Sweet syndrome in a patient with Hidradenitis Suppurativa.

Neutrophilic Dermatoses should be considered in the differential diagnosis, if a patient with abrupt onset of painful erythematous plaques/nodules and elevated erythrocyte sedimentation rate is not responding to antibiotics.

Current use of phosphodiesterase inhibitors in urology.

The causes of male erectile dysfunction (ED) are quite variable and are now commonly divided into etiologies such as ischemia, smooth muscle damage, or altered blood flow. Although varying rates of ED have been reported in literature, the number of men with ED is projected to increase worldwide by 2025 to approximately 322 million. Since the introduction of phosphodiesterase 5 (PDE5) inhibitors, there has been a paradigm shift in the treatment of ED because PDE5 inhibitors address a broad spectrum of etiologies for ED. Today, the American Urological Association recommends the use of three PDE5 inhibitors (sildenafil, tadalafil, and vardenafil) as a first-line therapy for the treatment of ED. This review evaluates the pharmacological mechanism of PDE5 inhibitors along with the impact and use of sildenafil, vardenafil, tadalafil, and avanafil. By increasing intracellular cGMP levels, PDE5 inhibitors have been shown to be effective in the treatment of ED. Through their effects on other cellular signaling pathways, PDE5 inhibitors have the potential for treating other urologic conditions as well. The use of PDE5 inhibitors can also be combined to produce a synergistic effect in conditions such as male hypogonadism and benign prostatic hyperplasia in addition to ED.

Association Between Testosterone Supplementation Therapy and Thrombotic Events in Elderly Men.

OBJECTIVE: To determine the prevalence of thrombotic events and all-cause mortality in men older than 65 years with hypogonadism treated with testosterone therapy (TST). PATIENTS AND METHODS: We retrospectively reviewed the charts of 217 hypogonadal men >65 years. We compared men who received TST (n = 153) to hypogonadal men (n = 64) who did not receive TST. We evaluated all-cause mortality, prevalence of myocardial infarction (MI), transient ischemic attack (TIA), cerebrovascular accident (CVA or "stroke"), and deep vein thrombosis/pulmonary embolism (DVT/PE). All events were verified by contacting patients. We excluded men with previous thrombotic events, men previously on androgen deprivation therapy, and men who had used TST before age of 65 years. RESULTS: Median age and Charlson Comorbidity Index of men on TST (74y; 5.1) was similar to hypogonadal men not on TST (73y, P = .48; 5.3, P = .36). Median follow-up was 3.8 vs 3.5 years (TST vs no TST). No man on TST died, whereas 5 hypogonadal men who did not receive TST died (P = .007). There were 4 thrombotic events (1 MI, 2 CVA/TIA, and 1 PE) in men who received TST and 1 event (CVA/TIA) among men who did not receive TST (P = .8). All events (1 death, 6-month follow-up) occurred at least after 2 years of follow-up. CONCLUSION: There was increased all-cause mortality in hypogonadal men not treated with testosterone compared to men who received TST. There was no difference in prevalence of MI, TIA/CVA, or PE between patients treated with testosterone and hypogonadal men not treated with testosterone.