Cited by 218Rheumatoid Arthritis Research and TherapiesDiabetes, Cardiovascular Risks, and LipoproteinsAdipokines, Inflammation, and Metabolic Diseases

Insulin resistance and impaired beta cell function in rheumatoid arthritis

Dessein, Patrick H., Joffe, Barry I.·2006·Arthritis & Rheumatism

Abstract

Objective: To identify factors that regulate glucose metabolism in rheumatoid arthritis (RA). Methods: We evaluated the homeostatic model assessment of insulin resistance (HOMA‐IR) and beta cell function (HOMA‐B) in 94 RA patients. We investigated the relationship between characteristics known to affect glucose metabolism in the general population (age, abdominal obesity [waist circumference], hypertension, antihypertensive therapy) as well as characteristics of RA (disease activity, glucocorticoid therapy) and insulin resistance and beta cell function. Results: Patients with high‐grade inflammation (high‐sensitivity C‐reactive protein value >1.92 mg/liter) (n = 81) were more insulin resistant than patients with low‐grade inflammation (n = 13), whereas beta cell function was similar in both groups. Insulin resistance and beta cell function were similar in both groups after adjustment for waist circumference. All recorded characteristics except for age were associated with HOMA‐IR or/and HOMA‐B in univariate analyses. In mixed regression models, abdominal obesity and patient's assessment of disease activity (by visual analog scale) were predictors of insulin resistance. The Disease Activity Score assessed using 28‐joint counts for swelling and tenderness, tender joint count, and patient's assessment of disease activity were associated with reduced beta cell function, and the cumulative dose of glucocorticoids was associated with enhanced beta cell function. The cumulative glucocorticoid dose in all study patients was a mean of only 536 mg (95% confidence interval 239–1,173). In patients with high‐grade inflammation, age was further associated with impaired beta cell function, whereas use of angiotensin‐converting enzyme inhibitors or angiotensin II type 1 receptor blockers was associated with enhanced beta cell function. Conclusion: The modifiable factors of abdominal obesity, antihypertensive therapy, disease activity, and use of glucocorticoids appear to affect glucose metabolism in RA.

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Crossref · 10.1002/art.22053

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Authors
Dessein, P. H., & Joffe, B. I.
Affiliations
University of the Witwatersrand (ZA)
Venue
Arthritis & Rheumatism
Publisher
Wiley
Published
2006-08-31
Volume
54
Issue
9
Pages
2765-2775
ISSN
  • 0004-3591 (ISSN-L)
  • 1529-0131
OpenAlex
W2061390926
Cited by
218
References
50
Citations by year
2026: 5 · 2025: 6 · 2024: 7 · 2023: 3 · 2022: 9 · 2021: 9 · 2020: 7 · 2019: 10 · 2018: 15 · 2017: 9 · 2016: 14 · 2015: 15 · 2014: 17 · 2013: 20 · 2012: 13
FWCI
6.28
Type
journal article
Language
en
Open access
closed
Locations
  • Arthritis & Rheumatism (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Keywords
rheumatoid arthritis, insulin resistance, beta-cell function, glucose metabolism, disease activity, C-reactive protein, abdominal obesity, glucocorticoid therapy, ACE inhibitors, angiotensin receptor blockers, antihypertensive therapy
MeSH terms
Arthritis, Rheumatoid, Blood Glucose, Blood Pressure, C-Reactive Protein, Diabetes Mellitus, Female, Homeostasis, Humans, Inflammation, Insulin Resistance, Islets of Langerhans, Male, Middle Aged, Models, Biological, Obesity, Body Mass Index, Body Size

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