Male hormone deficiency treatment

While the insulin tolerance test is considered the “gold-standard,” it is not a perfect test. It can be safely conducted in experienced centres [ 23 ] but is contraindicated in patients with a history of seizures or heart disease. Also, it is unpleasant for the patient who requires hospital admission and close medical supervision, and adequate hypoglycaemia is not always achieved [ 24 ]. This consumes considerable healthcare resources and reduces its appeal among some endocrinologists, as illustrated in a recent US study which found that only % of patients evaluated for GHD underwent an insulin tolerance test [ 16 ].

Testosterone (T) improves the ability of estrogen to improve bone health. A 2008 study on post-menopausal women receiving hormone replacement therapy found that women receiving testosterone saw greater improvement in bone density than with estrogen (E) replacement alone. “The favourable estrogenic effects on lipids were preserved in women treated with T, in association with beneficial changes in body composition.” They also noted that the, “addition of testosterone resulted in a significantly greater improvement compared to E for sexual activity (P < ), satisfaction (P < ), pleasure (P < ), orgasm (P < ) and relevancy (P < ).” In the statistical world, those are some nice looking P values. The smaller the P value, in this case, the more likely it is you will see the same benefit.

When measuring testosterone levels, it is critical to determine the levels of both free and total testosterone to understand the cause of any observed symptoms of deficiency (Khosla et al 2008).

Because of difficulties with equipment standardization and inter-laboratory variability, it is recommended that physicians consistently use the same local laboratories and gain familiarity with the accuracy, precision and definition of normal values for the assays offered in their communities (Morales et al 2010).

McNay et al. (2007) determined the contribution of HESX1 genetic defects to the etiology of hypopituitarism. Nonfamilial patients (724) with either septooptic dysplasia (314 patients) or isolated pituitary dysfunction, optic nerve hypoplasia, or midline neurologic abnormalities (410 patients) originally screened by SSCP were rescreened by heteroduplex detection for mutations in the coding and regulatory regions of HESX1. In addition, direct sequencing of HESX1 was performed in 126 patients with familial hypopituitarism from 66 unrelated families and in 11 patients born to consanguineous parents. All patients studied had at least 1 of the 3 classic features associated with septooptic dysplasia (optic nerve hypoplasia, hypopituitarism, and midline forebrain defects). The overall incidence of coding region mutations within the cohort was less than 1%. McNay et al. (2007) concluded that mutations within HESX1 are a rare cause of septooptic dysplasia and hypopituitarism, and that the large number of familial patients with septooptic dysplasia in whom no mutations were identified is suggestive of an etiological role for other genetic factors.

Male hormone deficiency treatment

male hormone deficiency treatment

McNay et al. (2007) determined the contribution of HESX1 genetic defects to the etiology of hypopituitarism. Nonfamilial patients (724) with either septooptic dysplasia (314 patients) or isolated pituitary dysfunction, optic nerve hypoplasia, or midline neurologic abnormalities (410 patients) originally screened by SSCP were rescreened by heteroduplex detection for mutations in the coding and regulatory regions of HESX1. In addition, direct sequencing of HESX1 was performed in 126 patients with familial hypopituitarism from 66 unrelated families and in 11 patients born to consanguineous parents. All patients studied had at least 1 of the 3 classic features associated with septooptic dysplasia (optic nerve hypoplasia, hypopituitarism, and midline forebrain defects). The overall incidence of coding region mutations within the cohort was less than 1%. McNay et al. (2007) concluded that mutations within HESX1 are a rare cause of septooptic dysplasia and hypopituitarism, and that the large number of familial patients with septooptic dysplasia in whom no mutations were identified is suggestive of an etiological role for other genetic factors.

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