title: Insulin resistance in systemic lupus erythematosus patients: contributing factors and relationship with subclinical atherosclerosis.
abstract: OBJECTIVE
  Insulin resistance (IR) plays a role in the increased cardiovascular risk of systemic lupus erythematosus (SLE) patients. This study aimed to determine the potential association of IR with disease activity, drug exposure and subclinical atherosclerosis in patients with SLE.
  
  
  METHODS
  This cross-sectional study encompassed 87 non-diabetic SLE patients and 82 sex-matched controls. Insulin and C-peptide serum levels, IR indexes by homeostatic model assessment (HOMA2) (both insulin-based: HOMA2-IR, and with C-peptide: HOMA2-IR-C-peptide) and lipid profiles were assessed in patients and controls. Activity (SLEDAI), severity (Katz) and damage (SLICC) index scores, as well as carotid intima-media thickness (cIMT) and carotid plaques, were determined in SLE patients. A multivariable regression analysis, adjusted for classic IR related factors, was performed to evaluate the differences in IR indexes between patients and controls and how IR is associated with disease-related characteristics, including carotid ultrasound results, in SLE patients.
  
  
  RESULTS
  SLE patients had higher C-peptide serum levels (2.61±1.51 vs. 1.34±0.62 ng/ml, p=0.00) and elevated HOMA2-IRC-peptide index (1.90±1.12 vs. 0.97±0.45, p=0.00) than controls. These differences remained statistically significant after adjusting for classic cardiovascular risk factors and prednisone intake. Traditional IR-related factors, such as body mass index, waist circumference or hypertension, and prednisone intake were significantly associated with HOMA2-IR and HOMA2-IRC-peptide in SLE patients. SLICC damage index was independently associated with HOMA2-IR-C-peptide. The presence of carotid plaques and cIMT values were associated with IR indexes in SLE patients only in the univariate analysis.
  
  
  CONCLUSIONS
  C-peptide serum levels are independently up-regulated in SLE patients. Although classic IR factors and prednisone are associated with IR, SLE damage over time also contributes to IR in an independent way.
authors.affiliation: Division of Rheumatology, Hospital Universitario de Canarias, Tenerife, Spain.
authors.forename: Hiurma
authors.initials: H
authors.lastname: Sánchez-Pérez
authors.affiliation: Division of Rheumatology, Hospital Universitario de Canarias, Tenerife, Spain.
authors.forename: Beatriz
authors.initials: B
authors.lastname: Tejera-Segura
authors.affiliation: Central Laboratory Division, Hospital Universitario de Canarias, Tenerife, Spain.
authors.forename: Antonia
authors.initials: A
authors.lastname: de Vera-González
authors.affiliation: Central Laboratory Division, Hospital Universitario de Canarias, Tenerife, Spain.
authors.forename: Alejandra
authors.initials: A
authors.lastname: González-Delgado
authors.affiliation: Division of Internal Medicine, Hospital Universitario Marqués de Valdecilla-IDIVAL, Universidad de Cantabria, RETICEF; and School of Medicine, University of Cantabria, Santander, Spain.
authors.forename: José Manuel
authors.initials: JM
authors.lastname: Olmos
authors.affiliation: Division of Internal Medicine, Hospital Universitario Marqués de Valdecilla-IDIVAL, Universidad de Cantabria, RETICEF; and School of Medicine, University of Cantabria, Santander, Spain.
authors.forename: José Luis
authors.initials: JL
authors.lastname: Hernández
authors.affiliation: Div. of Rheumatology, Hosp.Univ. Marqués de Valdecilla, IDIVAL, School of Medicine, Univ.of Cantabria; and Epidemiology, Genetics and Atherosclerosis Res. Group on Systemic Inflammatory Diseases, Hosp.Univ. Marqués de Valdecilla, IDIVAL, Santander, Spain.
authors.forename: Alfonso
authors.initials: A
authors.lastname: Corrales
authors.affiliation: Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Hospital Universitario Marqués de Valdecilla, IDIVAL, Santander, Spain.
authors.forename: Raquel
authors.initials: R
authors.lastname: López-Mejías
authors.affiliation: Division of Rheumatology, Hosp. Universitario Marqués de Valdecilla, IDIVAL, School of Medicine, University of Cantabria, Santander, Spain; and Cardiovascular Pathophysiology & Genomics Research Unit, Univ.of the Witwatersrand, Johannesburg, South Africa.
authors.forename: Miguel Angel
authors.initials: MA
authors.lastname: González-Gay
authors.affiliation: Division of Rheumatology, Hospital Universitario de Canarias, Tenerife, Spain. iferrazamaro@hotmail.com.
authors.forename: Iván
authors.initials: I
authors.lastname: Ferraz-Amaro
mesh_terms: D000328:Adult; D000368:Aged; D050197:Atherosclerosis / Q000209:etiology*; D002096:C-Peptide / Q000097:blood; D002318:Cardiovascular Diseases / Q000209:etiology; D059168:Carotid Intima-Media Thickness; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D007333:Insulin Resistance; D008180:Lupus Erythematosus, Systemic / Q000097:blood / Q000150:complications*; D008297:Male; D008875:Middle Aged; D011241:Prednisone / Q000627:therapeutic use
chemical_list: D002096:C-Peptide; D011241:Prednisone