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At least 1,369 records · Page 76Linked to original sources
PubMed2004

The effects of androgen depletion on human erectile function: a prospective study in male-to-female transsexuals.

The objective of the study was to determine the effects of androgen depletion on erectile function in a population of male-to-female transsexuals. The erectile function of 25 consecutive male-to-female transsexuals on androgen depletion treatment and scheduled for surgical gender reassignment was prospectively evaluated using medical and sexual history, physical examination, total serum testosterone, International Index of Erectile Function (IIEF-15) questionnaire, penile colour-coded Doppler ultrasonography (CDU) after pharmacological stimulation and nocturnal penile tumescence (NPT) test. All but one had undetectable or low testosterone. Subjective erectile function, according to IIEF-15 scores, and penile CDU findings did not correlate with testosterone levels, whereas NPT test findings correlated well with testosterone levels. These findings would suggest that nocturnal erections are androgen-dependent whereas sexually induced erections are androgen-independent. It can also be assumed that testosterone is important but not essential for male erectile function and that other androgen-independent pathways can be responsible for sexually induced erections.

5-alpha Reductase Inhibitors↗
PubMed1997

Involvement of neurosteroids in the effect of the endogenous benzodiazepine receptor ligand octadecaneuropeptide (ODN) on gonadotropin-releasing hormone gene expression in rat brain.

We have recently demonstrated that different activators of the GABAA receptor complex including reduced progesterone metabolites and the endozepine octodecaneuropeptide (ODN) exert an inhibitory influence on GnRH gene expression. In order to investigate the possible involvement of neurosteroids, especially progesterone metabolites in the effect of ODN, we have evaluated in adrenalectomized and castrated male rats the influence of pretreatment with an inhibitor of 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) trilostane (TRIL) and an inhibitor of 5 alpha-reductase MK-906 on GnRH mRNA levels in ODN-treated rats. TRIL completely prevented the inhibitory influence of ODN on GnRH mRNA. It was also found that the inhibitor of 3 beta-HSD as well as pregnenolone sulfate (PREG-S), which has been shown to be increased following TRIL treatment, could induce an increase in GnRH mRNA. MK-906 could also completely reverse the negative influence of ODN. When administered alone, this antagonist of 5 alpha-reductase induced an increase in GnRH mRNA. These results clearly indicate that the inhibition of two key enzymes for the synthesis of reduced progesterone metabolites can completely prevent the inhibitory influence of the endozepine ODN, suggesting that the effect of this endogenous ligand might be completely or partially mediated by an activation of the synthesis of active progesterone metabolites. On the other hand, it remains possible that, as a consequence of enzymatic inhibition, an increase in some precursors known as antagonists of GABAA may play a role in the prevention of the ODN effect by the two enzyme antagonists.

3-Hydroxysteroid Dehydrogenases↗
PubMed1997

Anaemia associated with androgen deprivation in patients with prostate cancer receiving combined hormone blockade.

OBJECTIVE: To describe the incidence, time to onset and extent of anaemia occurring in patients with prostate cancer receiving combined hormone blockade (CHB) and the timing and extent of recovery from anaemia in those patients where CHB was discontinued. PATIENTS AND METHODS: Patients with prostate cancer were evaluated prospectively by physical examination and laboratory tests at baseline and at routine intervals while receiving CHB. Of 142 patients who received CHB, 133 were evaluable for the assessment of anaemia; CHB was discontinued in 76 patients, of whom 64 were assessable for recovery from their anaemia. RESULTS: Haemoglobin levels declined significantly in all patients from a mean baseline of 149 g/L to means of 139 g/L, 132 g/L and 131 g/L at 1, 2 and 3 months, respectively. Haemoglobin levels continued to decline during CHB to a mean nadir of 123 g/L at a mean of 5.6 months of CHB, representing a mean absolute haemoglobin decline at nadir of 25.4 g/L. In 120 of the 133 (90%) patients, the relative decline in haemoglobin at nadir was > or = 10% and was > or = 25% in 17 (13%) others, representing a mean absolute haemoglobin decline in this subset of 42.7 g/L. Significant symptoms related to anaemia occurred in 17 patients (13%). Anaemia and symptoms in these patients were easily corrected with the subcutaneous administration of recombinant human erythropoietin. CONCLUSIONS: The anaemia associated with androgen deprivation is significant and occurs routinely in men receiving CHB. It is normochromic, normocytic, temporally-related to the initiation of androgen blockade and usually resolves after CHB is discontinued. We suggest that patients receiving CHB undergo haematological testing at baseline, 1-2 months after initiating CHB and periodically thereafter. Patients developing anaemia should be questioned about symptoms reflecting physiological compromise (e.g. angina, dyspnoea on exertion). In the absence of other causes, CHB should be suspected in the development of anaemia in patients receiving this treatment.

Age Factors↗
PubMed2005

[Prevention of prostate cancer].

Prostate cancer has become the most frequently diagnosed male cancer next to non-melanotic skin cancer in the Western world. Preventive measures would therefore have important potential effects on the incidence and prevalence of this disease. A potential for effective prevention of prostate cancer is currently seen in dietary changes and perhaps in dietary supplementation with vitamins D and E or selenium. Pharmacological prevention seems a possibility with drugs acting on intraprostatic testosterone metabolism. Several large randomised trials are ongoing to clarify the potential for successful prostate cancer prevention.

5-alpha Reductase Inhibitors↗