The aim of the present study was to examine the effect of new phosphodiesterase type 5 inhibitor vardenafil on endothelial function of cavernous and brachial arteries in healthy men and in patients with different forms of erectile dysfunction (ED). This prospective, double-blind, placebocontrolled study was performed on 135 men with ED and 30 healthy controls. Complex evaluation was performed in all patients with ED. All participants also underwent our modification of ultrasound (US) assessment of postocclusive changes in the diameter of cavernosal arteries and endothelium-dependent flow-mediated dilation (FMD) of the brachial artery before and 1 h after administration of 20 mg of vardenafil or placebo. After study drug administration, PICAD and FMD significantly increased in patients receiving vardenafil (Po0.001) but not in patients receiving placebo. Increase in PICAD values was significantly greater in patients with arteriogenic ED compared with patients with organic nonarterial ED (P ¼ 0.007), psychogenic ED (Po0.001) and controls (P ¼ 0.001). The most prominent increase in brachial artery FMD values were found in patients with arteriogenic ED, although statistically significant differences were present only between patients with arteriogenic ED and control group (P ¼ 0.035). We have found a moderate negative correlation between initial PICAD and its increase after vardenafil and between pretreatment flow-mediated vasodilation of brachial arteries and its increase after vardenafil administration (r ¼ À0.57 and À0.55, respectively). These findings suggest that the use of vardenafil restores impaired endothelial function of cavernous and brachial arteries.

Introduction There is considerable clinical and scientific evidence that endothelial dysfunction may be an important clinical link connecting erectile dysfunction (ED) with cardiovascular diseases. Aims To modify the method of assessment of endothelial function of cavernosal arteries, to develop a new algorithm for evaluating its results, and to investigate the relationship between postocclusive changes in the diameter of brachial and cavernous arteries. Methods The study participants were 212 patients presenting to our department complaining of ED and 40 healthy volunteers without sexual problems, which formed the control group. All patients with ED underwent complex evaluation and ultrasound assessment of postocclusive changes in the diameter of cavernosal arteries modified by us and standard ultrasound assessment of endothelium-dependent flow-mediated dilation of the brachial artery. Main Outcome Measures As the main outcome measure, the percent of increase of the cavernosal arteries diameter (PICAD) was recorded. Results In the patients with arteriogenic ED, PICAD values were significantly less than in other groups (P < 0.001 for pairs of comparison). At the same time there were no differences between the control group and groups of patients with psychogenic and organic nonarterial ED. The sensitivity and specificity of a PICAD value of 50% in diagnosis of arteriogenic ED were 100% and 98.2%, respectively. In all groups and in the entire sample of patients studied we did not find a correlation between PICAD and postocclusive changes in the diameter of brachial arteries. Conclusion The method of ultrasound assessment of postocclusive changes in the diameter of cavernosal arteries is reliable and a highly informative tool for diagnosis of arteriogenic ED. It cannot be substituted by techni-cally simpler method of ultrasound examination of brachial arteries, while results of the latter could help to define the necessity of performing an examination of cavernous arteries.

This study was designed to investigate whether angiotensin-converting enzyme (ACE) insertion/ deletion (I/D) polymorphism is associated with erectile dysfunction (ED) in Russian men with metabolic syndrome (MS). A total of 331 men with MS were studied. All patients underwent complex evaluation including the International Index of Erectile Function (IIEF) questionnaire. The ACE I/D polymorphism was determined by polymerase chain reaction. Overall, 182 men (55.0%) had ED according to the IIEF erectile function domain score. In the ED group, the prevalence of DD genotype was found to be significantly higher compared to the non-ED group (Po0.001). In both groups, patients with DD genotype were significantly younger than patients with other genotypes (Po0.001). In addition, in the ED group, the disease affected patients with DD genotype at a significantly younger age (Po0.001). Obtained results give evidence to support the finding that the D allele is a risk factor for the micro-and macrovascular diseases.

OBJECTIVE To investigate whether the results of the ultrasonographic (US) measurement of post‐occlusive changes in the diameters of cavernosal arteries after administering phosphodiesterase type 5 (PDE‐5) inhibitor vardenafil could be associated with the response to vardenafil in patients with erectile dysfunction (ED), as currently there are no reliable methods for predicting the success rate of oral PDE‐5 inhibitors. PATIENTS AND METHODS The study included 122 men with ED; after a complex evaluation, the endothelial function of the cavernosal arteries was assessed in all patients before and 1 h after oral ingestion of vardenafil (20 mg), using our modification of the US assessment of post‐occlusive changes in the diameter of cavernosal arteries. After the evaluation, all patients received vardenafil 20 mg on demand for 4 weeks. A successful response was defined using two endpoints, i.e. the normalization of the International Index of Erectile Function Erectile Function domain score (≥26) and positive answers to both Sexual Encounter Profile questions 2 and 3 on ≥ 75% of occasions, based on the diary data collected. RESULTS In all patients the mean (sd) initial percentage increase in the cavernosal artery diameter (PICAD) in responders and nonresponders was not statistically different, at 49 (24) and 43 (26), respectively (P = 0.168), but PICAD values after vardenafil were significantly greater in responders, at 73 (16) vs 55 (23) (P < 0.001). Analysis of data from patients with different causes of ED showed statistically significant differences in PICAD between responders and nonresponders only in those with arteriogenic ED. The sensitivity and specificity of a PICAD of ≥ 50% after taking vardenafil 20 mg for predicting a positive response to the same dose of the drug in patients with arteriogenic ED were 94.9% and 91.3%, respectively. CONCLUSION The results of the US assessment of post‐occlusive changes in the diameter of cavernosal arteries after vardenafil administration are significantly associated with the clinical efficacy of the drug in patients with arteriogenic ED.

Introduction. There is considerable clinical and scientific evidence that endothelial dysfunction may be an important clinical link connecting erectile dysfunction (ED) with cardiovascular diseases. Aims. To modify the method of assessment of endothelial function of cavernosal arteries, to develop a new algorithm for evaluating its results, and to investigate the relationship between postocclusive changes in the diameter of brachial and cavernous arteries. Methods. The study participants were 212 patients presenting to our department complaining of ED and 40 healthy volunteers without sexual problems, which formed the control group. All patients with ED underwent complex evaluation and ultrasound assessment of postocclusive changes in the diameter of cavernosal arteries modified by us and standard ultrasound assessment of endothelium-dependent flow-mediated dilation of the brachial artery. Main Outcome Measures. As the main outcome measure, the percent of increase of the cavernosal arteries diameter (PICAD) was recorded. Results. In the patients with arteriogenic ED, PICAD values were significantly less than in other groups (P < 0.001 for pairs of comparison). At the same time there were no differences between the control group and groups of patients with psychogenic and organic nonarterial ED. The sensitivity and specificity of a PICAD value of 50% in diagnosis of arteriogenic ED were 100% and 98.2%, respectively. In all groups and in the entire sample of patients studied we did not find a correlation between PICAD and postocclusive changes in the diameter of brachial arteries. Conclusion. The method of ultrasound assessment of postocclusive changes in the diameter of cavernosal arteries is reliable and a highly informative tool for diagnosis of arteriogenic ED. It cannot be substituted by technically simpler method of ultrasound examination of brachial arteries, while results of the latter could help to define the necessity of performing an examination of cavernous arteries. Mazo E, Gamidov S, Anranovich S, and Iremashvili V. Testing endothelial function of brachial and cavernous arteries in patients with erectile dysfunction. J Sex Med 2006;3:323-330.

1.25-dihydroxy-vitamin D3 (1.25 (OH)2D3) was tested in seven patients with myelodysplastic syndrome. The study was undertaken because 1.25 (OH)2D3 promotes differentiating myeloid cells in vitro and because of a prior report of potential benefit in a clinical study. The drug was given orally at a dose of 2.5 micrograms/day for a minimum of 8 weeks (range 8-28). After therapy, there were no significant changes in any of the parameters observed in peripheral blood or bone marrow. We did not observe any feature of granulocytic-monocytic differentiation. Treatment was well tolerated. One patient died because of bone marrow failure. Survivors have persisting myelodysplastic syndrome and continue to be transfusion dependent. 1.25 (OH)2D3 has no beneficial effect in patients with myelodysplastic syndrome with this dose regimen.

In a recent annotation published in this journal, McCarthy (1 98.5) reviewed the causes and underlying mechanism of the deposition of collagen in bone marrow and discussed the possibility of using 1,25(OH)2 vit D3 to control such deposition and its ability to reverse myelofibrosis. He had published this suggested form of treatment previously (McCarthy ef al, 1984). The theory is that the active metabolite of vitamin D3 is able to inhibit the proliferation of megakaryocytes which usually promote collagen synthesis by releasing PDGF: in addition. that it can facilitate the reabsorption and increase the catabolism of collagen by being able to promote differentiation of CFIJ-GM in macrophages and monocytes which producc collagenase.Following the original suggestion (McCarthy et al, 1984), other authors (Arlet et al, 1984) published the results of treating three patients. One of these had myelofibrosis associated with chronic myelomonocytic leukaemia (CMML), one had myelofibrosis associated with posthypoparathyroid thrombocythacmia and one had 'acute myelofibrosis'; there was apparent improvement in all the patients, and particularly in thc third, after treatment with 1 .2.5(OH)2 vit D 3 was started.We treated four patients in whom a diagnosis of idiopathic myelofibrosis had been made previously with 1,25(OH), vit D3 at a dose of 2.5 pg/d for 6 months. These patients had becri followed up for 1-7 years before treatment. None of these patients were transfusion dependent. Haematological data before and after treatment is given in Table 1. In addition, the collagen content of a bone marrow biopsy was assessed by two separate observers. In order to prevent the onset of secondary hypercalcaemia a calcium-deficient diet was given and fluid intake was increased; serum calcium, phosphorus and creatinine and urinary calcium and Correspondence creatinine (urinary calcium/creatinine ratio) were measured at intervals. After treatment for 6 months (Table I) there were no significant changes in any of the parameters observed; the number of reticulin fibres in marrow biopsy had risen in one of the patients. There were no modifications in the others. Treatment was tolerated very well and there were no complications associated with the development of hypercalcaemia.In spite of the small number of patients concerned, it is difficult to accept at present that this form of treatment has any beneficial effect in patients with primary myelofibrosis. The results published by Arlet et a1 (1984) have not been confirmed by others and it is important to bear in mind that myelofibrosis was 'secondary' in two of their patients which, as they themselves point out, makes it difficult to assess the effect of 1,2 5(OH)z vit D3.The intrinsic mechanism by means of which 1 , 2 5 ( 0 H )~ vitD3 promotes in vitro differentiation in HI, 60 cells from human promyelocytic leukaemia appears to be associated with the presence in these cells of receptors which are specific for the vitamin D3 metabolite and with the concentration achieved, since the greate...

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