21 beta hydroxysteroid dehydrogenase

Hypercortisolism can occur in several disorders other than Cushing's syndrome [ 1,2 ]. When such patients present with clinical features consistent with Cushing's syndrome, they may also be referred to as having physiologic hypercortisolism or pseudo-Cushing's syndrome. Clinically, patients with these physiologic forms of hypercortisolism seldom have the cutaneous (ie, easy bruising, thinning, and friability) or muscle (ie, proximal muscle atrophy and weakness) signs of Cushing's syndrome [ 3 ]. However, these conditions/disorders should be excluded when evaluating patients for Cushing's syndrome. (See "Establishing the diagnosis of Cushing's syndrome", section on 'Exclude physiologic hypercortisolism' .)

Dehydroepiandrosterone comes into subsequent oxidative transformation with production of 16Alpha-hydroxydehydroepiandrosterone . This oxidation is catalyzed by Cytochrome P450, family 3, subfamily A, polypeptide 7 ( CYP3A7) [10] , [11] , [12] and Cytochrome P450, family 3, subfamily A, polypeptide 4 ( CYP3A4) [13] , [10] , [11] . Oxidative metabolite of this reaction as well as Dehydroepiandrosterone can be further sulfated by steroid sulfatase (microsomal), isozyme S ( STS ) [14] , [15] , [16] , [15] , [14] . Dehydroepiandrosterone and Dehydroepiandrosterone sulfate can be transformed into other compounds with hormonal activity, Androstendiol and Androstendiol sulfate , respectively. These two reactions are catalyzed by Hydroxysteroid (17-beta) dehydrogenase 1 ( HSD17B1) [17] , [18] , [17] , [18] , Hydroxysteroid (17-beta) dehydrogenase 2 ( HSD17B2) [19] , [20] , [20] , [21] , and Hydroxysteroid (17-beta) dehydrogenase 7 ( HSD17B7 ) [22] , [23] , [23] , [24] .

Hmmmm interesting. Funny you mention it because I was taking gaba not too long ago and it was in a mixture with some other stuff. Anyways, I think it was causing me to wake up kind of uncoordinated and feeling just kind of weird. Dissociative I guess you could say, which makes sense because it’s related to the NMDA receptors somehow I think. It supposedly “can’t” cross the blood brain barrier, at least this is repeated despite the fact that it can and does, it’s just an unreliable mechanism in which it does. Low levels of gaba were insinuated to absorb more in the brain also. I didn’t have this issue as if I took the full 750 mg I felt very strange consistently and none of the other supplements in the mixture would seem to do this.

Stikkelbroeck et al. (2001) investigated the prevalence of testicular tumors in 17 adolescent and adult male patients with CAH aged 16 to 40 years. In 16 of 17 patients, one or more testicular tumors ranging in maximal length from to cm were found on ultrasonography. In 6 patients, the testicular tumors were palpable. Undertreatment, defined as the presence of a salivary androstenedione level above the upper reference morning level, was found in 5 of 17 patients at the time of investigation. The other 12 patients were treated adequately or even overtreated at the time of investigation. Nevertheless, 11 of these 12 patients showed testicular tumors on ultrasonography. Tumor size was significantly larger in patients who were heterozygous or homozygous for deletion or conversion of the CYP21 gene than in patients who did not have this genotype. Impairment of Leydig cell function as manifested by decreased plasma levels of testosterone was found in 6 of 17 patients. Semen analysis in 11 patients revealed azoospermia in 3 patients and poor semen quality in 4 patients. The authors concluded that, when carefully sought for, testicular adrenal rest tumors are frequently present in adolescent and adult males with CAH and are often accompanied by impaired spermatogenesis and Leydig cell failure.

21 beta hydroxysteroid dehydrogenase

21 beta hydroxysteroid dehydrogenase

Stikkelbroeck et al. (2001) investigated the prevalence of testicular tumors in 17 adolescent and adult male patients with CAH aged 16 to 40 years. In 16 of 17 patients, one or more testicular tumors ranging in maximal length from to cm were found on ultrasonography. In 6 patients, the testicular tumors were palpable. Undertreatment, defined as the presence of a salivary androstenedione level above the upper reference morning level, was found in 5 of 17 patients at the time of investigation. The other 12 patients were treated adequately or even overtreated at the time of investigation. Nevertheless, 11 of these 12 patients showed testicular tumors on ultrasonography. Tumor size was significantly larger in patients who were heterozygous or homozygous for deletion or conversion of the CYP21 gene than in patients who did not have this genotype. Impairment of Leydig cell function as manifested by decreased plasma levels of testosterone was found in 6 of 17 patients. Semen analysis in 11 patients revealed azoospermia in 3 patients and poor semen quality in 4 patients. The authors concluded that, when carefully sought for, testicular adrenal rest tumors are frequently present in adolescent and adult males with CAH and are often accompanied by impaired spermatogenesis and Leydig cell failure.

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