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Objective To determine if hyperuricemia and gouty arthritis are independent risk factors for acute myocardial infarction (MI) and, if so, whether they are independent of renal function, diuretic use, metabolic syndrome, and other established risk factors. Methods We performed multivariable logistic and instrumental variable probit regressions on data from the Multiple Risk Factor Intervention Trial (MRFIT). Results Overall, there were 12,866 men in the MRFIT who were followed up for a mean of 6.5 years. There were 118 events of acute MI in the group with gout (10.5%) and 990 events in the group without gout (8.43%; P = 0.018). Hyperuricemia was an independent risk factor for acute MI in the multivariable regression models, with an odds ratio (OR) of 1.11 (95% confidence interval [95% CI] 1.08–1.15, P < 0.001). In multivariable regressions in which the above risk factors were used as covariates, gout was found to be associated with a higher risk of acute MI (OR 1.26 [95% CI 1.14–1.40], P < 0.001). Subgroup analyses showed that a relationship between gout and the risk of acute MI was present among nonusers of alcohol, diuretics, or aspirin and among those who did not have metabolic syndrome, diabetes mellitus, or obesity. In separate analyses, a relationship between gout and the risk of acute MI was evident among those with and without those hyperuricemia. Conclusion The independent risk relationship between hyperuricemia and acute MI is confirmed. Gouty arthritis is associated with an excess risk of acute MI, and this is not explained by its well-known links with renal function, metabolic syndrome, diuretic use, and traditional cardiovascular risk factors.

The relationship between serum uric acid (SUA) and cardiovascular disease has been controversial. Here we review recent literature assessing whether hyperuricemia is an independent risk factor for adverse cardiovascular outcomes. Studies from the past 6 years evaluating the association of SUA with cardiovascular disease were identified through MEDLINE, EMBASE, and Cochrane library searches, bibliography cross-referencing, and review articles. Twenty-one cohort studies in healthy and high-risk patients with cardiovascular disease were identified and reviewed. In studies of high-risk patients, in which more overall events were recorded, 10 of 11 studies were supportive of an independent association. In 10 studies of healthy patients, 6 suggested an independent association of SUA with adverse cardiovascular outcomes. Increasing SUA is likely an independent risk factor for cardiovascular disease in high-risk individuals. However, the magnitude of excess risk attributable to high SUA is likely to be small in healthy individuals. Trials of SUA-lowering therapy in hyperuricemic patients evaluating the effect on cardiovascular outcomes are justified in high-risk patients.

Lupus erythematosus profundus is a rare complication of systemic lupus erythematosus characterized by the presence of deep, tender subcutaneous nodules. A 22-year-old African-American female with extensive lupus profundus resistant to conventional therapies was treated with two infusions of the anti-CD20 monoclonal antibody, rituximab, at a dosage of 1,000 mg each. The patient demonstrated a remarkable clinical response as indicated by the disappearance of the nodules. B-cell depletion therapy with rituximab used alone or in combination with other therapies may be a viable option in patients with lupus profundus refractory to current therapies.

Objectives Early predictors of progression in structural joint damage in RA are lacking. We evaluated if early MRI measures of inflammation & erosion at baseline (BL), 12 & 24wks could predict subsequent progression in structural damage as measured by standard x-ray at 1 & 2 yrs of follow-up among 256 pts from GO-BEFORE, a large randomized trial of golimumab+MTX vs MTX alone in RA pts who were MTX-naive. Methods Methods & results of the original trial have been published 1 . MRIs (contrast-enhanced; 1.5T) of the wrist & the 2 nd -5 th metacarpophalangeal joints of the dominant hand at BL & wks12, 24, 52, & 104 were obtained. MRIs were scored by 2 independent, blinded readers using the RA MRI Scoring (RAMRIS) system. X-rays (hands, wrists, forefeet at BL, wk 52, & 104) were scored by 2 other, blinded readers using the van der Heijde-Sharp (vdHS) system. X-ray progression was defined as a change in vdHS score > 0.5 as it was in the original trial. MRI synovitis & bone edema scores were evaluated as continuous variables (per unit difference or change). Change in RAMRIS bone erosion scores was highly skewed, & was therefore dichotomized at >0.5. Multivariable logistic regression was used to determine if BL & early measures of change in component RAMRIS scores predicted x-ray progression independent of clinical disease activity [DAS28(CRP)], change in DAS28(CRP), age, sex, BL vdHS score, & treatment group. Results Higher BL synovitis scores & less improvement in synovitis over the first 24 wks of follow-up were both significantly & independently associated with a greater risk of x-ray progression at 1- & 2 yrs (Table). Higher BL bone edema & less improvement in bone edema were independently associated with a greater risk of x-ray progression at 1yr, & tended to be associated with progression at 2yrs. An increase in RAMRIS bone erosion score >0.5 at wk 24 significantly predicted x-ray progression at 1- & 2 yrs. BL & wk12 changes in MRI scores all significantly predicted x-ray progression at wk52 (all p Conclusions Early MRI measures at 12 & 24 wks independently predict x-ray changes at 1 & 2 yrs of follow-up. These data support the use of MRI in clinical trials for early identification of pts with (OR who will develop) structural joint damage progression during follow-up. This has implications for clinical trial design. References Ostergaard M, Emery P, Conaghan PG, et al. Arthritis Rheum 2011; 63(12): 3712-3722. Disclosure of Interest J. Baker Grant/research support from: Janssen R&D, LLC, M. Ostergaard Grant/research support from: Janssen R&D, LLC, P. Emery Grant/research support from: Janssen R&D, LLC, E. Hsia Employee of: Janssen R&D, LLC, J. D. Lu Employee of: Janssen R&D, LLC, D. Baker Employee of: Janssen R&D, LLC, P. G. Conaghan Grant/research support from: Janssen R&D, LLC

AIM To determine the scope of acute hypoglycemic effects for certain anti-rheumatic medications in a large retrospective observational study. METHODS Patients enrolled in the Veterans Affairs Rheumatoid Arthritis (VARA) registry were selected who, during follow-up, initiated treatment with tumor necrosis factor inhibitors (TNFi’s, including etanercept, adalimumab, infliximab, golimumab, or certolizumab), prednisone, or conventional disease-modifying anti-rheumatic drugs (DMARDs), and for whom proximate random blood glucose (RBG) measurements were available within a window 2-wk prior to, and 6 mo following, medication initiation. Similar data were obtained for patients with proximate values available for glycosylated hemoglobin A1C values within a window 2 mo preceding, and 12 mo following, medication initiation. RBG and A1C measurements were compared before and after initiation events using paired t-tests, and multivariate regression analysis was performed including established comorbidities and demographics. RESULTS Two thousands one hundred and eleven patients contributed at least one proximate measurement surrounding the initiation of any examined medication. A significant decrease in RBG was noted surrounding 653 individual hydroxychloroquine-initiation events (-3.68 mg/dL, P = 0.04), while an increase was noted for RBG surrounding 665 prednisone-initiation events (+5.85 mg/dL, P < 0.01). A statistically significant decrease in A1C was noted for sulfasalazine initiation, as measured by 49 individual initiation events (-0.70%, P < 0.01). Multivariate regression analyses, using methotrexate as the referent, suggest sulfasalazine (β = -0.58, P = 0.01) and hydroxychloroquine (β = -5.78, P = 0.01) use as predictors of lower post-medication-initiation RBG and A1C values, respectively. Analysis by drug class suggested prednisone (or glucocorticoids) as predictive of higher medication-initiation event RBG among all start events as compared to DMARDs, while this analysis did not show any drug class-level effect for TNFi. A diagnosis of congestive heart failure (β = 4.69, P = 0.03) was predictive for higher post-initiation RBG values among all medication-initiation events. CONCLUSION No statistically significant hypoglycemic effects surrounding TNFi initiation were observed in this large cohort. Sulfasalazine and hydroxychloroquine may have epidemiologically significant acute hypoglycemic effects.