Metabolic syndrome, testosterone deficiency and erectile dysfunction never come alone

Until a decade ago the ailments of elderly men, such as atherosclerosis, hypertension, diabetes mellitus, lower urinary tract symptoms and erectile dysfunction (ED), were regarded as distinct diagnostic/therapeutic entities but there is a growing awareness that these entities are not disparate and, to improve the health of the ageing male, require an integral approach. There is an inter-dependence between the metabolic syndrome, ED and patterns of testosterone in ageing men. The main features of the metabolic syndrome are abdominal obesity, insulin resistance, hypertension and dyslipidaemia, significant factors in the aetiology of erectile function. The metabolic syndrome is associated with lower-than-normal testosterone levels. A new concept of the role of testosterone in male physiology suggests that testosterone plays also a significant role in the development and maintenance of bone and muscle mass and is a determinant of glucose homeostasis and lipid metabolism. Testosterone is not only a factor in libido but exerts also essential effects on the anatomical and physiological substrate of penile erection. With these recent insights, the health problems of elderly men must be placed in a context that allows an integral approach. Treatment of testosterone deficiency is to become part and parcel of this approach.     

Prevalence of erectile dysfunction in patients with metabolic syndrome

AIM: We wished to investigate the relationship between metabolic syndrome and erectile dysfunction (ED). MATERIALS AND METHODS: A total of 268 patients were included in this study. All of the patients were asked to fill in an International Index for Erectile Function (IIEF) questionnaire. The presence of metabolic syndrome was determined when any three or more of the five risk factors were present according to the National Cholesterol Education Program (NCEP) Adult Treatment Panel (ATP)-III. The relationship between risk factor for metabolic syndrome and ED status was determined according to logistic regression analysis. RESULTS: Eighty-nine patients (33%) constituted the metabolic syndrome group. IIEF-EF domain scores of patients with and without metabolic syndrome were 17.7 +/- 7.9 and 21.7 +/- 7.5, respectively (P < 0.001). Seventy-four percent of patients with metabolic syndrome and 50% of patients without metabolic syndrome had ED (P < 0.001; odds ratio 2.9; 95% CI 1.7-5.0). Erectile function domain scores significantly decreased as the number of metabolic risk factors increased (P < 0.001). Patients with the risk factor of fasting blood glucose (FBG), waist circumference (WC), or hypertension (HT) had lower erectile function domain scores than the patients with other metabolic risk factors. Logistic regression analysis revealed that FBG and WC were the most important criteria for ED. CONCLUSIONS: Metabolic syndrome seems to be a potential risk factor for ED. We recommend patients with metabolic syndrome should be questioned about ED, and WC measurement might take part in the evaluation of ED.     

Severity of erectile dysfunction in married impotent patients: Interrelationship with anthropometry, hormones, metabolic profiles and lifestyle

OBJECTIVE: This study was designed to evaluate the effects of risk factors for erectile dysfunction (ED) or cardiovascular disease on the disease severity in impotent men. METHODS: A total of 87 men, 25-75 years old (mean age, 53.4) were included in the study. Patients were evaluated with anthropometry, hormones, metabolic profiles and lifestyle. Baseline erectile function (EF) was evaluated using the International Index of Erectile Function (IIEF). The severity of ED was classified into the following four grades based on the six-item EF domain of the IIEF: severe (6-10); moderate (11-16); mild to moderate (17-21); and mild (22-25). Patients were deemed to have metabolic syndrome (MS) if they had three or more of five criteria according to National Cholesterol Education Program, with some modification. RESULTS: Of 87 patients, 15 patients (17.2%) had mild, 11 (12.6%) had mild to moderate, 33 (37.9%) had moderate and 28 (32.3%) had severe ED. There was no correlation between scores of IIEF or EF domain and continuous parameters. On the multivariate model used, hypertensive patients had 26-fold higher risk (odds ratio, 26.195; 95% confidence interval, 1.463-46.072; P = 0.027) of severe ED than those without hypertension. Other factors were not significant. CONCLUSION: The results of the study indicate that MS might not influence the severity of ED in impotent men. However, our findings suggest that hypertension plays a role in the disease severity in these patients.     

Clinical and metabolic evaluation of subjects with erectile dysfunction: a review with a proposal flowchart

Erectile function is a haemodynamic phenomenon depending on the integrity of neurological, vascular, endocrinological, tissue (corpora cavernosa), psychological and relational factors; changes in any one of these components may lead to erectile dysfunction (ED). ED and its comorbid conditions share common risk factors such as endothelial dysfunction, atherosclerosis and metabolic and hormonal abnormalities. Furthermore, although cross-sectional studies have shown a clear age-dependent association between ED, diabetes mellitus, hypertension, metabolic syndrome (MetS) and cardiovascular diseases, longitudinal evidence has recently emphasized that ED could be an early marker of these conditions. Recently, the European Association of Urology and American Urology Association provided consensus guidelines for the management of ED patients. However, the metabolic aspect of ED is rather neglected or not sufficiently treated. In this study, more emphasis will be placed on the presence of ED comorbid metabolic factors. The primary and secondary goals of therapy, according to current guidelines and to prevent their clinical evolution, will also be provided. We review the concepts of metabolic diseases related to ED and their treatment. Criteria for the diagnosis and treatment of hypogonadism, metabolic and vascular disease related to ED were analysed. ED can mark the starting point for the evaluation and prevention of significant severe diseases (such as diabetes, MetS, dyslipidaemia, arteriosclerosis, hypertension, ischaemic cardiopathy, neuropathy, etc.) hitherto unknown by the patients. Most widely used criteria for the diagnosis and treatment of these diseases were reported. We suggest a clinical approach which allows the identification of metabolic and others systemic pathologies contributing to the development of ED. This approach may constitute an improvement in disease prognosis and either induce a spontaneous reduction of ED or facilitate its specific therapy.     

Hypogonadism, ED, metabolic syndrome and obesity: a pathological link supporting cardiovascular diseases

Hypogonadism, erectile dysfunction (ED), visceral adiposity, insulin resistance and metabolic syndrome (MetS) often coexist in the same subjects. This cluster of abnormalities is associated with an increased risk of diabetes and cardiovascular diseases (CVD), affecting not only quality of life but also life expectancy. Longitudinal studies have also demonstrated that ED and male hypogonadism could be considered surrogate markers of incident CVD and MetS. However, how androgens signal fat depots and lessen them is still a matter of active research and whether or not low testosterone could play a pathogenetic role in CVD is still under debate. Hence, pathogenetic mechanisms linking hypogonadism with obesity and insulin resistance appear to be complex and often multi-directional. Visceral obesity can probably be considered a relevant cause of hypogonadism but at the same time, hypogonadism could be a cause of obesity and insulin resistance, consequently establishing a vicious cycle. To provide a critical analysis of these issues, a comprehensive literary search was carried out to discuss the relationship between insulin resistance ED, visceral adiposity, MetS and hypogonadism focusing on their possible involvement in the development of CVD.     

Cardiovascular diseases and erectile dysfunction: the two faces of the coin of androgen deficiency

Traditionally, clinical conditions synonymous with the ageing male included cardiovascular disease (CVD), type 2 diabetes mellitus (DM) and sexual dysfunction, and were widely regarded as independent clinical entities. Over the last decade, interrelationship of clinical conditions has been convincingly demonstrated. Declining testosterone levels in the elderly, once regarded as an academic endocrinological question, appear to be central to the listed pathologies. It is now clear that erectile dysfunction is an expression of endothelial dysfunction. Testosterone deficiency is associated with an increased incidence of CVD and DM. The latter is often the sequel of the metabolic syndrome. Visceral obesity, a pivotal characteristic of the metabolic syndrome, suppresses the hypothalamic-pituitary-testicular axis leading to diminished testosterone production. Conversely, substantial androgen deficiency leads to signs and symptoms of metabolic syndrome. It is erroneous not to include testosterone measurements in the progress of the CVD, DM and erectile dysfunction. These conditions correlate strongly with testosterone deficiency.     

Lack of sexual activity from erectile dysfunction is associated with a reversible reduction in serum testosterone

The role of androgenic hormones in human sexuality, in the mechanism of erection and in the pathogenesis of impotence is under debate. While the use of testosterone is common in the clinical therapy of male erectile dysfunction, hypogonadism is a rare cause of impotence. We evaluated serum testosterone levels in men with erectile dysfunction resulting either from organic or non-organic causes before and after non-hormonal impotence therapy. Eighty-three consecutive cases of impotence (70% organic, 30% non-organic, vascular aetiology being the most frequent) were subjected to hormonal screening before and after various psychological, medical (prostaglandin E1, yohimbine) or mechanical therapies (vascular surgery, penile prostheses, vacuum devices). Thirty age-matched healthy men served as a control group. Compared to controls, patients with impotence resulting from both organic and non-organic causes showed reduced serum levels of both total testosterone (11.1 +/- 2.4 vs. 17.7 +/- 5.5 nmol/L) and free testosterone (56.2 +/- 22.9 vs. 79.4 +/- 27.0 pmol/L) (both p < 0.001). Irrespective of the different aetiologies and of the various impotence therapies, a dramatic increase in serum total and free testosterone levels (15.6 +/- 4.2 nmol/L and 73.8 +/- 22.5 pmol/L, respectively) was observed in patients who achieved normal sexual activity 3 months after commencing therapy (p < 0.001). On the contrary, serum testosterone levels did not change in patients in whom therapies were ineffective. Since the pre-therapy low testosterone levels were independent of the aetiology of impotence, we hypothesize that this hormonal pattern is related to the loss of sexual activity, as demonstrated by its normalization with the resumption of coital activity after different therapies. The corollary is that sexual activity may feed itself throughout the increase in testosterone levels.     

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.     

Impact of the association between elevated oestradiol and low testosterone levels on erectile dysfunction severity

Our aim was to assess the impact of the association between elevated oestradiol (E₂) and low testosterone (T) levels on erectile dysfunction (ED) severity. A total of 614 male patients with ED and a normal or low T level in association with normal or elevated E₂ levels were enrolled. Patients underwent routine laboratory investigations in addition to measurements of total T, total E₂, follicle-stimulating hormone (FSH), luteinizing hormone (LH) and prolactin. We compared the responses to the erectile function domain, Q3 (achieving erection) and Q4 (maintaining erection) of the International Index for Erectile Function (IIEF) score in patients with the following: normal T and E₂ levels; low T level; low T level and elevated E₂ level; and elevated E₂ level. Of the patients included, 449 (73.1%) had normal T and E₂ levels, 110 (17.9%) had a low T level, 36 (5.9%) had a low T level and an elevated E₂ level, and 19 (3.1%) had an elevated E₂ level. Increased ED severity was significantly associated with low T levels, elevated E₂ levels, and both a low T level and an elevated E₂ level. Additionally, the mean values of the EF-domain, Q3 and Q4 were significantly lower in patients with both a low T level and an elevated E₂ level compared to patients with any condition alone. In conclusion, a low T level had the primary effect on erectile function; however, a concomitantly elevated E₂ level had an additive impairment effect.     

Hypogonadism and metabolic syndrome: implications for testosterone therapy

PURPOSE: Metabolic syndrome, characterized by central obesity, insulin resistance, dyslipidemia and hypertension, is highly prevalent in the United States. When left untreated, it significantly increases the risk of diabetes mellitus and cardiovascular disease. It has been suggested that hypogonadism may be an additional component of metabolic syndrome. This has potential implications for the treatment of metabolic syndrome with testosterone. We reviewed the available literature on metabolic syndrome and hypogonadism with a particular focus on testosterone therapy. MATERIALS AND METHODS: A comprehensive MEDLINE review of the world literature from 1988 to 2004 on hypogonadism, testosterone and metabolic syndrome was performed. RESULTS: Observational data suggest that metabolic syndrome is strongly associated with hypogonadism in men. Multiple interventional studies have shown that exogenous testosterone has a favorable impact on body mass, insulin secretion and sensitivity, lipid profile and blood pressure, which are the parameters most often disturbed in metabolic syndrome. CONCLUSIONS: Hypogonadism is likely a fundamental component of metabolic syndrome. Testosterone therapy may not only treat hypogonadism, but may also have tremendous potential to slow or halt the progression from metabolic syndrome to overt diabetes or cardiovascular disease via beneficial effects on insulin regulation, lipid profile and blood pressure. Furthermore, the use of testosterone to treat metabolic syndrome may also lead to the prevention of urological complications commonly associated with these chronic disease states, such as neurogenic bladder and erectile dysfunction. Physicians must be mindful to evaluate hypogonadism in all men diagnosed with metabolic syndrome as well as metabolic syndrome in all men diagnosed with hypogonadism. Future research in the form of randomized clinical trials should focus on further defining the role of testosterone for metabolic syndrome.     

Randomized study of testosterone gel as adjunctive therapy to sildenafil in hypogonadal men with erectile dysfunction who do not respond to sildenafil alone

PURPOSE: We compare the efficacy of testosterone gel (T-gel) versus placebo as adjunctive therapy to sildenafil in hypogonadal men with erectile dysfunction who do not respond to sildenafil alone. MATERIALS AND METHODS: A randomized, placebo controlled, double-blind, parallel group, multicenter study was performed. A total of 75 hypogonadal men (18 to 80 years old, morning serum total testosterone 400 ng/dl or less) with confirmed lack of response to sildenafil monotherapy were randomized (1:1) to receive a daily dose of 1% T-gel or 5 gm placebo gel as adjunctive therapy to 100 mg sildenafil during a 12-week period. Subjects were evaluated for sexual function, primarily based on the International Index of Erectile Function (IIEF), quality of life and serum testosterone levels at baseline and weeks 4, 8 and 12. RESULTS: Testosterone treated subjects had greater improvement in erectile function compared to those who received placebo, reaching statistical significance at week 4 (4.4 vs 2.1, p = 0.029, 95.1% CI 0.3, 4.7). Similar trends were observed for improvements in orgasmic function, overall satisfaction, total IIEF score and percentage of IIEF responders. T-gel significantly (p < or =0.004) increased total and free testosterone levels throughout the study, although no significant correlations were made between testosterone levels and the IIEF at end point. CONCLUSIONS: T-gel taken with sildenafil may be beneficial in improving erectile function in hypogonadal men with erectile dysfunction who are unresponsive to sildenafil alone.     

Serum testosterone levels in diabetic men with and without erectile dysfunction

Diabetes mellitus is a common chronic disease, affecting 0.5–2% worldwide. The Massachusetts Male Aging Study reported that up to 75% of men with diabetes have a lifetime risk of developing ED. Type 2 diabetes is associated with low total serum testosterone (TT) identified in several cross‐sectional studies and systemic analyses. There is a lack of consensus regarding what constitutes the lowest level of testosterone within the boundaries of normality. In this retrospective study, we sought to evaluate the effect of associated co‐morbidities on serum total testosterone (TT) level in men with type 2 diabetes DM, either with or without erectile dysfunction (ED). Three hundred and ninety‐one patients were evaluated for erectile function using an abridged, five‐item version of the International Index of Erectile Function‐5. Measurements of TT, fasting lipid profile, blood sugar and glycated haemoglobin (HbA1c) were conducted. Penile hemodynamics was assessed using intracavernosal injection and penile duplex study. Hypogonadism was found in 126 cases (33.2%), and normal TT was observed in 254 (66.8%). ED was detected in 119 cases in the hypogonadal group (94.4%) as compared to 155/254 (61.0%) in eugonadal group, P = 0.0001. TT was lower in diabetic men with ED as compared to those with normal erectile function (EF), 392.4 ± 314.9 versus 524.3 ± 140.2 ng dl^?1, respectively, P < 0.0001. After exclusion of patients with hypertension and dyslipidaemia, 185 men were evaluated, and there was no difference in the mean TT level among men with ED 490.6 ± 498.2 ng dl^?1 versus normal EF 540.6 ± 133.4 ng dl^?1 although, HbA1c remained lower in men with normal erectile function. Receiver operating characteristic (ROC) curve of TT in men without associated co‐morbidities showed that EF was compromised at TT = 403.5 ng dl^?1 or less. Sensitivity of 63.3% and a specificity of 94.0% were detected. At this level, ED was found in 33/38 (86.8%) men with TT 403.5 ng dl^?1, whereas ED was observed in 57/147 (38.8%) men with TT ≥ 403.5 ng dl^?1 (P < 0.0001). We propose a cut‐off value of 403.5 ng dl^?1 of TT blood levels as an indicator for initiation of testosterone replacement therapy in diabetic men with ED. Further prospective controlled trials are recommended.     

Determination of serum testosterone in experimental diabetes with erectile dysfunction

To study the mechanisms of erectile dysfunction (ED) in ex-perimental diabetic (DM) rats, streptozotocin (STZ) was injectedintraperitoneally into Sprague-Dewley rats to make experimentalmodels of DM. Rats showing apparent ED after apomorphine injec-tion were selected for the experiment. Penile erections were studiedon the 6th, 8th and 12th week after injection of apomorphine. Theconcentration of LH, FSH and testosterone (T) were examined andmicrostructure of testes were observed. Results indicated that theserum T was decreased significantly with marked changes in testicu-lar histology; the degree of both was closely related to the durationof DM. The concentration of LH did not change on the early days,but decreased significantly later in the course. FSH concentrationswere not changed. As conclusions, penile erection and synthesis oftestosterone are affected seriously by DM, and the decrease of Tconcentration may be one of the most important mechanisms.(Chin J Androl 2000; 4: 227 - 230)     

Effects of taking tadalafil 5 mg once daily on erectile function and total testosterone levels in patients with metabolic syndrome

We aimed to evaluate the efficacy of tadalafil 5 mg once‐daily treatment on testosterone levels in patients with erectile dysfunction (ED) accompanied by the metabolic syndrome. A total of 40 men with metabolic syndrome were evaluated for ED in this study. All the patients received 5 mg tadalafil once a day for 3 months. Erectile function was assessed using the five‐item version of the International Index of Erectile Function (IIEF) questionnaire. Serum testosterone, follicle‐stimulating hormone and luteinising hormone levels were also evaluated, and blood samples were taken between 08.00 and 10.00 in the fasting state. All participants have three or more criteria of metabolic syndrome. At the end of 3 months, mean testosterone values and IIEF scores showed an improvement from baseline values (from 3.6 ± 0.5 to 5.2 ± 0.3, from 11.3 ± 1.9 to 19 ± 0.8 respectively). After the treatment, serum LH levels were decreased (from 5.6 ± 0.6 to 4.6 ± 0.5). There was significantly difference in terms of baseline testosterone and luteinising hormone values and IIEF scores (p < .05). Based on our findings, we recommend tadalafil 5 mg once daily in those men with erectile dysfunction especially low testosterone levels accompanied by metabolic syndrome.     

Effects of testosterone replacement therapy on metabolic syndrome among Japanese hypogonadal men: A subanalysis of a prospective randomised controlled trial (EARTH study)

We investigated the effects of testosterone replacement therapy (TRT) on metabolic factors among hypogonadal men with a metabolic syndrome. From the study population of the EARTH study, which was a randomised controlled study in Japan, 65 hypogonadal patients with a metabolic syndrome, comprising the TRT group (n = 32) and controls (n = 33), were included in this study analysis. The TRT group was administered 250 mg of testosterone enanthate as an intramuscular injection every 4 weeks for 12 months. Waist circumference, body mass index, body fat volume and blood pressure were measured in all patients at baseline and at 12 months. In addition, blood biochemical data, including total cholesterol, triglyceride (TG), HDL cholesterol, fasting plasma glucose (FPG) and haemoglobin A1c (HbA1c) levels, were also evaluated. Changes in these categories from baseline to 12 months were compared between the TRT and control groups, with significant differences observed in waist circumference, body fat percentage, FPG, TG and HbA1c levels. No significant differences were observed in other parameters. TRT for 1 year was associated with improvements in some metabolic factors among Japanese men with hypogonadism and metabolic syndrome.     

Endothelial dysfunction and erectile dysfunction in the aging man

Penile erection is a vascular event that requires an intact endothelium to occur. A dysfunctional endothelium is an early marker for the development of atherosclerotic changes and can also contribute to the occurrence of acute cardiovascular events. The pathogenesis of both endothelial and erectile dysfunction (ED) is intimately linked through decreased expression and activation of endothelial nitric oxide (NO) synthase, and the subsequent blunted physiological actions of NO naturally occurring with aging. It is now well-understood that ED is a symptom of underlying disease rather than a disease itself; for this reason in the near future both general practitioners, internal medicine practitioners and many specialists will have to interplay with sexual medicine. Aging in the man is also associated with several changes in arterial structure and function, part of them related to the decline of circulating levels of steroids, that is, testosterone and estradiol. These changes may be responsible, in part, for the lack of efficacy of ED treatments. The recent discovery that chronic administration of phosphodiesterase type 5 inhibitors may improve erectile and endothelial responsiveness of men previously non-responsive to on-demand regimes, and the knowledge that testosterone is one of the main modulators of the expression of penile phosphodiesterase type 5 isoenzyme, opens a new scenario in the treatment of men with ED and co-morbidities. The aim of this review is to discuss the pathophysiology of endothelial dysfunction and its relationship with ED in the aging male, and to suggest possible strategies to improve arterial function with regard to sexual dysfunctions.     

Testosterone and erectile function in hypogonadal men unresponsive to tadalafil: results from an open-label uncontrolled study

The study was aimed at investigating the efficacy of tadalafil (Cialis) in combination with transdermal testosterone (Testogel) for the treatment of tadalafil-refractory erectile dysfunction in hypogonadal patients. In an open-label, retrospective trial, 69 hypogonadal nonresponders to tadalafil monotherapy (mean age: 59 years, total testosterone < or =3.4 ng ml(-1)) were randomly divided into two homogeneous groups. Group I (n = 35) received Testogel (5 g containing 50 mg testosterone, daily) for 4 weeks, followed by concurrent therapy with tadalafil (20 mg, twice a week). Group II (n = 34) was assigned to treatment with Testogel (5 g containing 50 mg testosterone, daily) for a duration of 10 weeks before adjunctive therapy with tadalafil was initiated. Total testosterone levels were measured at baseline, week 4 and week 10. Sexual function was assessed employing the International Index of Erectile Function (IIEF). As an additional measure of efficacy, a questionnaire completed by the patients' partner was used. Mean testosterone levels were observed to increase from baseline to study end. Following 4 weeks of therapy, an improvement in Erectile Function (EF) from baseline was observed, which was greater in group I than in group II. The assessment after week 10 showed that EF had further increased and was quite similar now in both groups. Partners found that erectile capacity had greatly improved from baseline to study end. No adverse effects have been observed. These data suggest that combination therapy with testosterone and tadalafil is an effective means in a subset of hypogonadal patients who did not respond to tadalafil alone. We assume that testosterone-induced remodelling of penile tissue structure is one underlying reason for the observed improvement of erectile function. The results imply that this process may require a longer period of testosterone administration than 4 weeks.     

Testosterone deficiency and risk factors in the metabolic syndrome: implications for erectile dysfunction

The most common cause of erectile dysfunction (ED) is penile vascular insufficiency. This is usually part of a generalized endothelial dysfunction and is related to several conditions, including type 2 diabetes mellitus, hypertension, hyperlipidemia, and obesity. These conditions underlie the pathophysiology of metabolic syndrome (MetS). Hypogonadism, or testosterone deficiency (TD), is an integral component of the pathology underlying endothelial dysfunction and MetS, with insulin resistance (IR) at its core. Testosterone replacement therapy for TD has been shown to ameliorate some of the components of the MetS, improve IR, and may serve as treatment for decreasing cardiovascular and ED risk.     

Pathogenetic aspects of erectile dysfunction in patients with the metabolic syndrome

BackgroundAlthough it is well known that the metabolic syndrome is a common cause of erectile dysfunction (ED) the pathogenesis of the latter in this group of patients is poorly understood. The present study aimed to improve our knowledge in this area.MethodsThe study included 385 men with ED (control group) who underwent a full evaluation, including laboratory and ultrasound assessment of endothelial function.ResultsThe full complex evaluation showed that arteriogenic impairment in the cavernosal circulation was the primary pathogenic factor for ED in patients with the metabolic syndrome. The ultrasound-assisted measurement of postocclusive changes in the diameter of the cavernosal arteries, which reflects the local endothelial function, was the most valuable method in the diagnosis of this form of ED. In addition, a considerable number of patients with the metabolic syndrome demonstrated both hormonal and neurological disorders which also contribute to the pathogenesis of ED in this cohort of men.ConclusionThe pathogenesis of ED in patients with the metabolic syndrome is multifactorial in nature: ED is primarily caused by arteriogenic disorders which are combined with neuropathic disorders in almost every second patient and with hormonal factors in every third one. In addition, psychomotor status has an impact on the development of ED in patients with metabolic syndrome.     

Testosterone therapy has positive effects on anthropometric measures,metabolic syndrome components (obesity,lipid profile,Diabetes Mellitus control), blood indices,liver enzymes,and prostate health indicators in elderly hypogonadal men

To alleviate late‐onset hypogonadism, testosterone treatment is offered to suitable patients. Although testosterone treatment is commonly given to late‐onset hypogonadism patients, there remains uncertainty about the metabolic effects during follow‐ups. We assessed the associations between testosterone treatment and wide range of characteristics that included hormonal, anthropometric, biochemical features. Patients received intramuscular 1,000 mg testosterone undecanoate for 1 year. Patient anthropometric measurements were undertaken at baseline and at each visit, and blood samples were drawn at each visit, prior to the next testosterone undecanoate. Eighty‐eight patients (51.1 ± 13.0 years) completed the follow‐up period. Testosterone treatment was associated with significant increase in serum testosterone levels and significant stepladder decrease in body mass index, total cholesterol, triglycerides and glycated haemoglobin from baseline values among all patients. There was no significant increase in liver enzymes. There was an increase in haemoglobin and haematocrit, as well as in prostate‐specific antigen and prostate volume, but no prostate biopsy intervention was needed for study patients during 1‐year testosterone treatment follow‐up. Testosterone treatment with long‐acting testosterone undecanoate improved the constituents of metabolic syndrome and improved glycated haemoglobin in a stepladder fashion, with no adverse effects.