Paget's disease of the skull causing hyperprolactinemia and erectile dysfunction: a case report

<p>Abstract</p> <p>Introduction</p> <p>Hyperprolactinemia is an uncommon cause of erectile dysfunction in men. Paget's disease of the skull is a relatively common disease. This case proposes a rare example of a causative link between the two and how treatment of the Paget's disease with bisphosphonates helped the patient regain erectile function.</p> <p>Case presentation</p> <p>A 67-year-old man with Paget's disease of the skull presented with prostatitis, erectile dysfunction, and hyperprolactinemia. Radio-isotope scanning showed increased vascularity around the sphenoid bone. Treatment with intravenous bisphosphonates improved the active Paget's disease as indicated by declining alkaline phosphatase levels and the patient's erectile function while serum prolactin levels became normal and serum testosterone levels remained unchanged.</p> <p>Conclusion</p> <p>It is possible that hyperprolactinemia is unrecognised in other patients with Paget's disease of the skull. Normalizing elevated prolactin levels by using bisphosphonates in treating Paget's disease appears to be more appropriate than traditional treatment for hyperprolactinemia.</p

Tadalafil 5 mg Alone or in Combination with Tamsulosin 0.4 mg for the Management of Men with Lower Urinary Tract Symptoms and Erectile Dysfunction: Results of a Prospective Observational Trial.

Tadalafil 5 mg represents the standard for men with Erectile dysfunction (ED) and lower urinary tract symptoms (LUTS)/benign prostatic enlargement (BPE). We carried out an observational trial aiming to assess the efficacy and safety of Tadalafil compared with Tadalafil plus Tamsulosin. Seventy-five patients complaining of ED and LUTS were treated for 12-weeks with Tadalafil plus placebo (TAD+PLA-group) or with combination therapy tadalafil plus tamsulosin (TAD+TAM-group). Efficacy variables were: International Index of Erectile Function (IIEF), International Prostate Symptom Score (IPSS), maximum urinary flow rate (Qmax) and safety assessments. Data were evaluated using paired samples T-test (baseline vs. 12-weeks) and analysis of variance (&Delta;group-TAD+PLA vs. &Delta;group-TAD+TAM). At baseline, both groups presented similar characteristics and symptoms scores (all: p &gt; 0.05). From baseline to 12-weeks, all the subjects showed a significant improvement of IIEF, total-IPSS, storage-IPSS, Qmax (all: p &lt; 0.001). Conversely, a significant improvement of voiding-IPSS was observed in TAD+TAM-group (&minus;3.5 points, p &lt; 0.001). Indeed, TAD+PLA-group showed a not significant improvement of voiding-IPSS (&minus;2.0 points, p = 0.074). When we compared between-groups differences at 12-weeks, IIEF (p = 0.255), total-IPSS (p = 0.084) and storage-IPSS (p = 0.08) did not show any statistically significant differences, whereas, voiding-IPSS and Qmax were significantly better in TAD+TAM-group (p = 0.006 and p = 0.027, respectively). No severe treatment adverse events (TAEs) were reported in both groups. Tadalafil achieved the same improvements of IIEF, total-IPSS, storage-IPSS when compared to combination therapy. Instead, Qmax and voiding-IPSS were better managed with combination therapy, without change of TAEs

Coupling of alpha(1)-Adrenoceptors to ERK1/2 in the Human Prostate

Introduction: alpha(1)-Adrenoceptors are considered critical for the regulation of prostatic smooth muscle tone. However, previous studies suggested further alpha(1)-adrenoceptor functions besides contraction. Here, we investigated whether alpha(1)-adrenoceptors in the human prostate may activate extracellular signal-regulated kinases (ERK1/2). Methods: Prostate tissues from patients undergoing radical prostatectomy were stimulated in vitro. Activation of ERK1/2 was assessed by Western blot analysis. Expression of ERK1/2 was studied by immunohistochemistry. The effect of ERK1/2 inhibition by U0126 on phenylephrine-induced contraction was studied in organ-bath experiments. Results: Stimulation of human prostate tissue with noradrenaline (30 mu M) or phenylephrine (10 mu M) resulted in ERK activation. This was reflected by increased levels of phosphorylated ERK1/2. Expression of ERK1/2 in the prostate was observed in smooth muscle cells. Incubation of prostate tissue with U0126 (30 mu M) resulted in ERK1/2 inhibition. Dose-dependent phenylephrine-induced contraction of prostate tissue was not modulated by U0126. Conclusions: alpha(1)-Adrenoceptors in the human prostate are coupled to ERK1/2. This may partially explain previous observations suggesting a role of alpha(1)-adrenoceptors in the regulation of prostate growth. Copyright (C) 2011 S. Karger AG, Base