The high disease activity is associated with derangements in glucose metabolism.
There is a significant increase in the short-term risk of type 2 diabetes mellitus in patients who have rheumatoid arthritis, a study found. The high disease activity is associated with derangements in glucose metabolism.
Although rheumatoid arthritis is known to be an inflammatory autoimmune disease that affects joints, the condition is also associated with important comorbidities, Piero Ruscitti and colleagues in Italy noted. They pointed out that a significant number of patients with rheumatoid arthritis are affected by type 2 diabetes and that cardiometabolic comorbidity remains underdiagnosed and undertreated in these patients.
Studies suggest that certain proinflammatory mediators, such as tumor necrosis factor and interleukin-1Î², may be shared between rheumatoid arthritis and type 2 diabetes.
The researchers presented the results of their prospective investigation into the relationship between cardiovascular risk factors, rheumatoid arthritis risk factors, and new-onset type 2 diabetes in a recent PLoS ONE article.
The authors conducted a longitudinal observational cohort study to determine the risk of type 2 diabetes in patients with rheumatoid arthritis; 439 consecutive patients were included.
Type 2 diabetes predictors
• Type 2 diabetes developed in 7.1% of subjects (31/439).
• The combination of high blood pressure, impaired fasting glucose, and high disease activity scores in 28 joints with erythrocyte sedimentation rate (DAS28[ESR]) proved to significantly increase the risk of type 2 diabetes by logistic regression (x2=79.32, p<0.0001).
• High blood pressure conferred 6.83 times the risk of type 2 diabetes (odds ratio [OR], 6.83; 95% confidence interval [CI], 2.18-21.34, p=0.001).
• For patients who did not see reductions in their disease activity score in 28 joints at month 12, a 75.22-fold higher risk of type 2 diabetes was found (OR, 75.22; 95% CI, 23.33–242.72, p<0.0001).
• Impaired fasting glucose and poor disease activity scores in 28 joints increased the risk of type 2 diabetes in patients with rheumatoid arthritis by 30.55 times and 33.598 times, respectively (OR, 30.55; 95% CI, 6.53–142.76, p < 0.0001 and OR, 33.59; 95% CI, 6.95–162.21, p < 0.0001, respectively).
• No association was found between treatment with corticosteroids and development of type 2 diabetes (OR, 3.22; 95% CI, 0.58–17.95, p = 0.18).
• Higher DAS28(ESR) correlated with increased likelihood of type 2 diabetes with the area under the receiver operator characteristic curve being 0.79 (95% CI, 0.63–0.79, p < 0.0001) and sensitivity and specificity of 80% and 63%, respectively, for disease activity scores over 3.71.
Impaired fasting glucose predictors
• While not meeting criteria for type 2 diabetes, 7.7% of patients displayed impaired fasting glucose.
• High blood pressure conferred 5.71 times the risk of impaired fasting glucose (OR, 5.71; 95% CI, 1.40–23.27, p = 0.015).
• Unexpectedly, having a body mass index >30 kg/m2 was not associated with impaired fasting glucose.
• Higher DAS28(ESR) correlated with increased likelihood of developing type 2 diabetes with the area under the receiver operator characteristic curve being 0.71 (95% CI, 0.64–0.77, p < 0.0001) and sensitivity and specificity of 91% and 51%, respectively, for disease activity scores over 3.30.
Implications for physicians
• There is an increased prevalence of type 2 diabetes in patients with rheumatoid arthritis over the general population.
• Patients with rheumatoid arthritis patients who have high blood pressure or high DAS28(ESR) are at higher risk for both impaired fasting glucose and development of type 2 diabetes.
• DAS28(ESR) over 3.30 predicted increased risk of impaired fasting glucose. Similar scores over 3.71 predicted the development of type 2 diabetes in patients with rheumatoid arthritis.
Ruscitti P, Ursini F, Cipriani P, et al. “Poor clinical response in rheumatoid arthritis is the main risk factor for diabetes development in the short-term: a 1-year, single-centre, longitudinal study.” PLoS One. 2017;12:e0181203. doi: 10.1371/journal.pone.0181203. eCollection 2017.