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For men with a reduced testosterone level, treatment with testosterone usually improves sexual appetency. This has been demonstrated for gel and plaster as well as intramuscular and oral forms of treatment. However, from our current stand point such disturbances in sexual appetency can only be treated pharmacologically if these result from an endocrinological or other disease.
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There is increasing awareness of the significant and varied actions of endogenous androgens in women, and acknowledgement that women might experience symptoms secondary to androgen deficiency. There is also substantial evidence that prudent testosterone replacement is effective in relieving both the physical and psychological symptoms of androgen insufficiency in clinically affected women. However, our understanding of the actions of testosterone in women is incomplete, with no consensus as to what constitutes either biochemical or clinical testosterone deficiency. The focus of the limited research into testosterone replacement has been on sexuality, primarily sexual desire. However, the influence of testosterone on mood and well being also requires further exploration.
Individual problems, difficulties in the partnership, handicaps of the body and the influence of society contribute to sexual problems. In this article a definition of hypoactive sexual desire disorders (HSDD) is given. Then the author tries to show the many different reasons of disturbed sexual desire to help to see the problem from different points of view. Often it is very important for the patients to understand why they are unable to feel sexual wishes. In clarifying the personal reasons change begins and the couple can find out which next steps may be useful to solve the problem of not wanting to want.
We present the case of a 60 year old male patient with incidentally detected visual abnormalities. Detailed personal history revealed a hypogonadism that had been present for several years. Further investigations established the diagnosis of an infiltrative macroadenoma. Medical treatment with cabergoline led to a rapid regression of ophthalmologic symptoms and, subsequently, of tumor size. In male subjects symptoms of hypogonadism are often reported only late in the course of the disease, thereby leading to a generally larger tumor size at the point of diagnosis. In contrast to other pituitary tumors that are mainly treated by surgery, medical treatment with dopamine agonists is the principal therapeutic option in prolactinomas.
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The assessment of female sexual dysfunction (FSD) is often challenging in the clinical setting. Although androgen deficiency is regarded as a major cause for FSD, the causes of this condition are multifactorial. Women presenting with FSD require thorough clinical evaluation to determine the cause of FSD. Androgen therapy should be used in women only when clinical and biochemical parameters indicate that FSD stems from androgen deficiency. This review outlines the various causes of FSD, clinical and biochemical investigations required to diagnose androgen deficiency, and options for treatment of the woman found to have androgen deficiency as a cause of FSD.
A prior study has shown that premenopausal women could have decreased testosterone levels and still have regular menstrual cycles (Guay, 2001). Since ovarian function in such women was normal, the question of a possible adrenal dysfunction causing androgen deficiency was considered. If this was true, the question then arose as to whether the same defect could be seen in postmenopausal women. We studied 105 women who presented during a 6-month period of time with the chief complaint of decreased sexual desire. On subsequent testing, 74 of the women (70%) were found to have decreased total testosterone, free testosterone, and dehydroepiandrosterone sulfate (DHEA-S). Thirty-six of these women were premenopausal (ages range 24-50 years), and 38 were postmenopausal (ages range 47-78 years). All androgen levels for the women were lower than age-matched control groups found in the literature. The decreased DHEA-S levels suggest a a defect in adrenal steroidogenesis, which was seen in both premenopausal and postmenopausal women. Possible defects in regulatory mechanisms of adrenal steroidogenesis are discussed.
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