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A study presented at the same AUA meeting found that unpadded seats reduce penile blood flow more than padded seats. The width of the padded seats wasn't a factor.
There have been rare reports of priapism (prolonged and painful erections lasting more than 6 hours) with the use of PDE5 inhibitors such as sildenafil, vardenafil, and tadalafil, especially when sildenafil is used in combination with injection of medications into the corpora cavernosa or intraurethral suppositories. Patients with blood cell diseases such as sickle cell anemia, leukemia, and multiple myeloma have higher than normal risks of developing priapism. Priapism untreated can cause injury to the penis and lead to permanent impotence. Therefore, sildenafil should not be used in combination with intraurethral suppositories and corpora cavernosa injections. If there is prolonged erection (longer than 4 hours), immediate medical assistance should be obtained.
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Fig. S1 shows that PDE-5 inhibitors reduce tumor growth but that persistent tumors show evidence of immune editing. In Fig. S2, the antitumor effect of sildenafil is maintained even with delayed treatment. Fig. S3 shows that sildenafil increases CD8+ TILs. Fig. S4 depicts sildenafil as it fails to induce an antitumor effect in 4T1-HA–bearing Rag-2–/– mice. In Fig. S5, sildenafil fails to augment proliferation of purified T cells. Fig. S6 shows that sildenafil does not alter IL-13 or IFN- production from CD11b+ cells. Online supplemental material is available at http://www.jem.org/cgi/content/full/jem.20061104/DC1.
Having demonstrated that PDE5 inhibition can impair MDSC suppressive mechanisms in BALB/c and C57BL/6 tumor-bearing mice, we next sought to determine whether similar results could be obtained in humans. Head and neck cancers are known to be highly immunosuppressive. Their high levels of GM-CSF production are likely the major mediator of immune suppression observed in these patients and are probably responsible for the intratumoral infiltration by MDSCs (36). In fact, peripheral blood lymphocytes (PBLs) from these patients are functionally impaired in their ability to be activated and to proliferate upon stimulation (37). Similar results were also seen in prostate cancer (38) and in nonsmall cell cancer (35). Although this anergic state in solid tumors may be attributable to the ARG1- and/or NOS-dependent suppressive activity of MDSCs, MDSC-mediated immunosuppression has not been previously reported in hematological malignancies. PBMCs from MM patients were stimulated with anti-CD3/CD28 antibody-coated beads in the presence of N-(omega)-hydroxy-nor-L-arginine (NorNOHA; an ARG1-specific inhibitor), NG-monomethyl-L-arginine (L-NMMA; an NOS2 inhibitor), both inhibitors, or neither. As shown in Fig. 8 A (top), T cell expansion was considerably enhanced in the presence of both NorNOHA and L-NMMA, whereas the single inhibitors failed to increase T cell proliferation over the baseline. Interestingly, sildenafil yielded results equivalent to the combination of NorNOHA and L-NMMA. These results suggest involvement of both ARG1 and NOS2 in MDSC-mediated immunosuppression in myeloma and confirm the in vitro results demonstrating the ability of PDE5 inhibitors to affect both pathways. Recent data from our lab identified human MDSCs as ARG+, CD14+ cells (unpublished data). We therefore examined T cell expansion in CD14+-depleted PBMCs under the same conditions (Fig. 8 A, bottom). Although CD14+ depletion alone increased CD3+ T cell expansion fourfold, pharmacologic inhibitors failed to further enhance proliferation, suggesting that CD14+ cells are the mediators of ARG1- and NOS2-mediated immunosuppression in MM. As seen with purified mouse T cells (Fig. 5 B), sildenafil also failed to enhance the CD3+ T cell proliferation of CD14-depleted PBMCs from cancer patients.
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Significant adverse effects (eg, fluid retention, liver damage)
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Currently, any man who wishes to have erectile function can do so regardless of the etiology of the problem. Many therapeutic options are available, and the task of the physician is to help the patient seek the best solution. Finding a trained and understanding physician who is willing to take the time to understand the patient's problem is the first step in identifying which therapeutic option will ultimately be most appropriate and successful.
The study is published in the Nov. 9 online edition of the Proceedings of the National Academy of Sciences.
"PDE-5 inhibitors have been considered the mainstay of treatment for erectile dysfunction in the general population for many years. Diabetics are prone to this complication, and the etiology of their erectile dysfunction is multifactorial, thus making their treatment a special challenge for physicians and other health care professionals," Vardi said.
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