Hypogonadotropic hypogonadism anabolic steroids

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A 31-year-old man presenting with an 18-month history of sexual dysfunction resulting from severe adult-onset IHH (LH U/L, FSH U/L, T nmol/L). Initial therapy with 50 mg of clomiphene citrate (CC) three times a day for 7 days, with overnight LH pulse profiling and 9 am T levels evaluated at baseline and on completion. A 2-month washout period, followed by low-dose maintenance therapy (25-50 mg/d) for 4 months.
MAIN OUTCOME MEASURE(S):Baseline and stimulated T levels and LH pulsatility; effect on sexual function.
RESULT(S):Clomiphene therapy resulted in complete normalization of pulsatile gonadotropin secretion, serum T level, and sexual function. CONCLUSION(S):Isolated hypogonadotropic hypogonadism may result from an acquired defect of enhanced hypothalamic sensitivity to E-mediated negative feedback. Whereas direct T replacement therapy can further suppress endogenous gonadotropin secretion, treating IHH men with gonadotropins can stimulate endogenous T secretion and enhance fertility potential. On theoretical grounds, reversal of gonadotropin deficiency with CC might be expected to have a similar biological effect.

Micropenis refers to an extremely small penis with a stretched penile length of less than SD below the mean for age or stage of sexual development. It should be differentiated from a buried or hidden penis and aphallia. It is important to use a standard technique of stretched penile measurement and nomograms for age to identify children with micropenis. All children above 1 year of age with a stretched penile length of less than cm need evaluation. Based on etiology they can be classified as hypogonadotropic hypogonadism (hypothalamic or pituitary failure), hypergonadotropic hypogonadism (testicular failure), partial androgen insensitivity syndrome and idiopathic groups. The help of a pediatric endocrinologist, geneticist, pediatric surgeon and/or urologist is often necessary. Growth velocity is an important determinant of associated hypothalamic or pituitary pathology. GnRH and/or hCG stimulation tests are often helpful in evaluating the etiology. Similarly chromosomal studies are indicated in a few. Often the diagnosis is inferred by the presence of clinical features suggestive of a syndrome usually associated with hypogonadotropic hypogonadism. Irrespective of the underlying cause a short course of testosterone should be tried in patients with micropenis and an assessment of the penis to respond should be made. Transdermal DHT has also been reported to be effective in prepubertal children. Children with hypopituitarism and GH deficiency respond to appropriate hormonal therapy. Surgical correction is not indicated in the common endocrine types of micropenis. Many studies have shown that most testosterone treated children have satisfactory gain in length of penis and sexual function. Thus sexual reassignment is done very infrequently now.

Kim et al. (2008) analyzed the CHD7 gene in 197 patients with Kallmann syndrome or normosmic hypogonadotropic hypogonadism and identified 7 different heterozygous mutations in 7 sporadic patients, 3 with KS and 4 with IHH, respectively (see, ., -). A splice site mutation () in a female KS patient with cleft lip and palate and hearing loss had previously been reported by Jongmans et al. (2008) in 2 brothers with 'relatively mild' CHARGE syndrome (214800), and a missense mutation () that was found in a male patient with IHH, cleft lip, and cryptorchidism had previously been reported by Delahaye et al. (2007) in a mother and 2 sons from a family with both typical and atypical CHARGE syndrome phenotypes. Kim et al. (2008) concluded that both normosmic IHH and Kallmann syndrome due to CHD7 mutations are mild allelic variants of CHARGE syndrome.

Hypogonadotropic hypogonadism anabolic steroids

hypogonadotropic hypogonadism anabolic steroids

Kim et al. (2008) analyzed the CHD7 gene in 197 patients with Kallmann syndrome or normosmic hypogonadotropic hypogonadism and identified 7 different heterozygous mutations in 7 sporadic patients, 3 with KS and 4 with IHH, respectively (see, ., -). A splice site mutation () in a female KS patient with cleft lip and palate and hearing loss had previously been reported by Jongmans et al. (2008) in 2 brothers with 'relatively mild' CHARGE syndrome (214800), and a missense mutation () that was found in a male patient with IHH, cleft lip, and cryptorchidism had previously been reported by Delahaye et al. (2007) in a mother and 2 sons from a family with both typical and atypical CHARGE syndrome phenotypes. Kim et al. (2008) concluded that both normosmic IHH and Kallmann syndrome due to CHD7 mutations are mild allelic variants of CHARGE syndrome.

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