Publications by authors named "Inger L Meek"

Objective: Gout and diabetes mellitus type 2 (DM) frequently co-exist. The pharmacological effects of metformin may include anti-inflammatory and urate lowering effects. The objective of this study was to test these effects in patients with gout starting uric acid lowering treatment (ULT) in secondary care.

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Background: Rheumatoid arthritis (RA) patients have an increased cardiovascular (CV) risk. Here, we aimed to investigate whether gender and age are contributing to the misclassification of CV risk in RA patients.

Methods: Prospectively collected data on cardiovascular risk factors and incident events from the Nijmegen inception cohort were analyzed, with up to 10 years follow-up.

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Objective: Tumor necrosis factor inhibitor (TNFi) biologic agents are an effective treatment for rheumatoid arthritis (RA). It is unclear whether patients whose disease is in remission or who have stable low disease activity need to continue use of TNFi or can stop this treatment. This study was undertaken to assess whether patients with established RA who are in remission or have stable low disease activity can effectively and safely stop their TNFi therapy.

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Article Synopsis
  • Systemic sclerosis is a rare disease where the body’s immune system attacks its own tissues, causing issues in the skin and organs.
  • It can lead to serious problems like lung, kidney, heart, and blood pressure issues that can be very dangerous.
  • Getting early treatment with special medications can help stop the disease from getting worse and make people healthier.
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Background: Gout and hyperuricaemia may be associated with increased cardiovascular risk, but analyses in different populations show conflicting results. This study investigates the impact of serum uric acid, inflammation and traditional CV risk parameters on CV event risk in patients with gouty arthritis and patients with non-gouty rheumatic disease.

Methods: cross-sectional and prospective multivariate analysis of the relation between tertiles of serum uric acid and individual traditional CV risk factors in a cohort of gouty arthritis (GA, n=172), rheumatoid arthritis (RA, n=480) and osteoarthritis (OA, n=206) patients.

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Background: Previous studies found increased case fatality after myocardial infarction and more frequent sudden death in RA patients compared to non-RA subjects. The RA associated CV risk might be explained by the combined effects of chronic systemic inflammation and increased lifestyle associated cardiovascular risk factors, and modified by the use of medication such as non steroidal anti-inflammatory drugs, corticosteroids and disease modifying anti-rheumatic drugs. Trends in case fatality rate in RA after the introduction of potent anti-inflammatory biologic therapies and treat-to-target treatment strategies aiming at remission are not known.

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A 65-year-old woman had an eschar after a holiday to Spain. A skin biopsy showed findings consistent with an ulcer but tested negative for fungi, atypical mycobacteria and Leishmania parasites. Rickettsia conorii serology was negative.

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Objectives: To study the prevalence of cardiovascular risk factors among patients attending a rheumatology outpatient clinic in comparison with the general population.

Methods: Cross-sectional comparison between a rheumatic outpatient cohort of consecutive patients (n = 1233) between 36 and 75 years of age attending the Arthritis Center Twente (ACT) in the year 2009: RA (n = 546), gout (n = 129), OA (n = 168), CTD (n = 85), PMR (n = 91) and chronic localized or generalized pain syndromes (CPSs; n = 214) and a random sample from a long-lasting population-based health study in the Netherlands (n = 4523). The main outcome measures were hypertension (systolic blood pressure ≥ 140 mmHg and/or a diastolic blood pressure ≥ 90 mmHg and/or the use of antihypertensive medication), abnormal cholesterol profile (total cholesterol ≥ 6.

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While aspirin may offer protection, other non-aspirin non-steroidal anti-inflammatory drugs (NSAIDs) can cause serious cardiovascular side effects and complications. This has led to a general "black box" warning for cardiovascular adverse events for NSAIDs. This review explores the different mechanisms underlying the protective effects of aspirin, the NSAID associated renovascular effects causing hypertension, edema and heart failure, the cardiovascular effects causing myocardial infarction and stroke, and the possible deleterious interaction between NSAIDs and aspirin.

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