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Volume 4, Number 2, June 2007
Insulin resistance is an independent risk factor for atherosclerosis in rheumatoid
arthritis
Giovanni La Montagna, Federico Cacciapuoti, Rosario Buono, Daniela Manzella,
Gianna Angela Mennillo, Alessandro Arciello, Gabriele Valentini, Giuseppe Paolisso
The objective of this study was to investigate the relationship
between insulin resistance (IR) and subclinical
atherosclerosis in patients with rheumatoid
arthritis (RA).
Carotid artery intima media thickness (IMT), using
ultrasound evaluation, and other clinical and laboratory
variables were investigated in 45 RA outpatients and in
48 controls with soft tissue disorders. IR was assayed by
homeostasis model assessment (HOMA2) and metabolic
syndrome by National Cholesterol Education Program
Adult Treatment Panel (NCEP ATP III) criteria.
Insulin resistance, as defined by HOMA2-IR>1, was
seen in 40 (88.9%) RA patients and in three (6.2%) controls
(p<0.001). No significant difference was detected in
the prevalence of metabolic syndrome. The median IMT
was greater in RA patients (0.76 mm; interquartile range
[IQR] 0.65, 0.85) than in the controls (0.66 mm; IQR
0.60, 0.72) (p<0.001). Dividing the RA patients according
to the cut-off IMT value (0.72 mm), a difference was
detected in both systolic (p=0.04) and diastolic blood
pressure (p=0.02), disease activity score (DAS28)
(p=0.008), HOMA2-IR (p<0.001) and cumulative oral
steroid dose (p=0.001). Moreover, the frequency of cases
with increased IMT was higher in glucocorticoid users
than in non-users (21/23 vs. 9/22, respectively)
(p<0.001). Spearman’s rho correlation showed a significant
positive relationship between IMT and HOMA2-IR
(p<0.001). Multivariate stepwise analysis selected
HOMA2-IR plus diastolic BP plus glucocorticoid exposure
as the best predictive model for subclinical atherosclerosis
(R2c=0.577, F=21, p<0.001).
In conclusion, this study showed a significantly higher
prevalence of IR in RA patients and pointed out a significant
association between IR and subclinical atherosclerosis.
This relationship may be driven primarily by exposure
to steroid therapy. Diabetes Vasc Dis Res 2007;4:130-135. View full PDF article (open in new window)
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