Racial and ethnic disparities in rheumatoid arthritis.

Racial and ethnic health disparities are a national health issue. They are well described in other chronic diseases, but in rheumatoid arthritis (RA), research into their causes, outcomes, and elimination is in its early stages. Health disparities occur in a complex milieu, with system-level, provider-level, and individual-level factors playing roles. Dissecting the overlapping aspects of race/ethnicity, socioeconomic variables, and how their individual components combine to explain the magnitude of disparities in RA can be challenging. Recent research has focused on the extent to which treatment preferences, adherence, trust in physicians, patient-physician communication, health literacy, and depression have contributed to observed disparities in RA. Practicing evidence-based medicine, improving patient-physician communication skills, reducing language and literacy barriers, improving adherence to therapies, raising awareness of racial/ethnic disparities, and recognizing comorbidities such as depression are steps clinicians may take to help eliminate racial/ethnic disparities in RA.

Relation of platelet C4d with all-cause mortality and ischemic stroke in patients with systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is an autoimmune disease associated with significant morbidity, including premature cardiovascular disease, and mortality. Platelets bearing complement protein C4d (P-C4d) were initially determined to be specific for diagnosis of SLE and were later found to be associated with acute ischemic stroke in non-SLE patients. P-C4d may identify a subset of SLE patients with a worse clinical prognosis. This study investigated the associations of P-C4d with all-cause mortality and vascular events in a lupus cohort. A cohort of 356 consecutive patients with SLE was followed from 2001 to 2009. Primary outcome was all-cause mortality. Secondary outcomes were vascular events (myocardial infarction, coronary artery bypass graft, percutaneous coronary transluminal angioplasty, ischemic stroke, venous thromboembolism, pulmonary embolism, or other thrombosis). P-C4d was measured at study baseline. Seventy SLE patients (19.7%) had P-C4d. Mean follow-up was 4.7 years. All-cause mortality was 4%. P-C4d was associated with all-cause mortality (hazard ratio 7.52, 95% confidence interval (CI) 2.14-26.45, p = 0.002) after adjusting for age, ethnicity, sex, cancer, and anticoagulant use. Vascular event rate was 21.6%. Patients with positive P-C4d were more likely to have had vascular events compared to those with negative P-C4d (35.7 vs. 18.2%, p = 0.001). Specifically, P-C4d was associated with ischemic stroke (odds ratio 4.54, 95% CI 1.63-12.69, p = 0.004) after adjusting for age, ethnicity, and antiphospholipid antibodies. Platelet-C4d is associated with all-cause mortality and stroke in SLE patients. P-C4d may be a prognostic biomarker as well as a pathogenic clue that links platelets, complement activation, and thrombosis.