Home About us Contact
|
Home About us Contact | ||
|
|
||
Hypogonadotropic Hypogonadism (hypogonadotropic + hypogonadism)
Selected AbstractsLetrozole normalizes serum testosterone in severely obese men with hypogonadotropic hypogonadismDIABETES OBESITY & METABOLISM, Issue 3 2005H. De Boer Background:, Morbid obesity is associated with increased estradiol production as a result of aromatase-dependent conversion of testosterone to estradiol. The elevated serum estradiol levels may inhibit pituitary LH secretion to such extent that hypogonadotropic hypogonadism can result. Normalization of the disturbed estradiol-testosterone balance may be beneficial to reverse the adverse effects of hypogonadism. Aim:, To examine whether aromatase inhibition with Letrozole can normalize serum testosterone levels in severely obese men with hypogonadotropic hypogonadism. Patients and Methods:, Ten severely obese men, mean age 48.2 ± 2.3 (s.e.) years and body mass index 42.1 ± 2.6 kg/m2, were treated with Letrozole for 6 weeks in doses ranging from 7.5 to 17.5 mg per week. Results:, Six weeks of treatment decreased serum estradiol from 120 ± 20 to 70 ± 9 pmol/l (p = 0.006). None of the subjects developed an estradiol level of less than 40 pmol/l. LH increased from 4.5 ± 0.8 to 14.8 ± 2.3 U/l (p < 0.001). Total testosterone rose from 7.5 ± 1.0 to 23.8 ± 3.0 nmol/l (p < 0.001) without a concomitant change in sex hormone-binding globulin level. Those treated with Letrozole 17.5 mg per week had an excessive LH response. Conclusion:, Short-term Letrozole treatment normalized serum testosterone levels in all obese men. The clinical significance of this intervention remains to be established in controlled, long-term studies. [source] Nutritional hypogonadotropic hypogonadism presented with decreased ejaculatory volumeINTERNATIONAL JOURNAL OF UROLOGY, Issue 2 2005KOICH UDAGAWA Abstract A 19-year-old male college student presented with decreased ejaculatory volume. Endocrinological examinations demonstrated a hypogonadotropic hypogonadism (HH) caused by a gonadotropin-releasing hormone deficiency from the hypothalamus. Cranial magnetic resonance imaging did not demonstrate any abnormalities. The possible causative factor of this adult-onset HH was excessive weight-loss (,26% in 1 year) due to inadequate food intake and an irregular lifestyle. Semen analyses and serum gonadotropin and testosterone values gradually improved as the patient became accustomed to his new life and regained weight. [source] Abstracts of the 8th Meeting of the Italian Peripheral Nerve Study Group: 43JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2003S Amadio Study aim: the Ebf gene family has been implicated in several developmental processes, ranging from B-cell development to neuronal differentiation. As the murine Ebf2 gene is expressed in numerous sites of nervous system, Ebf2-null mice develop hypogonadotropic hypogonadism, due to defective migration of gonadotropin releasing hormone-synthesizing neurons, and a peripheral neuropathy as well. Therefore, we aimed to study whether electrophysiological tests would be able to detect abnormalities of peripheral nerve function. Methods: 2 groups of mice were studied, which consisted of 8 Ebf2-/- mice and 9 age-matched controls. The sciatic nerve was stimulated at the ankle and at the ischiatic notch; the compound motor action potential (cMAP) was recorded from the paw muscles with a pair of needle electrodes to measure the motor conduction velocity (MCV). Results: MCV mean values were lower in Ebf2-/-(21.8 m/sec; SD 2.9) than in controls (35.2 m/sec; SD 2.6) and the difference was significant (p < 0.001). The mean cMAP amplitude was also decreased in Ebf2-/-(6.2 mV; SD 2.7) as compared to controls (9.3 mV; SD 2.6, p < 0.05). Conclusions: electrophysiological tests demonstrated a sharp decrease of sciatic MCV in Ebf2-/- mouse, as consequence of defective axon sorting, segmental dysmyelination and axonal damage revealed by pathological study. [source] Mutations in a G protein-coupled receptor cause hypogonadotropic hypogonadism in humans and miceCLINICAL GENETICS, Issue 3 2004MLE MacDonald No abstract is available for this article. [source] | ||||||||||