A 6-month study of the efficacy and safety of tadalafil in the treatment of erectile dysfunction: a randomised, double-blind, parallel-group, placebo-controlled study in Australian men.

The efficacy and safety of tadalafil for the treatment of erectile dysfunction (ED) were assessed in a 6-month, randomised, double-blind, placebo-controlled study. Australian men with mild, moderate or severe ED of organic, psychogenic or mixed aetiology were randomised to tadalafil 20 mg as needed (n = 93) or placebo (n = 47). Efficacy assessments included the international index of erectile function (IIEF) and the sexual encounter profile (SEP) diary. Tadalafil significantly improved erectile function compared with placebo (p < 0.001, all measures). At the end of the study, the mean per-patient proportion of successful sexual intercourse attempts (SEP question three) was 73.5% for patients treated with tadalafil and 26.8% for placebo-treated patients. Improved erections were reported by 78% of tadalafil-treated patients compared to 12.8% of placebo-treated patients. The most common treatment-emergent adverse events--headache and dyspepsia--were generally mild or moderate. Tadalafil was effective and well tolerated in Australian men with mild to severe ED.

The association of autoimmune diseases and anti-IgA antibodies in patients with selective IgA deficiency.

The prevalence of antibodies to immunoglobulin A (IgA) was studied in eighty-three subjects with selective IgA deficiency (SIgAD), thirty-three normal individuals, thirty-two children with juvenile rheumatoid arthritis (JRA) and normal or elevated IgA, seventeen children with systemic lupus erythematosus (SLE) and normal or elevated IgA, and thirteen patients with hypogammaglobulinaemia. Anti-IgA antibodies were detected by haemagglutination of human erythrocytes coated with one of two IgA myelomas by the chromic chloride technique. Antibodies to IgA were not found in significant titre in individuals with normal or elevated IgA or in those with hypogammaglobulinaemia. In IgA deficient patients, elevated titres were found in 25--30% of those who were healthy or who had non-rheumatic diseases, 50% of those with rheumatoid arthritis, 77% of those with JRA and 100% of those with SLE. Patients with rheumatic diseases and SIgAD may therefore be particularly at risk of developing anti-IgA-mediated reactions to blood products.