title: In prehypertension leukocytosis is associated with body mass index but not with blood pressure or incident hypertension.
abstract: BACKGROUND
  Previous studies reported increased white blood cell counts (WBCCs), an inflammatory marker, in hypertension, prehypertension and metabolic syndrome. Evidence suggests that inflammation precedes blood pressure (BP) elevation and may contribute to incident hypertension. Angiotensin receptor blockers (ARBs) may reduce inflammation. We analyzed WBCC trends in TRial Of Preventing HYpertension (TROPHY) to determine if this inflammatory marker predicted incident hypertension in prehypertensive individuals and whether randomized assignment to the ARB candesartan (391 individuals) for 2 years, lowered WBCC compared with placebo-treated controls (381 individuals).
  
  
  METHODS
  A new analysis of TROPHY trial data.
  
  
  RESULTS
  In the total population, baseline BMI correlated with WBCC (r = 0.185, P < 0.0001), neutrophils (r = 0.135, P < 0.001) and lymphocytes (r = 0.204, P < 0.0001). Baseline triglycerides also correlated significantly with inflammatory markers. Despite a wide range of home BP (HBP) values, HBP did not correlate with baseline WBCC counts. After 2 years, candesartan decreased placebo corrected HBP by -5.5/-2.5 mmHg, (P < 0.0001), but WBCC, neutrophil and lymphocyte counts were not different in placebo and in candesartan groups. Baseline WBCC, neutrophils and lymphocyte counts did not predict incident hypertension in the placebo group.
  
  
  CONCLUSIONS
  In TROPHY, candesartan lowered BP but did not alter WBCC. Baseline WBCC did not predict incident hypertension. Our findings do not support the hypothesis that inflammation contributes to incident hypertension or that ARB treatment suppresses inflammation. The significant independent association of WBCC with baseline BMI and triglycerides is consistent with the evidence that obesity and insulin resistance are associated with inflammation. The findings highlight the importance of effective lifestyle modification in prehypertension to reduce inflammatory cardio-metabolic risk and suppress transition to hypertension.
authors.affiliation: aDivision of Cardiovascular Medicine, University of Michigan, Ann Arbor, Michigan bDepartment of Medicine, Medical University of South Carolina, Charleston, South Carolina cCenter for Human Growth and Development, University of Michigan, Ann Arbor, Michigan dDepartmentof Internal Medicine, University of Texas Southwestern, Dallas, Texas eDivision of Cardiovascular Disease, Scripps Clinic, La Jolla, California, USA.
authors.forename: Stevo
authors.initials: S
authors.lastname: Julius
authors.forename: Brent M
authors.initials: BM
authors.lastname: Egan
authors.forename: Niko A
authors.initials: NA
authors.lastname: Kaciroti
authors.forename: Shawna D
authors.initials: SD
authors.lastname: Nesbitt
authors.forename: Andrew K
authors.initials: AK
authors.lastname: Chen
mesh_terms: D000328:Adult; D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use; D001562:Benzimidazoles / Q000627:therapeutic use; D001713:Biphenyl Compounds; D001794:Blood Pressure; D015992:Body Mass Index; D004311:Double-Blind Method; D005260:Female; D006801:Humans; D006973:Hypertension / Q000209:etiology / Q000517:prevention & control*; D007249:Inflammation / Q000150:complications / Q000188:drug therapy; D007958:Leukocyte Count; D007964:Leukocytosis / Q000150:complications* / Q000188:drug therapy; D008297:Male; D008875:Middle Aged; D058246:Prehypertension / Q000150:complications* / Q000188:drug therapy; D012307:Risk Factors; D013777:Tetrazoles / Q000627:therapeutic use
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D001562:Benzimidazoles; D001713:Biphenyl Compounds; D013777:Tetrazoles; C081643:candesartan