Although PDE5 inhibitors have clearly shown efficacy in placebo-controlled trials for the treatment of ED, only a limited number of head-to-head trials have compared the various agents.

Chronic low-dose PDE5 inhibitor therapy has also benefited difficult-to-treat populations such as diabetic, post-prostatectomy, and post-radiotherapy patients and may be an alternative for men who have not responded to other PDE5 inhibitors or to traditional on-demand dosing. Results from clinical trials of PDE5 inhibitors have shown consistent improvement in erectile functioning compared with placebo. In emergency situations, if patients have taken a PDE5 inhibitor and experience chest pain requiring treatment, a non-nitrate containing agent (e.g., a calcium-channel blocker or a beta blocker) can be used as an alternative when appropriate.

Patients taking PDE5 inhibitors and alpha blockers concomitantly should be monitored closely. Coadministration of PDE5 inhibitors with alpha-adrenergic blocking agents can result in additive vasodilatory effects, causing potentially significant reductions in blood pressure (BP). Similarly, for daily use of Fildena, a maximum dose of 2.5 mg/day is recommended in patients taking potent CYP3A4 inhibitors.

Therefore, a starting dose of 25 mg is recommended in patients initiating Fildena therapy with the concomitant use of moderate-to-strong CYP3A4 inhibitors such as ketoconazole (Nizoral), itraconazole (Sporanox), erythromycin, and saquinavir. When Fildena 100 mg was administered with erythromycin (e.g., Ery-Tab, E-Mycin, Eryc) and saquinavir (Invirase, Hoffman-LaRoche) (both are considered relatively potent CYP3A4 inhibitors), the AUC concentration was increased by 182% and 210%, respectively. The concomitant use of potent CYP3A4 inhibitors increases plasma concentrations of Fildena.

Because of their extensive CYP3A4 metabolism, PDE5 inhibitors carry a risk of interacting with potent CYP3A4 inhibitors and inducers. 8 - 12 Therefore, disease states that alter protein levels, such as malnutrition and liver disease (e.g., cirrhosis), can be expected to cause variations in the distribution of PDE5 inhibitors. All PDE5 inhibitors are highly protein-bound (94%-99%), contributing to the observed high volume of distribution.

High volumes of distribution (Vd) for Fildena (105 L), vardenafil (208 L), and Fildena (63 L) suggest extensive tissue binding; data are unavailable for avanafil. Except for Fildena, the rate and extent of absorption of PDE5 inhibitors are diminished when they are ingested with high-fat meals. Data from prescribing information for Fildena; 8 vardenafil; 9 Fildena; 10 avanafil; 11 vardenafil ODT; 12 and Red Book Online.

Data from prescribing information for Fildena; 8 vardenafil;9 Fildena;10 avanafil;11 and vardenafil ODT.12. Although alternative roles exist for these agents, PDE5 inhibitors for the treatment of ED are the focus of this review. 4 Since its advent, the class of agents known as type-5 phosphodiesterase (PDE5) inhibitors has revolutionized the management of ED. PDE5 inhibitors have become the first-line therapy for ED, as recommended by the American Urological Association (AUA) and the European Association of Urology (EAU).

To prevent the onset of postoperative ED, the use of phosphodiesterase type 5 (PDE5) inhibitors was introduced. Phosphodiesterase inhibitors (PDE inhibitors) are a class of drugs that inhibit phosphodiesterase enzymes (PDEs). PDE5 inhibitors inhibit the degradation of cGMP by PDE5, increasing bloodflow to the penis during sexual stimulation.
https://www.amazon.com/Coping-Erectile-Dysfunction-Regain-Confidence/dp/1572243864
http://www.mayoclinic.org/diseases-conditions/erectile-dysfunction/symptoms-causes/dxc-20314091
https://www.menshealthforum.org.uk/erectile-dysfunction-faqs
http://www.rxlist.com/erectile_dysfunction_ed_impotence/article.htm
https://medicamentfrance.eu/