Steroid 21-hydroxylase deficiency genotype may not predict phenotype

Q. Had FMS for almost twenty years now, tried almost everything. Is Lyrica in the "steroid" family? Any one in this community could help me? I have given my few questions to find out an answer. I Had FMS for almost twenty years now, tried almost everything. I'm considering Lyrica but I'd like more info. Is Lyrica in the "steroid" family? If you go on Lyrica for a while & see no improvement with pain, is going off of it a big deal like with other med's, or can you simply just stop taking it? I take Ambien, will that have any interactions? I'm seeing my Doc about this at the end of the month, but I was hoping to get some personal experiences about it. Thanks for any thoughts! Thanks for your answers, keep them coming! A. according to this-
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there is a moderate interaction. that means you can take them both but be checked regularly for depression of breath.

Congenital adrenal hyperplasia (CAH) is an autosomal recessive disorder, and occurs in approximately 1 in 15000 births globally. [17] [18] There are multiple forms of CAH, broken down into classical and nonclassical forms based on the amount of function retained. The classical forms include salt-wasting (SW), and simple-viralizing (SV). Mutations that interfere with the active site—the heme group or residues involved in substrate binding—result in a complete loss of enzymatic activity, the salt-wasting type. [19] Cortisol and aldosterone deficits are associated with life-threatening salt-loss (hence salt-wasting), as the steroids play roles in regulating sodium homeostasis . Retaining minimal enzyme activity, the simple-viralizing type is associated with mutations in conserved hydrophobic regions or near the transmembrane domain. Simple viralizing CAH patients maintain adequate sodium homeostasis, but exhibit other phenotypical symptoms shared by SW, including accelerated growth in childhood and ambiguous genitalia in female neonates. Nonclassical forms retain 20-60% of hydroxylase function—this form is associated with normal cortisol expression, but an excess of androgens post-puberty. [20] [21]

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, dehydroepiandosterone (DHEA) and androstenedione. Thus, fasciculata and reticularis cells can make corticosteroids and the adrenal androgens, but not aldosterone.

Steroid 21-hydroxylase deficiency genotype may not predict phenotype

steroid 21-hydroxylase deficiency genotype may not predict phenotype

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steroid 21-hydroxylase deficiency genotype may not predict phenotypesteroid 21-hydroxylase deficiency genotype may not predict phenotypesteroid 21-hydroxylase deficiency genotype may not predict phenotypesteroid 21-hydroxylase deficiency genotype may not predict phenotypesteroid 21-hydroxylase deficiency genotype may not predict phenotype

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