Infliximab maintains a high degree of clinical response in patients with active psoriatic arthritis through 1 year of treatment: results from the IMPACT 2 trial.

OBJECTIVE: To evaluate the efficacy and safety of infliximab through 1 year in patients with psoriatic arthritis (PsA) enrolled in the IMPACT 2 trial. METHODS: In this double blind, placebo controlled, phase III study, 200 patients with active PsA were randomised to receive infusions of infliximab 5 mg/kg or placebo at weeks 0, 2, 6, and every 8 weeks thereafter through 1 year. Patients with persistent disease activity could enter early escape at week 16, and all remaining placebo patients crossed over to infliximab at week 24. Patients randomised to infliximab who had no response or who lost response could escalate their dose to 10 mg/kg starting at week 38. Clinical efficacy was assessed based on the proportion of patients achieving ACR 20 and PASI 75 responses. Major clinical response (that is, maintenance of ACR 70 response for 24 continuous weeks) was assessed for the first time in PsA. RESULTS: Through 1 year of treatment, 58.9% and 61.4% of patients in the randomised infliximab and placebo/infliximab groups, respectively, achieved ACR 20; corresponding figures for PASI 75 were 50.0% and 60.3%. At week 54, major clinical response was achieved by 12.1% of patients in the infliximab group. The safety profile of infliximab through week 54 was consistent with that seen through week 24. Two malignancies occurred: basal cell skin cancer (placebo) and stage I Hodgkin's lymphoma (infliximab). CONCLUSION: Infliximab maintains a high degree of clinical efficacy and continues to be well tolerated in patients with PsA through 1 year of treatment.

Thoracic outlet syndrome mimicking angina pectoris with elevated creatine phosphokinase values.

Four patients with elevated creatine phosphokinase (CPK) values and recurrent chest pain were found to have thoracic outlet syndrome. This association of abnormal CPK levels and chest pain due to thoracic outlet syndrome has not been previously reported. Symptoms and CPK values improved with anti-inflammatory medications and/or proper posture instruction. It is proposed that CPK values become elevated by ischemic or neurologic compromise of muscles supplied by the subclavian artery or brachial plexus respectively. Accordingly, chest pain in the same dermatomal distribution as that of angina pectoris may be simulated by ischemic skeletal muscle. Thoracic outlet syndrome therefore should be suspected in any patient with chronically abnormal CPK values and chest pain in whom no other etiology can be determined.