Abstract
ObjectivesTo evaluate the correlation between inflammatory measures and whole-body insulin sensitivity in psoriatic arthritis (PsA) patients.MethodsFor the present study, 40 nondiabetic PsA patients were recruited. A standard oral glucose tolerance test (OGTT) was performed. The insulin sensitivity index (ISI), insulinogenic index (IGI) and oral disposition index (ODI) were calculated from dynamic values of glucose and insulin obtained during OGTT.ResultsIn our study population, mean ISI was 3.5 ± 2.5, median IGI was 1.2 (0.7–1.8), mean ODI 4.5 ± 4.5. In univariate correlation analysis, ISI correlated inversely with systolic blood pressure (sBP) (R = -0.52, p = 0.001), diastolic blood pressure (dBP) (R = -0.45, p = 0.004) and complement C3 (R = -0.43, p = 0.006) and ODI correlated inversely with sBP (R = -0.38, p = 0.02), dBP (R = -0.35, p = 0.03) and complement C3 (R = -0.37, p = 0.02). No significant correlations were found between analyzed variables and IGI. In a stepwise multiple regression, only complement C3 entered in the regression equation and accounted for approximately 50% of the variance of ISI. Using a receiver operating characteristic (ROC) curve we identified the best cut-off for complement C3 of 1.32 g/L that yielded a sensitivity of 56% and a specificity of 96% for classification of insulin resistant patients.ConclusionsIn conclusion, our data suggest that serum complement C3 could represent a useful marker of whole-body insulin sensitivity in PsA patients.
Highlights
Skin psoriasis (Pso) and psoriatic arthritis (PsA) are inflammatory diseases characterized by an increased risk of major cardiovascular events [1]
Using a receiver operating characteristic (ROC) curve we identified the best cut-off for complement C3 of 1.32 g/L that yielded a sensitivity of 56% and a specificity of 96% for classification of insulin resistant patients
Our data suggest that serum complement C3 could represent a useful marker of whole-body insulin sensitivity in PsA patients
Summary
Skin psoriasis (Pso) and psoriatic arthritis (PsA) are inflammatory diseases characterized by an increased risk of major cardiovascular events [1]. Among conventional cardiovascular disease (CVD) risk factors, type 2 diabetes mellitus (T2DM) plays a major role [2]. Glucose homeostasis abnormalities have been considered for a long time a peculiarity of rheumatoid arthritis (RA) [3, 4], but a recent large-scale UK study demonstrated that the risk of incident T2DM in PsA and Pso could be even higher to that conferred by RA [5]; a recent work confirmed that abnormal metabolic status is more prevalent in PsA than RA [6]. Metabolic syndrome (MS), a condition characterized by the clustering of different CVD risk factors (including glucose disturbances, visceral adiposity, elevated blood pressure, and abnormal lipid profile), is highly prevalent among patients with Pso [7] and PsA [8]. The so-called “inflammatory” hypothesis is supported by the evidence that disease-modifying antirheumatic drugs (DMARDs) [13] and biologic agents [14,15,16,17,18] have been demonstrated to improve insulin sensitivity in inflammatory arthritis patients
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