Testosterone levels in men with erectile dysfunction

OBJECTIVE: To investigate the frequency of hypogonadism in men with erectile dysfunction (ED) and to assess which factors are related with low testosterone levels. PATIENTS AND METHODS: In all, 165 men with ED were assessed; the evaluation included: hormonal profiles, serum total and free testosterone (using Vermeulen's formula) levels, and self-reported questionnaires on erectile function and desire domains of the International Index of Erectile Function. The frequency of hypogonadism was established using total and free testosterone levels as diagnostic criteria. The factors that might influence testosterone levels were evaluated by univariate and multivariate statistical analysis, and a logistic regression was used to determine which factors can predict free testosterone levels below normal limits (biochemical hypogonadism). RESULTS: Using the total testosterone levels, 4.8% of the men were hypogonadal, whereas when using the free testosterone levels, 17.6% were hypogonadal. In the univariate analyses, not smoking and hypertension were associated with lower total and free testosterone levels. Ageing, absence of nocturnal erections and a lower erectile function score were only associated with lower free testosterone serum levels. There was no association between total and free testosterone levels and desire. In the multivariate analysis, only total testosterone levels were related to hypertension, while free testosterone levels were related to age and nocturnal erections. For biochemical hypogonadism, simple logistic regression analysis selected age, erectile function score and aetiological diagnosis of ED as predictors. In the multivariate analysis only the erectile function score had significant independent prognostic value. CONCLUSIONS: The frequency of hypogonadism is higher when free testosterone levels are used for diagnosis. The total and free testosterone levels were not related to the level of sexual desire in men with ED. The free testosterone levels could be related to the quality and frequency of nocturnal erections, and when ED is more severe, it is more probable that free testosterone levels are below the 'normal' limit.     

Testosteron und erektile Dysfunktion

Primary hypogonadism represents a classic but rare cause of erectile dysfunction (ED) in men. Therapy with testosterone as monotherapy is therefore unlikely to cure ED in the typical ED patient. However, recent developments indicate a much greater role of testosterone in erectile function than has been supposed in the past. Serum testosterone levels decline in men with increasing age. Aging men might develop late-onset hypogonadism (LOH) associated with characteristic symptoms. Typical symptoms of LOH are represented by decreased libido and sexual function, osteoporosis, altered distribution of body fat, overall reduction in physical strength, and alterations in the general mood. Experimental and clinical studies over the last few years have also pointed out that hypogonadism results in characteristic alterations of the erectile tissue of the penis. These alterations might be reversible in response to hormone therapy with testosterone. Particularly testosterone might be a helpful supportive therapy in cases where PDE-5 antagonists have tended to lose their effectiveness on the erectile tissue in the treatment of ED.     

Testosterone and Erection: Practical Management for the Patient with Erectile Dysfunction

Although erectile dysfunction (ED) and testosterone deficiency syndrome are two independently distributed disorders, there is a degree of overlap between them. Testosterone replacement therapy, either alone or combined with other treatments such as a phosphodiesterase type 5 (PDE5) inhibitor, may therefore be useful in some men with ED. Corrective treatment of ED includes sex therapy, risk factor modification, chronic usage of PDE5 inhibitors, and testosterone replacement. Studies have shown that testosterone replacement in men with hypogonadism improves libido and erectile function in a significant proportion of cases. If corrective treatment fails or is not indicated, symptomatic treatments such as oral PDE5 inhibitors or intraurethral/intracavernous therapy are available. PDE5 inhibitors are an excellent first-line choice, although a significant proportion of men still fail to respond to monotherapy. Testosterone deficiency may be overlooked in some men with ED and, because this may be associated with lower expression of PDE5 in the penis, it could result in failure of PDE5 inhibitor therapy. Recent recommendations, therefore, suggest the need for combination therapy in some patients. In conclusion, all men presenting with ED should have their testosterone levels checked, and testosterone replacement should be considered in those with low levels. Testosterone replacement should also be considered in hypogonadal men with ED not responding to PDE5 inhibitors. If erections remain insufficient after 3 mo, a combination of testosterone and a PDE5 inhibitor may be beneficial.     

Effects of testosterone on erectile function: implications for the therapy of erectile dysfunction

Sexual potency declines with age, as does the efficiency of erection. Many studies show that different patterns of erectile dysfunction (ED), varying from occasional inability to obtain a full erection, impairment throughout intercourse and total absence of erectile response, might not be triggered by psychological factors only. Recent research indicates that ED relies on organic causes, and has challenged the development of new therapies. One therapeutic approach in patients who have testosterone deficiency is based on androgen therapy. Thus, we reviewed data on testosterone-induced effects relative to erectile function, summarizing the results from studies reported in 1991-2006 on testosterone therapy in patients with ED and hypogonadism, with a special focus on men not responding to phosphodiesterase-5 (PDE-5) inhibitors. We searched several computerized databases parallel with printed bibliographic references. Many studies have established animal models, which confirm that testosterone is important in modulating the central and peripheral regulation of ED. Testosterone deprivation has a strong negative impact on the structure of penile tissues and erectile nerves, which can be prevented by androgen administration. Combined therapy regimens with PDE-5 inhibitors and testosterone might improve ED in patients with hypogonadism of different causes. Thus, androgen treatment in hypogonadic patients, including those unresponsive to PDE-5 inhibitors, often results in an improvement of ED. Testosterone therapy is safe and convenient, while rapidly correcting low testosterone levels.     

Testosterone and erectile dysfunction

Aging is associated with a decline in several important health factors in men, including libido. Serum testosterone concentrations also decrease with age, and many age-related clinical features are closely associated with androgen deficiency, including erectile function (ED). Approximately 70% of ED is of organic origin, with the major risk factors being diabetes mellitus, hypercholesterolemia, smoking and chronic medical illnesses. These are also established risk factors for atherosclerosis, which is the predominant predisposing factor of vasculogenic ED. The introduction of phosphodiasterase-5 (PDE-5) inhibitors for the treatment of ED made a significant impact both in terms of clinical efficacy, and increasing the awareness of the condition. In spite of this, some patients fail to respond to PDE-5 inhibitors alone. Both animal and clinical studies indicate that testosterone therapy improves both erectile function and the response to PDE-5 inhibitors in patients with ED and hypogonadism. Indeed, interventional studies demonstrate that testosterone replacement therapy improves erectile function in hypogonadal men who have previously failed to respond to PDE-5 inhibitors alone. Furthermore, it has been demonstrated that the full therapeutic potential of PDE5 inhibitors will only become manifest in a eugonadal state. Recent studies have demonstrated a close relationship between testosterone and ED and suggest that testosterone therapy may be a valuable option for an increasing number of affected men. European guidelines recommend that all men presenting with ED should have their testosterone concentrations measured.     

Prevalence and management of mild hypogonadism: introduction

Although male hypogonadism can adversely affect the well-being of otherwise healthy men, physicians sometimes overlook it as a possible contributing factor to decreased libido, erectile dysfunction (ED), irritability, osteoporosis, and decreased muscle mass. However, hypogonadism is easily treated by testosterone replacement therapy, which may provide benefits such as mood improvement, increased bone density, and possibly reduced risk of type II diabetes. Articles in this supplement focus on populations that may benefit from testosterone replacement therapy (eg, men with type II diabetes, HIV, and ED). An overview of male 'andropause' is also provided. The authors discuss the surprisingly high prevalence of hypogonadism in certain patient populations and its impact on quality of life. Although testosterone has been used therapeutically for years, much remains to be learn about this hormone and its positive effects.     

Erectile dysfunction, testosterone deficiency, metabolic syndrome and prostatic disease in Taiwan

The purpose of this article is to review the current status and associations between erectile dysfunction (ED), testosterone deficiency (hypogonadism), the metabolic syndrome (MS) and prostatic disease in Taiwan. The prevalence of ED among Taiwanese men older than 40 years was 17.7%, and self-reported ED was lower than International Index of Erectile Function (IIEF)-5 defined ED. Phosphodiesterase type 5 (PDE-5) inhibitors are the first line treatment, but intracavernosal injection and penile prosthesis still have their place. The serum total testosterone (TT) level showed a decline with age, and is one of the major factors that reduces quality of life (QoL). Testosterone deficiency and hypogonadism are associated with ED, which can be improved by testosterone replacement. The MS was reported to have a prevalence of 14–16% in Taiwanese men, and was associated with an increase in all-cause and cardiovascular disease (CVD) mortality. It was also reported to be associated with hypogonadism and ED. The incidence of prostate cancer (PCa) has been rapidly increasing, and its management has also been changing in Taiwan. In conclusion, we need to pay more attention to men's health in Taiwan.     

Endocrine causes of impotence (nondiabetes)

The endocrine system has a major role in erections in normal men and it can also be a cause of significant morbidity. The relationship between serum testosterone measurement and erectile function is complex. Androgen treatment should certainly be considered in patients without prostate cancer but with a clinical picture that suggests a relevant contribution of hypogonadism to the ED. Other, nondiabetic, endocrine abnormalities may need to be considered in the management or the patient with ED.     

Hypogonadism is associated with overt depression symptoms in men with erectile dysfunction

Depression and hypogonadism are associated with erectile dysfunction (ED). We evaluated the prevalence of both conditions in men presenting to an ED specialty clinic, and tested whether hypogonadism correlated with the presence of depressive symptoms using a validated questionnaire. From July 2001 to June 2003, 157 men referred to an ED specialty clinic prospectively filled the Center for Epidemiologic Studies Depression Scale (CES-D), the abbreviated International Index of Erectile Function (IIEF-5) and had testosterone serum levels drawn. Median age was 53 (range=21-85 years). Hypogonadism, defined as serum T (testosterone)<300 mg/dl, was present in 36% of patients. This proportion was higher in men over the median age compared to younger patients (45 and 26%, respectively, P=0.002). Overt depression symptoms, defined as a CES-D> or =22, were found in 24% of men. Mean age of men with overt depression was 49.9+/-10.1 years vs 55.1+/-15.8 years for those with CES-D<22 (P=0.02). Hypogonadal men were more likely to have overt depression scores compared to eugonadal counterparts (35 vs 18%, P=0.02). This association was statistically stronger after correcting for age in a multivariate linear model (P=0.005). The relative risk of having overt depression was 1.94 times higher in men with hypogonadal testosterone level (95% confidence interval: 1.13 to 3.7). We conclude that in an ED referral population, symptoms of hypogonadism and depression symptoms are fairly prevalent, and that overt depression symptoms are strongly associated with hypogonadism. Clinicians should consider testosterone measurements in all men with high depression symptom scores.     

Clomiphene increases free testosterone levels in men with both secondary hypogonadism and erectile dysfunction: who does and does not benefit?

Secondary hypogonadism is more common than primary gonadal failure and is seen in chronic and acute illnesses. Although testosterone has a role in erections, its importance in erectile dysfunction (ED) has been controversial. Hypogonadism produced by functional suppression of pituitary gonadotropins has been shown to correct with clomiphene citrate, but with a modest effect on sexual function. We wondered if longer treatment would produce improved results. A total of 178 men with secondary hypogonadism and ED received clomiphene citrate for 4 months. Sexual function improved in 75%, with no change in 25%, while significant increases in luteinizing hormone (P<0.001) and free testosterone (P<0.001) occurred in all patients. Multivariable analysis showed that responses decreased significantly with aging (P<0.05). Decreased responses also occurred in men with diabetes, hypertension, coronary artery disease, and multiple medication use. Since these conditions are more prevalent with aging, chronic disease may be a more important determinant of sexual dysfunction. Men with anxiety-related disorders responded better to normalization of testosterone. Assessment of androgen status should be accomplished in all men with ED. For those with lower than normal age-matched levels of testosterone treatment directed at normalizing testosterone with clomiphene citrate is a viable alternative to giving androgen supplements.     

Obesity, low testosterone levels and erectile dysfunction

Obesity is an important risk factor for many common diseases including cardiovascular disease (CVD), type 2 diabetes, cancer and erectile dysfunction (ED). Adipose tissues produce a number of adipokines and cytokines, which affect endothelial and metabolic function resulting in insulin resistance and the metabolic syndrome (risks factors for CVD). Both ED and metabolic syndrome improve with a reduction in body mass index (BMI). The relationships among obesity, metabolic syndrome, ED, sex hormone-binding globulin (SHBG) and serum total and free testosterone levels are complex and often confusing to the physician. It is known that BMI is inversely proportional to serum total testosterone concentrations; low serum SHBG levels in obesity contribute to the low serum total testosterone. Recent studies show that BMI is also inversely proportional to free testosterone concentration. The characteristic low serum testosterone concentrations observed in obese men are also present in men with the metabolic syndrome and type 2 diabetes mellitus. A small proportion of men with ED have hypogonadism; however, the proportion increases if these men are obese with manifestations of the metabolic syndrome or type 2 diabetes mellitus. ED is a common symptom in patients with type 2 diabetes who also have low testosterone levels. This review describes the relationships between low serum testosterone concentrations and ED in obese patients and those with metabolic syndrome and type 2 diabetes mellitus.     

Predicting hypogonadism in men based upon age, presence of erectile dysfunction, and depression

Hypogonadism, a disorder associated with aging, can cause significant morbidity. As clinical manifestations of hypogonadism can be subtle, the challenge and the burden of diagnosis remain the responsibility of the clinician. Four different analytic methods were used to predict hypogonadism in men based upon age, the presence of erectile dysfunction (ED) and depression. 218 men were classified by age, serum testosterone level, the presence of ED and depression. Depression was determined by the Center for Epidemiologic Studies Depression Scale (CES-D). ED was assessed by the Sexual Health Inventory for Men (SHIM). Hypogonadism was defined as a serum testosterone level <300 ng/dl. An artificial neural network (ANN) was programmed and trained to predict hypogonadism based upon age, SHIM, and CES-D scores. Subject data was randomly partitioned into a training set of 148 (67.9%) and a test set of 70 (32.1%). The ANN processed the test set only after the training was complete. The discrete predicted binary output was set to (0) if testosterone level was <300 ng/dl or (1) if >300 ng/dl. The data was also analyzed by standard logistic regression (LR), linear and quadratic discriminant function analysis (LDFA and QDFA, respectively). Reverse regression (RR) analysis evaluated the statistical significance of each risk factor. The ANN can accurately predict hypogonadism in men based upon age, the presence of ED, and depression (receiver-operating characteristic=0.725). A four hidden node network was found to have the highest accuracy. RR revealed the depression index score to be most significant variable (P=0.0019), followed by SHIM score (P=0.00602), and then by age (P=0.015). Hypogonadism can be predicated by an ANN using the input factors of age, ED, and depression. This model can help clinicians assess the need for endocrinologic evaluation in men.     

Significance of hypogonadism in erectile dysfunction

To review the role and significance of hypogonadism, defined as a low testosterone (T) level, in erectile dysfunction (ED). Review of literature. Serum T is below 3 ng/ml in 12% of ED patients, including 4% before and 15% after the age of 50. Replacement studies in men with severe hypogonadism demonstrate that sexual desire and arousal, as well as the frequency of sexual activity and spontaneous erections are clearly T-dependant. Psychic erections are partly T-dependant. The effects of T upon sexual function are dose-dependant up to a threshold level that is consistent within an individual, but markedly variable between individuals, ranging from 2 to 4.5 ng/ml. More evidence is required to confirm a significant impact of T on the intrapenile vascular mechanisms of erections in men as it is the case in animals. No convincing association of T with ED has been found in epidemiological studies. As concerns clinical experience, although a meta-analysis of the randomized controlled trials established that T therapy consistently restores erectile function in young hypogonadal patients with T below 3.46 ng/ml, the effects of this treatment have been mostly disappointing when used alone in older patients consulting for ED who are subsequently diagnosed to have hypogonadism following routine T measurement. These poor results may probably be explained by the high prevalence of co-morbidities, and by the fact that ED itself may induce hypogonadism. Combination therapy with T and PDE5 inhibitor (PDE5I) may be effective in the hypogonadal ED patients when T therapy alone fails. However, more evidence is required to confirm the hypothesis that a minimum level of T is required for a complete effect of PDE5I in certain men, since a PDE5I was able to restore complete erections in severely hypogonadal men. Though a low T level is not always the only cause of ED in hypogonadal ED patients, there are important benefits in screening for hypogonadism in ED. A low T level justifies a 3 month trial of T therapy, before combining a PDE5I if T therapy alone fails     

Hypogonadism in the man with erectile dysfunction: What to look for and when to treat

Hypogonadism (low serum testosterone) is commonly associated with erectile dysfunction (ED). However, many urologists may lack appreciation of the relative merits of treating hypogonadism compared with oral phosphodiesterase inhibitors for sexual dysfunction. Testosterone-replacement therapy (TRT) may be the best treatment for men with ED when the presentation includes diminished libido or other sexual symptoms or when non-sexual symptoms such as depressed mood, decreased sense of vitality, and increased fatigue also exist. The health benefits of TRT also include improvements in body composition, bone density, cognition, and sense of well-being. Thus, there may be good reasons to use TRT as first-line therapy for the man with ED. Concerns regarding prostatic and cardiovascular risks of TRT have not been supported by the literature. Nevertheless, men receiving TRT must be monitored at regular intervals with digital rectal examination and blood testing for prostate-specific antigen. Hematocrit or hemoglobin also should be obtained regularly due to the risk of erythrocytosis. Awareness of the benefits of TRT in the man with ED may improve clinical outcomes.     

Getting Urology involved in the treatment of men with erectile dysfunction,the metabolic syndrome and hypogonadism

Urologists play a significant role in the diagnosis and treatment of male erectile dysfunction (ED). But the context of diagnosing and treating ED has profoundly changed over the past decade, in that it is no longer viewed as an independent entity. Rather it is recognized that in many (but not all) patients, there is a close association with the so called “metabolic syndrome” and on occasions with hypogonadism. In order to treat men with ED appropriately in this context, it is important for the urologist to become familiar with the intricacies of the metabolic syndrome and also with the diagnosis and treatment of male hypogonadism.While understanding of the metabolic syndrome involves the urologist in the understanding the management of hypertension, dyslipidaemia and diabetes, (most of which will be have changed considerably since he first learnt about them at medical school), an understanding of testosterone metabolism is much closer to home. Urologists are trained to use testosterone withdrawal as a treatment for prostate cancer, and it is only a short intellectual step to believing that there is an association between testosterone replacement and the development of prostate cancer. However, while the evidence for the former is considerable, the evidence to support the latter relationship is lacking.There is increasing evidence that there is a role for the responsible treatment of elderly men who are hypogonadal with testosterone while at the same exercising due caution in relation to any potentially harmful effects of testosterone administration on the prostate and the hematopoietic system. To this end a number of sets of guidelines for diagnosing and treating elderly men with testosterone deficiency have been developed.     

Screening for metabolic syndrome and testosterone deficiency in patients with erectile dysfunction: results from the first UK prospective study

Study Type – Diagnostic (exploratory cohort)
Level of Evidence 2b

OBJECTIVE

To screen patients with erectile dysfunction (ED) for the presence of metabolic syndrome (MetS), testosterone deficiency and cardiovascular (CV) risk factors, in a secondary referral centre in the UK, as men with ED have a high incidence of CV risk factors that might amount to MetS, with obesity, increased risk of coronary heart disease and type II diabetes; testosterone deficiency has also been associated with both ED and MetS.

PATIENTS AND METHODS

We assessed 124 men presenting with ED between March 2007 and August 2008. Data were collected prospectively for patient demographics, risk factors associated with MetS, and hypogonadism. MetS was assessed using the National Cholesterol Education Program Adult Treatment Panel III Criteria 2005 (based on three or more of five criteria: waist circumference, high triglycerides, low levels of high‐density lipoprotein cholesterol, hypertension and impaired glucose tolerance).

RESULTS

The mean (range) age of the men was 50 (16–76) years; 50 of 124 (40%) patients had MetS and 27% had hypogonadism. The latter was also associated with a low testicular volume and decreased libido. Ninety‐seven patients (82%) were either overweight or obese, and 64 (52%) were current or ex‐smokers.

CONCLUSIONS

Our audit confirms a high incidence of MetS and hypogonadism in patients with ED in the UK. We recommend routine screening for CV risk factors, MetS and testosterone deficiency in all patients in the UK with ED.     

Hypogonadism and erectile dysfunction: the role for testosterone therapy

The role of low testosterone levels in erectile dysfunction (ED) remains unclear. Both organic and psychogenic factors contribute to ED, with vasculogenic causes being the most common etiology. Approximately 10-20% of patients with ED are diagnosed with hormonal abnormalities. At the physiologic level, two second messenger systems are involved in mediating erections, one involving cyclic adenosine monophosphate (cAMP) and the other involving cyclic guanosine monophosphate (cGMP). PDE5 inhibitors such as sildenafil promote the cGMP pathway, while alprostadil affects the cAMP pathway. Evidence is strong that, in animal systems, testosterone has direct effects on erectile tissue. However, although testosterone clearly has an impact on libido in humans, its effect on penile function is less clear. Evaluation of ED includes medical, sexual, and psychosocial history assessments, as well as laboratory tests to check for diabetes and hormonal abnormalities. Initial interventions should involve correction of potentially reversible causes of ED, such as hypogonadism. First-line therapy for other patients is typically oral PDE5 inhibitors, such as sildenafil, tadalafil, or vardenafil. For patients who fail treatment with PDE5 inhibitors, local therapies such as intracavernous alprostadil are highly successful. Recent data also support the success of combination therapy with sildenafil and testosterone. This opens the possibility of other combinations of testosterone and other treatments of ED. The ability to exploit multiple pathways in the physiologic processes leading to erection may help improve therapy for ED.     

Following the common association between testosterone deficiency and diabetes mellitus, can testosterone be regarded as a new therapy for diabetes?

Type 2 diabetes mellitus (T2DM) is increasing at epidemic proportions worldwide, representing a risk factor for cardiovascular diseases. Nowadays, hypogonadism and erectile dysfunction (ED) are considered frequent, although often under-diagnosed, complications of T2DM. Recent evidence suggests that in a diabetic population ED itself is an efficient predictor of silent coronary heart diseases. Patients with T2DM have an impaired sexual life, which is worsened by hypogonadism. Low T in T2DM is in fact associated with more severe ED, hypoactive sexual desire and low intercourse frequency. Testosterone replacement therapy (TRT) has been proven to improve sexual function in hypogonadal men. In addition, TRT improves adiposity, insulin resistance and total cholesterol. Specific studies on the effect of TRT in T2DM are scanty. This review will evaluate the contribution of low testosterone in diabetic subjects with sexual dysfunction. In addition, we have also reviewed available evidence on potential metabolic benefits of testosterone supplementation in T2DM patients.     

The relationship between hypogonadism and erectile dysfunction

It is well known that testosterone enhances sexual interest leading to an increased frequency of sexual acts and an increase in the frequency of sleep-related erections. However, it has little effect on fantasy- or visually induced erections. Exact contribution to erection from testosterone in men remains unclear. Animal studies have well demonstrated that testosterone plays critical physiological (activity of nitric oxide synthases and phosphodiesterases), biochemical (through an endothelial-independent pathway and adrenergic tonicity) and structural (change of fibroelasticity and hollow cell accumulation) roles in erectile function. The supplementation of testosterone to castrated animals can restore erectile function. Clinically, reports of patients with erectile dysfunction (ED) combined with hypogonadism who receive testosterone therapy have inconsistent results. However, testosterone may ameliorate the expression of the phosphodiesterase-5 (PDE5) inhibitor, and the use of testosterone in conjunction with the PDE5 inhibitor revealed convincing results. Because of potential risks in clinical use, testosterone therapy should be individualized, carefully considered and closely monitored, especially, in patients with possible occult prostate cancer, and large benign prostatic hyperplasia. Lower urinary tract symptoms might be worsened by this treatment, since the prostate is an androgen-dependent tissue.     

Sexual functions of men with obstructive sleep apnoea syndrome and hypogonadism may improve upon testosterone administration: a pilot study

This study examined 72 patients with obstructive sleep apnoea syndrome (OSAS), confirmed by polysomnography. Thirty-two patients were suffering from erectile dysfunction (ED) assessed by IIEF-5 questionnaires and confirmed by nocturnal penile tumescence examination. Their testosterone levels were measured. Eight patients had normal testosterone levels and were treated with a PDE-5 inhibitor (vardenafil) only; after 6 months of treatment, 6 of these patients (75%) showed significant improvement in erectile function. The remaining 24 patients with OSAS, ED and hypogonadism (total testosterone <12 nmol l⁻¹), were divided into two groups based on the indication for continuous positive airway pressure (CPAP) therapy: five patients received CPAP therapy (group 1) and 19 patients did not (group 2). The patients of group 2 received only a PDE-5 inhibitor (vardenafil 20 mg) for ED; and eight patients (42%) showed an improvement after 3 months of treatment. The five patients receiving CPAP therapy were treated with a combination of parenteral testosterone undecanoate and a PDE-5 inhibitor (vardenafil) and all had normal erectile function after 3 months of therapy. The results suggest positive effects of addition of testosterone to treatment with PDE-5 inhibitors in hypogonadal men with OSAS, which should be confirmed in larger controlled studies.