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Psychogenic impotence is relatively uncommon. It is characterized objectively by the presence of good nocturnal and morning erections and negative findings from all other tests. During the interview, a history of highly variable erections that can be totally absent one day but virtually normal the next suggests a psychogenic cause. Virtually 100% of men with severe depression have erectile dysfunction (ED). Sildenafil (Viagra) works well for psychogenic ED; other treatment modalities are also effective because the tissues, nerves, hormone levels, and vasculature are normal. The authors usually recommend a full psychological evaluation in these patients so that the underlying etiology can be identified and treated appropriately rather than just treating the symptom of ED. Therefore, the authors defer treatment of the patient's ED until he has begun psychological testing and therapy for the underlying problem.
Erectile Dysfunction as Warning Sign
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Figure 1. Flow diagram of patient population in the study.
In her practice, Shaw finds that physical problems don't lie at the heart of most men's sexual problems.
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Yes, but because these drugs work the same way, it's unlikely that you'll have success with one if you've failed to achieve an adequate erection with another.
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Evidence of an immune-mediated, antitumor effect of PDE5 inhibition is further shown by tetramer analysis on splenocytes obtained from sildenafil-treated, CT26WT tumor- bearing mice, which revealed a higher number of CTLs specific for AH-1 (unpublished data), a CT26 tumor-associated antigen, as compared with their untreated counterparts (19). To confirm immune-mediated antitumor activity in the sildenafil-treated groups, we performed an in vivo cytotoxicity assay. BALB/c mice were injected with PBS (naive), vaccinated with -irradiated CT26WT or C26GM, or challenged with CT26WT or C26GM tumors on day 0. On day 12 (CT26WT) or day 5 (C26GM), all mice received carboxyfluorescein diacetate succinimidyl ester (CFSE)labeled splenocytes pulsed with the MHC class Irestricted AH-1 peptide (CFSEhigh), admixed with CFSE-labeled splenocytes pulsed with the irrelevant hemagglutinin (HA)-peptide (CFSElow). In vivo T cell cytotoxicity was determined 40 h later (Fig. 2). These time points were chosen based on the kinetics of tumor outgrowth observed in Fig. 1 A and Fig. 1 B, respectively, when tumor size significantly differed between untreated and sildenafil-treated mice. As expected, an endogenous AH1-specific immune response was observed in the vaccinated mice as compared with their tumor-bearing counterparts. PDE5 inhibition in the vaccine-primed mice failed to augment antigen-specific CD8 responsiveness compared with no treatment. In contrast, tumor-bearing mice treated with sildenafil early after tumor challenge generated antigen-specific immunity that was significantly greater then that observed in their untreated counterparts and similar, or even superior, to that induced by vaccination. Collectively, this is the first indication that PDE5 inhibitors can modulate antitumor immunity. Because the sildenafil-mediated antitumor immune response does not completely eradicate tumors, tumor escape mechanisms may be associated with their outgrowth. To test this hypothesis, the parental CT26WT cell line, as well as the CT26 tumor removed on day 24 from sildenafil-treated mice (either AH-1 pulsed or unpulsed), and BALB/c splenocytes were incubated with either AH-1 peptide-primed (Fig. S1 C) or tumor-primed (Fig. S1 D) effector T cells. Although effector T cells recognized the parental CT26WT line and released IFN- in the assay, they failed to recognize the sildenafil-derived tumor. Its recognition, however, was restored by loading the sildenafil-derived tumor with the AH-1 peptide. (Fig. S1, C and D). These results suggest that the immune response in sildenafil-treated mice does not result in complete tumor eradication but rather in the selection of antigen-escape variants.
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Arterial Disorders (peripheral vascular disease, hypertension; reduced blood flow to the penis).
Promotes and maintains secondary sex characteristics in androgen-deficient males. Depot injections can produce high levels of serum testosterone when administered in adequate doses.
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