase-2 (SRD5A2) or 17-beta hydroxysteroid dehydrogenase-3 (HSD17B3; 605573 ) gene defects. Using SSCP analysis and DNA sequencing, a new mutation in exon 5 of the SRD5A2 gene was detected in some male pseudohermaphrodites from this kindred. This single base (adenine) deletion caused a frameshift at amino acid position 251, resulting in the addition of 23 amino acids at the C terminus of this 254-amino acid isozyme. Expression of the mutant isozyme in CV1 cells showed a complete loss of enzymatic activity in the conversion of [14C]testosterone to dihydrotestosterone, without a change in the mRNA level compared to that of the wildtype isozyme. Analysis of the HSD17B3 gene in other male pseudohermaphrodites from this kindred revealed a G-to-A transition at the boundary between intron 8 and exon 9, disrupting the splice acceptor site of exon 9 ( ). In addition to finding male pseudohermaphrodites with either a homozygous SRD5A2 or HSD17B3 gene defect in this kindred, other affected males were found to be genetically more complex, ., homozygous for the SRD5A2 defect and heterozygous for the HSD17B3 defect, or homozygous for the HSD17B3 defect and heterozygous for the SRD5A2 defect. Also, phenotypically normal carriers were identified with either one or both gene defects. Homozygous male pseudohermaphrodites with SRD5A2 or HSD17B3 gene defects were phenotypically distinguishable by the presence of mild gynecomastia in the latter. Hormone data were consistent with the particular homozygous gene defect. The authors concluded that 2 gene defects, one in SRD5A2 and the other in HSD17B3, can each cause male pseudohermaphroditism in a large isolated Turkish kindred, and that the 2 defects segregate independently and can be inherited from 2 different progenitors. They stated that the analysis of a new mutation in exon 5 of the SRD5A2 gene supported the functional importance of the C terminus of the SRD5A2 isozyme.

The Female Panel of five hormones may highlight imbalances that can contribute to a number of different health conditions.   Low levels of estrogens may contribute to bone loss, fatigue, heart disease,  hot flashes, sleep disturbances, vaginal dryness and depression. Low testosterone may also contribute to bone loss, depression, fatigue, heart disease and vaginal dryness.  High estrogens or low progesterone may be a factor in anxiety symptoms, weight gain and breast cancer risk.  Fatigue often accompanies hormone imbalance and is frequently observed in postmenopausal women. Hormone imbalance may also be a feature of metabolic syndrome.

Steroid conversion ratio

steroid conversion ratio

The Female Panel of five hormones may highlight imbalances that can contribute to a number of different health conditions.   Low levels of estrogens may contribute to bone loss, fatigue, heart disease,  hot flashes, sleep disturbances, vaginal dryness and depression. Low testosterone may also contribute to bone loss, depression, fatigue, heart disease and vaginal dryness.  High estrogens or low progesterone may be a factor in anxiety symptoms, weight gain and breast cancer risk.  Fatigue often accompanies hormone imbalance and is frequently observed in postmenopausal women. Hormone imbalance may also be a feature of metabolic syndrome.

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