title: Longitudinal evolution of HIV-1-associated lipodystrophy is correlated to serum cortisol:DHEA ratio and IFN-alpha.
abstract: BACKGROUND
  We have previously shown that lipid alterations in HIV-1-associated lipodystrophy (LD) are correlated with decreased serum dehydroepiandosterone (DHEA) and increased cortisol:DHEA ratio and IFN-alpha levels.
  
  
  OBJECTIVE
  To evaluate in a longitudinal study whether steroid and cytokine modifications are associated with the evolution of physical changes and lipid alterations associated with LD.
  
  
  METHODS
  Thirty-four HIV-1-positive men were followed during 32.5 +/- 4.0 months and tested at four time-points. The patients were subdivided into five groups according to physical changes and anthropometric measurements: LD-negative, initially LD-negative becoming LD-positive, LD-positive unchanged, aggravated or improved. Serum lipids, apolipoproteins, adrenal steroids and cytokines were measured and compared with baseline values.
  
  
  RESULTS
  (1) LD aggravation is associated with persistent elevated lipids, a decrease in serum DHEA, an increase in cortisol:DHEA ratio and persistent high levels of IFN-alpha. (2) LD improvement is associated with normalization of serum lipids, an increase in serum DHEA leading to normalization in cortisol:DHEA ratio, and normalization of IFN-alpha levels. (3) In LD-positive men evolution of VLDL cholesterol is negatively correlated with DHEA (r = -0.56, P < 0.01) and positively with cortisol:DHEA ratio (r = 0.62, P < 0.004) and with IFN-alpha (r = 0.57, P < 0.01). (4) The switch to LD is associated with a decrease in serum DHEA. (5) Patients who remained LD-negative maintained normal lipids, elevated cortisol and DHEA, and normal cortisol:DHEA ratio and normal levels of IFN-alpha.
  
  
  CONCLUSIONS
  This study indicates that cortisol:DHEA ratio and serum IFN-alpha levels are closely associated with clinical evolution and atherogenic lipid alterations in LD.
authors.affiliation: Institut Pasteur, Hôpital Raymond Poincaré, Garches, CHU Bichat Claude Bernard, Paris Cedex, France.
authors.forename: N
authors.initials: N
authors.lastname: Christeff
authors.forename: P
authors.initials: P
authors.lastname: De Truchis
authors.forename: J-C
authors.initials: JC
authors.lastname: Melchior
authors.forename: C
authors.initials: C
authors.lastname: Perronne
authors.forename: M-L
authors.initials: ML
authors.lastname: Gougeon
mesh_terms: D000328:Adult; D023241:Antiretroviral Therapy, Highly Active; D016632:Apolipoprotein A-I / Q000032:analysis; D001055:Apolipoproteins B / Q000032:analysis; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D015243:Cholesterol, VLDL / Q000097:blood; D003687:Dehydroepiandrosterone / Q000097:blood*; D018450:Disease Progression; D015658:HIV Infections / Q000097:blood / Q000188:drug therapy; D015497:HIV-1; D039682:HIV-Associated Lipodystrophy Syndrome / Q000097:blood / Q000209:etiology*; D006801:Humans; D006854:Hydrocortisone / Q000097:blood*; D007328:Insulin / Q000097:blood; D016898:Interferon-alpha / Q000097:blood; D008137:Longitudinal Studies; D008297:Male; D018709:Statistics, Nonparametric; D014280:Triglycerides / Q000097:blood
chemical_list: D016632:Apolipoprotein A-I; D001055:Apolipoproteins B; D008076:Cholesterol, HDL; D015243:Cholesterol, VLDL; D007328:Insulin; D016898:Interferon-alpha; D014280:Triglycerides; D003687:Dehydroepiandrosterone; D002784:Cholesterol; D006854:Hydrocortisone