For follow-up children are treated with hydrocortisone in a dose of 10–15 mg/m 2 /day. Long-acting glucocorticoids such as dexamethasone and prednisolone, known to suppress growth in children, can be used during adulthood [7, 33, 67]. Compared to 21OHD it seems to be more difficult to suppress the androgens in 3βHSD2D, which could be speculated be due to the DHEAS as a constant source of DHEA, testosterone and DHT. This may result in a need for slightly higher doses of glucocorticoids in 3βHSD2D with subsequently more long-term negative outcomes. Mineralocorticoid replacement can be achieved with fludrocortisone 0.1 mg/day [33] with regular monitoring of plasma renin activity [1, 7, 67]. Sex hormone replacement therapy should be considered for patients who show delayed progression through puberty [16].
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The phenotype of 3βHSD2D varies according to the genetic defect from severe SW form in neonates to mild menstrual disorders in older females [13, 15, 20]. In normal 46,XY fetuses, androgens are required for penile development including the urethra and fusion of the labial-scrotal folds that normally takes place before 12 weeks of gestation [29]. Severe form of 3βHSD2D is associated with varying manifestations of incomplete masculinization including severe hypospadia, micropenis, bifid scrotum, and undescended testis [16, 20, 29]. Depending on the genetic mutations, 46,XX infants can show enlarged clitoris, incomplete labial fusion and genital hyperpigmentation [30]. In contrast, some girls can have normal external genitalia which may delay diagnosis and they can subsequently present with adrenal crisis [31]. Older girls and women with genetically confirmed non-SW 3βHSD2D can present with androgen symptoms of hirsutism, premature pubarche or menstrual disorders including oligomenorrhea and primary amenorrhea [16, 32]. Several deleterious mutations in the HSD3B2 gene have been described that can cause SW during the first few weeks of life and may be fatal if not treated adequately [31, 32]. Biochemical findings include hyponatremia, hyperkalemia, metabolic acidosis and hypoglycemia [15, 33]. Regulamento da aposta esportiva abaixo de 2.5.
Jager, C.G. Sweep, K. Noordam, A.R. Hermus, High prevalence of testicular adrenal rest tumors, impaired spermatogenesis, and Leydig cell failure in adolescent and adult males with congenital adrenal hyperplasia. J. Clin. Endocrinol. Metab. 86 (12), 5721–5728 (2001) ArticleCASPubMedGoogle Scholar M.
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