The Clinical Study Of Metabolic Syndrome In Systemic Lupus Erythematosus

ObjectivesTo investigate the prevalence of Metabolic Syndrome (MS) in SLE patients and its risk factors.In addition, we explore the mechanism of MS by evaluating insulin resistance and beta celldysfunction in SLE.Subjects and methods1. A total of187hospitalized patients admitted to the Department of Rheumatology andImmunology, Shenzhen’s Hospital were enrolled in the study, excluding those withpregnancy, infection or organ failure. All patients fulfilled the American College ofRheumatology (ACR)1997revised classification criteria for SLE. One hundred and sixtyfive healthy people were recruited from health check-up center of our hospital as controlgroup with age and gender well matched. Case control study was performed to explore therisk factors for MS in SLE patients.2. MS was defined according to the IDF/NHBIL/AHA/WHF/IAS/IASO Joint ScientificStatement definition of Chinese people. The prevalence of MS for SLE patients as well ascontrol group was calculated, respectively. Data were collected from case files, includinginflammation biomarker, SLEDAI, uric acid, homocysteine, organ lesion, cumulative dosageof prednisone, current dosage of prednisone, the use of hydroxychloroquine, etc.Comparison was made between SLE patients with and without MS.3. Among the187patients and165healthy people,87SLE patients and30non-SLE subjectsunderwent OGTT test. The insulin sensitivity in fasting state was assessed by homeostasismodel assessment of insulin resistance (HOMA-IR). Matsuda index (M-SI) was calculatedto evaluate insulin sensitivity after glucose loading. Homeostasis model assessment of isletbeta cell function (HOMA-β) was used to assess beta cell function in fasting state. Early andlate insulin secretion (EISI and LISI) were calculated to evaluate islet beta cell function afterglucose loading. Furthermore, risk factors for insulin sensitivity and beta cell function in SLE patients were analyzed.Results1. The prevalence of MS was much higher in SLE patients than that in control group (34.76%vs14.54%, P<0.05). The prevalence of MS for young people (≦40age old) in SLE patients(27.93%) was5.09times than that in control group (5.49%). The average waistcircumference, triglyceridemia and the lower high-density lipoprotein in SLE patients wereall significantly higher than that in controls (P <0.05). While, the total cholesterol level inSLE patients is significantly lower than that in control group (P <0.05).2. SLE patients with intercurrent MS presented a higher average-age, regarding duration ofdisease, body mass index, waist circumference, systolic blood pressure, diastolic bloodpressure, fasting blood-glucose, total choleserol, triglyceridemia compare with SLE patientswithout intercurrent MS (P <0.05).3. Regression analysis demonstrated that age, body mass index, renal involvement, homo-cysteine and uric acid were independent risk factors for MS in SLE, whilehydroxychloroquine is a protective factor for MS in SLE.4. Compared with normal control group, HOMA-IR, HOMA-β, EISI and LISI of SLE patientswere significantly higher. But no significant difference was observed in M-SI between thetwo groups. Compared with normal control group, HOMA-IR, HOMA-β, EISI and LISI ofSLE patients with glucocorticoids treatment were significantly higher. But no significantdifference was observed in M-SI between the two groups. Compared with normal controlgroup, HOMA-IR, HOMA-β, EISI and LISI of newly diagnosed SLE patients withoutglucocorticoids treatment were significantly higher, while difference of M-SI was notsignificant. Compared with newly diagnosed SLE patients without glucocorticoids treatment,HOMA-IR, HOMA-β, EISI, LISI and M-SI were not significantly different from SLEpatients with glucocorticoids treatment.5. HsCRP, SLEDAI and total glucocorticoids doses were risk of factors for HOMA-IR. HsCRPwere risk of factors for LISI.Conclusions1. There was a higher frequency of MS in SLE patients. 2. Hydroxychloroquine may be a protective factor against MS in SLE.3. Age, body mass index, homocysteine and uric acid were the risk factors for MS in SLE.4. Compared with normal control group, the insulin sensitivity of SLE patients withglucocorticoid treatment and newly diagnosed SLE patients without glucocorticoidstreatment were lower. While their beta cell function was bader than that of the controlgroup.5. HsCRP, SLEDAI and the total of glucocorticoids doses were independent risk factors forinsulin resistance in fasting state. HsCRP was independent risk factors for beta celldysfunction after glucose loading.6. High insulin resistence prevalence was found in SLE patients, Which may be one of mainmechanism for of MS in SLE patients.