Level of pain, morning stiffness and function was registered by the self-reported AUSCAN questionnaire.26 The occurrence of any adverse events was questioned at every visit. erosive evolution around the radiological image (3.7%) was seen in the adalimumab treated group compared to the placebo group (14.5%) (P = 0.009). GUSSTM scoring confirmed a less rapid rate of mean increase in the erosion scores during the first 6 months of treatment in patients in adalimumab-treated patients. Conclusion Palpable soft tissue swelling in IP joints in patients with erosive HOA is usually a strong predictor for erosive progression. In these joints adalimumab significantly halted the progression of joint damage compared to placebo. Moderate to severe hand osteoarthritis is usually estimated to occur in 5C8% Caucasian adults above the age of 60 years.1 2 Similar data have been reported in the USA.3 In this population, marked destructive changes4C7 occur mostly in the distal and proximal interphalangeal joints, which eventually result in considerable disability.8 9 Anamorelin As there is still lack of agreement concerning the nature and specificity of erosive osteoarthritis as a distinct subset of hand osteoarthritis, clear epidemiological data are scarce. In a survey on the entire health district in Anamorelin the Venetian area, radiographic erosive osteoarthritis of Rabbit Polyclonal to TEAD1 the interphalangeal joints occurred in 8.5% of subjects above Anamorelin the age of 40 years.10 These figures were confirmed in two large population studies in which the prevalence of radiographic erosive interphalangeal osteoarthritis in subjects over 55 years of age ranged between 5.0% and 9.9%.11 12 The changes in both the joint space and subchondral bone that characterise the erosive phase of the interphalangeal finger joints strongly suggest the involvement of pro-inflammatory cytokine cascades known to cause cartilage degradation and bone resorption. Among these, tumour necrosis ractor alpha (TNF) directly stimulates osteoclast progenitors of the monocyte/macrophage lineage into osteoclasts, enhances the production of a series of proinflammatory cytokines, eg, interleukin-1 (IL-1), receptor activator for nuclear factor B ligand, and increases the rate of tissue remodelling by matrix-degrading proteases.13C15 Adalimumab (Humira; Abbott Laboratories, Abbott Park, Illinois) is usually a bioengineered fully human monoclonal antibody that binds to TNF, preventing it from activating TNF receptors.16 In rheumatoid arthritis (RA), adalimumab slowed down progressive joint destruction.17C19 The authors evaluated the efficacy and safety of adalimumab, 40 mg subcutaneous administration, every 2 weeks, to control the structural damage Anamorelin to cartilage and bone, as determined by radiographic assessment, in erosive osteoarthritis of the interphalangeal finger joints in a double blind, placebo controlled randomised clinical trial of 1 1 year. Patients and methods Patient inclusion/exclusion criteria Sixty patients were recruited from the outpatient rheumatology clinic of the Ghent University Hospital between May 2006 and January 2008. Patients were eligible for study if: (1) they were 18 years or older; (2) had hand osteoarthritis (meeting the American College of Rheumatology criteria)20 characterised by painful, inflammatory episodes of the interphalangeal joints; (3) presented with at least one interphalangeal finger joint in the E phase as defined by Verbruggen and Veys7 on radiography; and (4) were willing to self-administer subcutaneous injections or allow a suitable person to perform this. Patients were excluded from the study if they had received previous treatment with any investigational agent within 30 days (or five half lives of the product when longer). Previous treatment with chondroitin sulfate, glucosamine, avocado-soybean unsaponifiables, tetracyclines, corticosteroids or any immunomodulating drug with possible Anamorelin effects on pro-inflammatory cytokine metabolism within 90 days was another reason for exclusion. Patients with chronic inflammatory rheumatic disease (eg, RA, spondylarthropathy, psoriatic arthritis, gout, chondrocalcinosis or other autoimmune diseases) were excluded as well as underlying comorbidities, eg, uncontrolled diabetes, unstable ischaemic heart disease, congestive heart failure, active inflammatory bowel disease, recent stroke (within 3 months before screening),.
Level of pain, morning stiffness and function was registered by the self-reported AUSCAN questionnaire