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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Male hypogonadism has a multifactorial etiology that includes genetic conditions, anatomic abnormalities, infection, tumor, and injury. Defects in the hypothalamic-pituitary-gonadal axis may also result from type II diabetes mellitus and treatment with a range of medications. Circulating testosterone levels have been associated with sexual function, cognitive function, and body composition. Apart from reduced levels of testosterone, clinical hallmarks of hypogonadism include absence or regression of secondary sex characteristics, reduced fertility (oligospermia, azoospermia), anemia, muscle wasting, reduced bone mass (and bone mineral density), and/or abdominal adiposity. Some patients, particularly those with partial androgen deficiency of the aging male, also experience sexual dysfunction, reduced sense of vitality, depressed mood, increased irritability, difficulty concentrating, and/or hot flushes in certain cases of acute onset. As many patients with male hypogonadism-like patients with erectile dysfunction-do not seek medical attention, it is important for clinicians to be acquainted with the signs and symptoms of hypogonadism, and to conduct appropriate laboratory testing and other assessments to determine the causes and inform the treatment of this condition.
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PMID:Male hypogonadism. Part II: etiology, pathophysiology, and diagnosis. 1609 14

We evaluated the prevalence and risk factors for erectile dysfunction (ED) and interest in ED treatment among Japanese men being treated for type 2 diabetes mellitus. Patients (40-79 years; n=1118) completed the 5-item version of the International Index of Erectile Function (IIEF-5), and questions related to interest in ED pharmacotherapy, subjective symptoms of diabetes, and general quality of life. A separate survey completed by physicians examined the relationships between age, diabetic treatments (insulin or oral), symptoms of diabetes (poor glycemic control, microangiopathy), complications of diabetes (hypertension, ischemic heart disease, cerebrovascular disease), and ED. The prevalence of ED in patients with diabetes was 90%, a rate double that of non-diabetic individuals. Multivariate analyses revealed that age, insulin therapy, microangiopathy, hypertension, history of cerebrovascular or cardiovascular disease, leg dysesthesia, dysuria, insomnia, and anorexia all represented significant risk factors for ED. Half of all respondents were interested (29%) or would consider pharmacotherapy for ED (21%). These findings suggest that ED is a significant problem in Japanese men with diabetes, and that specific risk factors increase the prevalence of ED. Furthermore, the survey results expose national attitudes toward treatment of ED.
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PMID:Prevalence and risk factors for erectile dysfunction in Japanese diabetics. 1612 26

Erectile dysfunction (ED) shares the same vascular risk factors (VRFs) with coronary arteries disease (CAD). A reduced biological activity of endothelium-derived nitric oxide links human atherosclerosis to ED and underscores the role of an altered endothelium in the pathogenesis of both conditions. ED is associated to a systemic endothelial cell activation/dysfunction independent from VRFs or from a diffuse vascular damage, indicating that ED is a marker of an early systemic endothelial damage, a relevant determinant of atherosclerosis. A diffuse vascular damage of carotid arteries indicative of pre-clinical atherosclerosis is significantly associated to an increased risk of severe ED in men with VRFs but without clinical atherosclerosis and ED was the most efficient predictor of angiographically verified silent CAD among different VRFs in uncomplicated type 2 diabetes. In conclusion, ED may be the only clinical correlate of a diffuse, unrecognized vascular damage that is associated to a documented future risk of acute vascular events. Searching ED might be of relevance in men with VRFs but no other clinical atherosclerosis to identify patients that should aggressively reduce their VRFs while treating ED.
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PMID:Vascular aetiology of erectile dysfunction. 1623 62

The past decade has witnessed a dramatic increase in the prevalence of obesity. Comorbidities of obesity include type 2 diabetes mellitus, hypertension, and lipid abnormalities, all of which contribute to cardiovascular disease (CVD) and are associated with endothelial dysfunction. These abnormalities frequently cluster in individuals, and the term metabolic syndrome is now widely used to define this cluster. The syndrome is frequently (although not invariably) associated with insulin resistance and CVD. Diabetes is associated with CVD, which may be asymptomatic in some cases, particularly when associated with autonomic neuropathy. This has implications for guidelines on the evaluation of patients with erectile dysfunction (ED) and CVD. Treatment of ED in men with diabetes has been revolutionized by the introduction of phosphodiesterase 5 inhibitors. However, men with diabetes tend to respond less positively to these agents, at least as currently prescribed. This decreased responsiveness may be related to the severity of endothelial function in patients with diabetes. Additional therapeutic strategies may be needed to overcome this problem.
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PMID:Endothelial and erectile dysfunction, diabetes mellitus, and the metabolic syndrome: common pathways and treatments? 1638 60

Assessment of cavernosal perfusion in men with erectile dysfunction (ED) relies on Doppler spectrum analysis of pharmachologically stimulated peak systolic velocity (sPSV) in cavernous arteries but its accuracy in identifying men affected by a cavernosal perfusion disorder correlated with atherosclerosis remains undefined. We estimated by B-mode ultrasound, the accuracy of sPSV of cavernous arteries to identify ED with an expected cavernosal perfusion disorder. This was predicted by an elevated intima-media thickness (IMT) of common carotid arteries, a reference methodology to estimate the degree of generalized atherosclerosis, in men exposed to vascular risk factors (VRFs). sPSV and IMT were evaluated in 269 men with ED, 49 had no VRFs, 100 were overweight with/or without hyperlipidaemia, 120 were affected by type 2 diabetes and/or essential hypertension. sPSV was significantly lower (p<0.05) in patients with VRFs associated with atherosclerosis (IMT>or=1 mm) (n=39) than in men with no VRFs and no atherosclerosis (n=49). sPSV correlated negatively with age (p<0.0001), with serum% of glycated haemoglobin (p=0.010) and with carotid artery IMT (p=0.013). An sPSV<or=30 cm/sec, the cut-off value which showed at receiver operating characteristic curve analysis the combined highest value of sensitivity and specificity, correctly identified only 57% of men in whom a cavernosal perfusion disorder was expected based on the presence of carotid artery IMT>or=1 mm combined to the exposure to VRFs. The ultrasonographic evaluation of sPSV had a very limited accuracy in discriminating ED with an expected cavernosal perfusion disorder, based on the presence of a generalized atherosclerosis in men with VRFs.
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PMID:Penile duplex pharmaco-ultrasonography of cavernous arteries in men with erectile dysfunction and generalized atherosclerosis. 1720 82

Hypogonadism may play a significant role in the pathophysiology of erectile dysfunction (ED). A threshold level of testosterone may be necessary for normal erectile function. Testosterone replacement therapy is indicated in hypogonadal patients and is beneficial in patients with ED and hypogonadism. Monotherapy with testosterone for ED is of limited effectiveness and may be most promising in young patients with hypogonadism and without vascular risk factors for ED. A number of laboratory and human studies have shown the combination of testosterone and other ED treatments, such as phosphodiesterase type 5 (PDE5) inhibitors, to be beneficial in patients with ED and hypogonadism, who fail PDE5 inhibitor therapy alone. There is increasing evidence that combination therapy is effective in treating the symptoms of ED in patients for whom treatment failed with testosterone or PDE5 inhibitors alone. Testosterone replacement therapy has potentially evolved from a monotherapy for ED in cases of low testosterone, to a combination therapy with PDE5 inhibitors. Screening for hypogonadism may be useful in men with ED who fail prior PDE5 inhibitors, especially in populations at risk for hypogonadism such as type 2 diabetes and the metabolic syndrome.
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PMID:The evolving role of testosterone in the treatment of erectile dysfunction. 1693 38

Erectile dysfunction (ED) affects up to 70% of men with diabetes. However, the pathophysiology of ED in diabetes remains uncertain with both neuronal and vascular factors cited. We examined whether ED is an indicator of generalized endothelial dysfunction. A unique group of diabetic patients free from established conventional cardiac risk factors were investigated. Forearm bloodflow responses to nitroprusside and acetylcholine on 11 diabetic men with ED and 11 potent diabetic men were measured by venous plethysmography. Patient characteristics between the impotent and potent patients were similar except for Hba1c which was higher in the group with ED (8.35% vs. 7.03%: p = 0.003). Both groups showed increases in FBF to incremental infusions of nitroprusside and acetylcholine but the area under curve (AUC) were similar in the ED and the non-ED groups (p = 0.16 and p = 0.17, respectively). We demonstrated that ED in patients with type 2 diabetes is not associated with additional generalized endothelial dysfunction.
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PMID:Diabetic erectile dysfunction--an indicator of generalised endothelial function per se? 1698 60

Erectile dysfunction is a common complication of diabetes. Diabetes can cause neuropathy or damage to nerves throughout your body, including the penis. Damaged nerves can't communicate properly. So even though you might be emotionally stimulated to have intercourse, nerve damage means that information isn't relayed to the penis, and it doesn't respond. In addition, poor blood sugar control can inhibit nitric oxide production. Lack of nitric oxide can prevent the pressure of blood in the corpora cavernosa from rising enough to close off penile veins, allowing blood to flow out of the penis instead of remaining trapped for an erection. This prospective, randomized, double-blind, placebo-controlled study included 176 patients with type 2 diabetes. The daily 4 g dose of inositol plus 400 microg of folic acid or placebo was divided and given in three doses. The present study demonstrates that Myoinositol/folic acid combination, deserves consideration as therapeutic agent for preventing and treating erectile dysfunction in diabetic men, probably by virtue of both their chronic metabolic, acute ROS scavenging, and NO protective beneficial effects.
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PMID:Myoinositol/folic acid combination for the treatment of erectile dysfunction in type 2 diabetes men: a double-blind, randomized, placebo-controlled study. 1712 17

The cyclic nucleotide (cGMP) signalling pathway mediates the smooth-muscle relaxing effects of nitric oxide necessary for normal erectile function. Down-regulation of this pathway is the pathophysiological pivot of many forms of erectile dysfunction (ED) and leads to the development of some chronic diseases, such as hypertension and type 2 diabetes mellitus. Therefore, selective inhibition of the enzyme that catalyses the degradation of cGMP promotes erectile responses to sexual stimulation. Recently, a new phosphodiesterase type 5 (PDE-5) inhibitor tadalafil has emerged, which has a prolonged half-life. Here is a review of recent studies on the safety of tadalafil in the treatment of ED.
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PMID:[The safety of tadalafil in the treatment of erectile dysfunction]. 1791 20

Low testosterone levels in men are associated with type 2 diabetes mellitus. Erectile dysfunction (ED) is a frequent complication of type 2 diabetes. The aim of our cross-sectional study was to investigate the relationship between ED and total, bioavailable and free testosterone levels in 198 men with type 2 diabetes. In addition, we examined the associations of various cardiovascular risk factors involved in the development of ED in type 2 diabetic men. We found that bioavailable and free testosterone levels were significantly lower in men with ED (p = 0.006 and 0.027 respectively) than those without ED. Sex hormone-binding globulin levels were also reduced, but there was no significant difference in total testosterone (TT) levels between men with and without ED. The severity of ED as assessed by International Index of Erectile Function scores was significantly associated with TT (r = 0.32; p < 0.001), bioavailable testosterone (r = 0.32; p < 0.001) and calculated free testosterone (r = 0.35; p < 0.001) levels. ED was more frequently observed in men with hypertension and a higher waist circumference (p = 0.03). There was also a higher prevalence of ED among smokers (p = 0.06), but there were no significant associations between ED and alcohol consumption or with BMI > 30. This study has shown that ED is associated with low bioavailable and free testosterone levels, age, visceral adiposity and hypertension in type 2 diabetic men.
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PMID:Erectile dysfunction is associated with low bioactive testosterone levels and visceral adiposity in men with type 2 diabetes. 1802 99


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