IMPORTANCE Hidradenitis suppurativa (HS) is a common skin disorder in which excessive inflammation is believed to have an important role. There is no specific therapy for HS. OBJECTIVE To investigate the safety and efficacy of the anti-inflammatory biological therapy anakinra in HS. DESIGN, SETTING, AND PARTICIPANTS Double-blind, randomized, placebo-controlled clinical trial with a 12-week treatment phase and a 12-week follow-up phase. The setting was Attikon University General Hospital, a tertiary care institution in Athens, Greece. Participants were 20 patients with Hurley stage II or III HS. The study and the analysis were conducted between

OSAHS may be a comorbidity in obese psoriasis patients with hypertension. Treatment with continuous positive airway pressure and weight loss interventions should be initiated.

SummaryBackground Recent evidence has suggested that deranged immune responses play a role in the pathogenesis of hidradenitis suppurativa (HS). Objectives To investigate the role of single nucleotide polymorphisms (SNPs) of the tumour necrosis factor (TNF) and Toll-like receptor 4 (TLR4) genes in the physical course of HS; these genes encode for proteins implicated in the immune response of the host. Methods DNA was isolated from 190 patients with HS and 84 healthy controls. SNPs at the promoter regions )376G ⁄A, )238G ⁄A and )308G ⁄A of the TNF gene and the Asp299Gly and Thr399Ile SNPs of the TLR4 gene were determined by polymerase chain reaction (PCR) and digestion of the PCR product by restriction enzymes; after electrophoresis on 2AE0% agarose gel, products were visualized on under ultraviolet radiation. Results The presence of the )238 TNF gene polymorphism was associated with a predisposition to HS (P = 0AE027). Susceptibility to the disease was strongly correlated with the presence of AGG ⁄GGA ⁄AGA ⁄GAA TNF haplotypes in 32 (17%) patients compared with two (2%) controls (P < 0AE001, odds ratio 8AE30, 95% confidence interval 1AE94-35AE52). The frequency of HS exacerbations and disease severity were greater in patients carrying any of the GAG ⁄AGG ⁄GGA ⁄AGA ⁄GAA haplotypes of the TNF gene. Thirty-two patients were given TNF antagonists. Nineteen of these patients were carriers of the GGG haplotype of the TNF gene, whereas 13 were carriers of other haplotypes; favourable responses as evidenced by the Sartorius score were registered in 15 (79%) and five (38%, P = 0AE025), respectively. Carriage of the TLR4 gene alleles was not associated with any disease parameter. Conclusions A significant role of SNPs at the promoter region of the TNF gene is indicated for susceptibility to HS and for response to TNF antagonists.

Aims: To assess the efficacy and safety of rituximab in refractory pemphigus and the possible benefit of an additional prophylactic infusion at 6 months. Methods: Seventeen patients with pemphigus vulgaris, 1 with pemphigus foliaceus and 1 with pemphigus vegetans were treated with 4 weekly infusions of rituximab (375 mg/m²). Nine patients received an additional prophylactic infusion after 6 months while the rest received no maintenance therapy. In case of recurrence, an additional single infusion was administered. Results: Control of the disease was obtained after 3-8 weeks. End of the consolidation phase for all patients was observed after 16 weeks. Patients remained in full remission for 7-42 months. All immunosuppressive agents, including prednisone, were discontinued after 2-12 months. The disease relapsed in 5 out of 9 patients who received the additional prophylactic infusion, and in 3 out of 10 patients among those skipping the prophylactic additional infusion. Conclusion: One course of rituximab and treatment of relapses is highly effective and well tolerated in the treatment of refractory pemphigus. In this pilot study of 19 patients, the prophylactic infusion does not appear to have provided any additional benefit to the patients receiving it.

Carriage of gene SNPs is protective against the development of acne conglobata even in the presence of P. acnes.