Cohort Description

By reference to the nation-wide Swedish Rheumatoid Arthritis Registry, all eligible patients from the four northern-most counties of Sweden diagnosed with early RA (i.e., symptomatic for <12 months), are since December 1995 consecutively included in a large survey on the progress of RA and development of co-morbidity, in particular cardiovascular disease (CVD). By April 2008, 700 patients (481 women, 219 men) registered with newly diagnosed early RA had been included into the study at diagnosis of RA (baseline, T0). Of these, 442 patients had suffered their disease for more than 5 years. All patients had been assessed regularly by their local rheumatologist during the follow-up period with special attention to established cardiovascular (CV) risk factors, any previous CV event, and clinical examination including blood pressure and laboratory tests. The following parameters were recorded at baseline and after 6, 12, 18, 24, 36, and 60 months: the 28-joint count of tender and swollen joints; VAS for pain and patient’s global assessment; completion of a HAQ and inflammatory markers, i.e., ESR and CRP. Disease activity score (DAS28) was calculated. Lipid levels (total cholesterol, high-density lipoprotein (HDL) and triglycerides) were analysed in the majority of cases at baseline, otherwise as soon as possible during the follow-up period. The presence of autoantibodies, i.e., (RF, and ANA), was detected at baseline by the routine methods at each hospital. Antibodies against cyclic citrullinated peptides/proteins (ACPA) were analysed at baseline using ELISA for anti-CCP antibodies type 2. Genotyping for PTPN22 1858C/T polymorphisms was performed for the majority of the patients. All patient records were carefully read and data collected according to a study protocol, both at inclusion at T0 and after five years at T5. In addition, the patients completed a self-reported questionnaire on co-morbidity at T0 and at T5. Recorded variables were: all co-morbidity including previous CVE, i.e., prior to inclusion, and new CVE during follow-up, i.e., myocardial infarction /coronary artery bypass grafting, stroke/transient ischaemic attack (TIA)/deep vein thrombosis (DVT)/pulmonary embolism, and ruptured aortic aneurysm. Myocardial infarction was recorded when the diagnosis had been made according to the World Health Organization (WHO) criteria. A cerebrovascular lesion was recorded when intra-cerebral haemorrhage or cerebral infarction had been diagnosed by either computerized tomography or magnetic resonance imaging, or when a typical clinical profile of neurological deficits had persisted for more than 24 h. A TIA was recorded in cases when the focal neurological deficit of presumed ischaemic origin had persisted for less then 24 h. Deep vein thrombosis/ pulmonary embolism was recorded when the diagnosis had been verified objectively or when the clinical signs combined with pulmonary radiography, electrocardiography, and laboratory changes resulted in full time warfarin treatment. The information regarding fatal CV events was obtained from the National Board of Health and Welfare. Furthermore, traditional CV risk factors (treatment for hypertension and current blood pressure, DM, smoking, BMI), rheumatoid nodules and time for development of Ex-RA were registered. Cumulated pharmacological treatment was registered (months) regarding corticosteroids and DMARDs, including biological agents at inclusion and at follow-up. Treatment with NSAIDs, before inclusion (T0) and any period during the follow up period (T5) was registered as “yes” or “no”, as was statin treatment. Time for treatment with selective COX-2 inhibitors was registered as exact as possible.

Ref: Innala et al. Arthritis research & therapy 2011:13(4):R131