Background/Purpose To determine the frequency of hypothyroidism in patients with rheumatoid arthritis (RA), and to elucidate the association of hypothyroidism and development of cardiovascular disease in these patients. Method A retrospective medical record review was performed using all incident cases of adult onset RA from a defined geographic population base that fulfilled criteria for RA in the years 1988–2007. Patients with and without thyroid disease were followed longitudinally for the development of cardiovascular disease (CVD). Results A cohort of 650 patients with RA and an age and sex matched comparison cohort of 650 patients without RA was assembled (both cohorts mean age 55.8; 69% female). There was no significant difference between cohorts in the presence of hypothyroid disease or subclinical hypothyroidism at time of RA diagnosis. No significant difference was found in the cumulative incidence of hypothyroid disease between the two cohorts. Hypothyroid disease was found to be significantly associated with CVD in patients with RA (hazard ratio 2; 95% confidence interval 1.1,3.6). This difference remained significant and unchanged after adjustment for traditional cardiovascular risk factors (HR: 2.0; 95% CI: 1.1, 3.6). Conclusion No significant difference was found in either incidence or prevalence of hypothyroidism between patients with or without RA. Hypothyroid disease was significantly associated with CVD in patients with RA, even after adjustment for other traditional cardiovascular risk factors.

Objective To investigate the risk profiles, treatment utilization, and outcomes of myocardial infarction (MI) patients with rheumatoid arthritis (RA) and matched MI patients without RA. Methods We utilized a population-based cohort of Olmsted County, Minnesota, residents with MI from 1979–2009. Among these, we identified 77 patients who fulfilled the American College of Rheumatology (ACR) 1987 criteria for RA and 154 age, sex, and calendar year matched MI patients without RA. Data collection from medical records included RA and MI characteristics, antirheumatic and cardioprotective medications, and reperfusion therapy as well as outcomes (mortality, heart failure, and recurrent ischemia). Results The mean age at MI was 72.4 and 55% were female in both cohorts. Cardiovascular risk factor profiles, MI characteristics, and treatment with reperfusion therapy or cardioprotective medications were similar in MI patients with and without RA. However, patients with RA experienced poorer long-term outcomes compared to patients without RA (for mortality: hazard ratio [HR]: 1.47; 95% confidence interval [CI]: 1.04, 2.08, and for recurrent ischemia: HR: 1.51; 95% CI: 1.04, 2.18). Conclusion MI patients with RA receive similar treatment with reperfusion therapy and cardioprotective medications, and have similar short-term outcomes compared to patients without RA. However, patients with RA have poorer long-term outcomes. Thus, despite similar treatment, MI patients with RA have worse long-term outcomes than MI patients without RA.

Opinion statement Purpose of review Neurologic disease is a common extraglandular manifestation of Sjögren’s syndrome (SS), the study of which has been hampered both by the lack of uniform definitions for specific neurologic complications and by the imprecision of the tools used to diagnose SS. There is a great need to develop consensus criteria for classifying these varied neurologic manifestations, as has been done in systemic lupus erythematosus (SLE) “Arthritis and rheumatism 42:599-608, 1999”. SS patients with certain forms of neurologic involvement, such as small fiber neuropathy and sensory ataxic ganglionopathy, frequently lack anti-SSA and anti-SSB antibodies and other serologic abnormalities. In these patients, neurologic disease is often their presenting manifestation, triggering a search for underlying SS. Given the frequent seronegativity of such patients, their diagnosis of SS rests heavily on the interpretation of a labial gland biopsy. However, these biopsies are prone to misinterpretation “Vivino etal. J Rheumatol 29:938-44, 2002”, and “positive” ones are found in up to 15% of healthy volunteers “Radfar et al. Arthrit Rheumatu 47:520-4, 2002”. Better diagnostic tools are needed to determine if the frequent seronegative status of these SS patients may be related to a unique disease pathogenesis. Recent findings Recent advances in diagnostic techniques have served to define a likely pathogenetic basis for certain neurologic manifestations of SS. The advent of punch skin biopsies to analyze intraepidermal nerve fiber density and morphology has helped define pure sensory small fiber neuropathy as common in SS and the basis for both length- and non-length-dependent patterns of neuropathic pain. New protocols for magnetic resonance imaging (MRI) have enabled the recognition of dorsal root ganglionitis, a finding originally detected in pathologic studies. The advent of the anti-aquaporin-4 (AQP4) antibody test in 2004 has Led to the appreciation that demyelinating disease in SS is often related to the presence of neuromyelitis optica spectrum disorder. The anti-AQP4 antibody is considered to be directly pathogenic in the brain, targeting the primary water channel proteins in the brain, expressed prominently on astrocytic foot processes. Summary There are no clinical trials evaluating the efficacy of systemic immune suppressive therapy for peripheral or central nervous system involvement. With the recent increase in clinical trials of biologic agents for SS, which utilize systemic disease manifestations as standardized outcome measures, there is an urgency to deveLop appropriate definitions of neuroLogic compLications of SS and cLear parameters for clinical improvement.

Scleroderma keratinocytes promote the activation of fibroblasts in a TGF-β-independent manner and demonstrate an imbalance in NF-κB1 and PPAR-γ expression leading to increased cytokine and CCL5 production. Further study of keratinocyte mediators of fibrosis, including CCL5, may provide novel targets for skin fibrosis therapy.

Pulmonary manifestations of SLE were more common in late-onset SLE patients compared to their younger peers, in particular ILD and serositis. Age-related changes of the immune system, tobacco exposure, race, and possible overlap with Sjögren's syndrome should be examined in future studies.