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Secondary hypogonadism is not an infrequent abnormality in older patients presenting with the primary complaint of erectile dysfunction. Because of the role of testosterone in mediating sexual desire and erectile function in men, these patients are usually treated with exogenous testosterone, which, while elevating the circulating androgens, suppresses gonadotropins from the hypothalamic-pituitary axis. The response of this form of therapy, although extolled in the lay literature, has usually not been effective in restoring or even improving sexual function. This failure of response could be the result of suppression of gonadotropins or the lack of a cause and effect relationship between sexual function and circulating androgens in this group of patients. Further, because exogenous testosterone can potentially increase the risk of prostate disease, it is important to be sure of the benefit sought, i.e. an increase in sexual function. In an attempt to answer this question, we measured the hormone levels and studied the sexual function in 17 patients with erectile dysfunction who were found to have secondary hypogonadism. This double blind, placebo-controlled, cross-over study consisted of treatment with clomiphene citrate and a placebo for 2 months each. Similar to our previous observations, LH, FSH, and total and free testosterone levels showed a significant elevation in response to clomiphene citrate over the response to placebo. However, sexual function, as monitored by questionnaires and nocturnal penile tumescence and rigidity testing, did not improve except for some limited parameters in younger and healthier men. The results confirmed that there can be a functional secondary hypogonadism in men on an out-patient basis, but correlation of the hormonal status does not universally reverse the associated erectile dysfunction to normal, thus requiring closer scrutiny of claims of cause and effect relationships between hypogonadism and erectile dysfunction.

Sexual dysfunction is common in hypertensive men and often is first reported by patients while receiving hypotensive therapy, leading to a widespread belief by patients and physicians that the sexual dysfunction is caused by a specific antihypertensive medication. However, it is unclear from the literature whether this problem is related to hypertension or to its therapy. Further, whether the erectile failures reported during therapy are a result of 1) reduced penile blood flow secondary to reduction of blood pressure after antihypertensive treatment or to obstructive vascular disease (or both) or 2) specific drug effects has not been well studied. Because of these unresolved issues, this common problem is not well managed and contributes to noncompliance with therapy by hypertensive male patients, which impedes the attainment of satisfactory blood pressure control. The present article reviews the literature related to hypertension and sexual function in men and outlines a management strategy for clinicians that attempts to document normalcy of sexual function before initiating treatment in newly diagnosed hypertensive patients. Further, it does not ascribe causality to specific antihypertensive agents for the sexual dysfunction reported by treated hypertensive patients but attempts instead to delineate the pathogenesis of the dysfunction. Once the pathogenesis is established, treatment plans can be implemented to restore normotension and maintain adequate sexual function among treated hypertensive men. The article also discusses how applied research in this area may be performed.