title: C-reactive protein and tumor necrosis factor-alpha in gestational hyperglycemia.
abstract: OBJECTIVE
  Increasing evidences support an inflammatory origin for gestational hyperglycemia. This paper aims at investigating, cross-sectionally and prospectively, the relationships between tumor necrosis factor-alpha (TNF-alpha) and C-reactive protein (CRP) levels in normoglycemic and hyperglycemic pregnancies of women with and without conventional risk factors for gestational diabetes (GDM).
  
  
  RESULTS
  Both at simple and multiple correlations TNF-alpha levels are associated to fasting insulin, homeostasis model assessment-insulin resistance (HOMA-IR) values and gestational hyperglycemia, while high sensitivity CRP (hsCRP) levels to body mass index (BMI). Furthermore, the TNF-alpha levels of the second trimester and their increments in the third trimester are significant predictors of insulin levels measured at 32-36 weeks in the subgroup of hyperglycemic women with < or = 35 yr, BMI <25 kg/m2 and the absence of a first-degree relative with Type 2 diabetes (respectively, beta=1.1; 95%CI 0.66-1.48; p=0.002 and beta=1.0; 95%CI 0.36-1.66; p=0.02), in a multiple regression model, after multiple adjustments. In a second cohort of women at low risk for GDM (<25 yr, BMI <25 kg/m2 and absence of a first-degree relative with Type 2 diabetes), 24-28 weeks TNF-alpha levels are highly associated with corresponding insulin and HOMA values in the same model (respectively, beta=0.27; 95%CI 0.11-0.43; p=0.001 and beta=0.30; 95%CI 0.14-0.46; p<0.001).
  
  
  CONCLUSIONS
  The data support the developing hypothesis that low-grade systemic inflammation is associated to GDM, in particular for pregnant women without conventional risk factors for gestational hyperglycemia, whose insulin resistance seems less explainable.
authors.affiliation: Department of Internal Medicine, University of Turin, Italy. sbo@molinette.piemonte.it
authors.forename: S
authors.initials: S
authors.lastname: Bo
authors.forename: A
authors.initials: A
authors.lastname: Signorile
authors.forename: G
authors.initials: G
authors.lastname: Menato
authors.forename: R
authors.initials: R
authors.lastname: Gambino
authors.forename: C
authors.initials: C
authors.lastname: Bardelli
authors.forename: M L
authors.initials: ML
authors.lastname: Gallo
authors.forename: M
authors.initials: M
authors.lastname: Cassader
authors.forename: M
authors.initials: M
authors.lastname: Massobrio
authors.forename: G F
authors.initials: GF
authors.lastname: Pagano
mesh_terms: D000328:Adult; D015992:Body Mass Index; D002097:C-Reactive Protein / Q000378:metabolism*; D003430:Cross-Sectional Studies; D003924:Diabetes Mellitus, Type 2 / Q000235:genetics; D016640:Diabetes, Gestational / Q000209:etiology; D005260:Female; D006801:Humans; D006943:Hyperglycemia / Q000097:blood*; D007249:Inflammation / Q000378:metabolism; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D010375:Pedigree; D011237:Predictive Value of Tests; D011247:Pregnancy; D011248:Pregnancy Complications / Q000097:blood*; D011262:Pregnancy Trimester, Second; D011263:Pregnancy Trimester, Third; D011446:Prospective Studies; D012016:Reference Values; D012044:Regression Analysis; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
chemical_list: D007328:Insulin; C439524:TNF protein, human; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein