title: A pilot study of telmisartan for visceral adiposity in HIV infection: the metabolic abnormalities, telmisartan, and HIV infection (MATH) trial.
abstract: BACKGROUND
  Visceral adiposity in the setting of HIV infection and antiretroviral therapy (ART) is not fully understood, and treatment options remain limited. Telmisartan, an angiotensin receptor blocker and partial PPAR-γ agonist, has been shown to decrease visceral fat and improve metabolic and inflammatory parameters in HIV-uninfected subjects.
  
  
  METHODS
  HIV-infected subjects with HIV-1 RNA <50 copies/mL on ART and (women/men) waist circumference >94/95 cm or waist: hip ratio >0.88/0.94 received open-label telmisartan 40 mg po daily for 24 weeks. Adipose tissue (AT) volumes were quantified by L4-L5 single slice computed tomography. Metabolic and inflammatory markers were obtained fasting. Thirty-five subjects provided 80% power to detect a 10% 24-week decrease in visceral AT (VAT, two-sided α = 0.05).
  
  
  RESULTS
  Thirty-five subjects enrolled and completed the protocol. At entry (median or %): age 49 years, 43% female, 77% non-white, 91% non-smokers, CD4+ T cell count 590 cells/mm(3), BMI 31 kg/m(2). AT responses were heterogeneous, with statistically significant losses of median (IQR) total (TAT, 2.9% (-9.8, 0.7), p = 0.03) and subcutaneous (SAT, -2.7% (-9.8, 1.1), p = 0.03) AT, but not VAT (-2.7% (-20.5, 14.2), p = 0.53). Significant decreases in waist circumference and waist:hip ratio occurred (both p<0.001) without BMI or weight changes. In an exploratory analysis, significant increases in TNF-α occurred among female subjects without changes in other inflammatory or metabolic markers. No related adverse events occurred.
  
  
  CONCLUSIONS
  Telmisartan was well tolerated. Small losses of AT from all depots were observed after 24 weeks of telmisartan therapy. Further study is needed to determine whether HIV-infected patients can receive metabolic benefits from telmisartan.
authors.affiliation: Division of Infectious Diseases, Department of Medicine, University of California Los Angeles, Los Angeles, California, USA. jlake@mednet.ucla.edu
authors.forename: Jordan E
authors.initials: JE
authors.lastname: Lake
authors.forename: Chi-Hong
authors.initials: CH
authors.lastname: Tseng
authors.forename: Judith S
authors.initials: JS
authors.lastname: Currier
mesh_terms: D050154:Adiposity / Q000187:drug effects*; D047228:Angiotensin II Type 1 Receptor Blockers / Q000008:administration & dosage / Q000009:adverse effects / Q000494:pharmacology*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000008:administration & dosage / Q000009:adverse effects / Q000494:pharmacology*; D023241:Antiretroviral Therapy, Highly Active; D001562:Benzimidazoles / Q000008:administration & dosage / Q000009:adverse effects / Q000494:pharmacology*; D001565:Benzoates / Q000008:administration & dosage / Q000009:adverse effects / Q000494:pharmacology*; D005260:Female; D005947:Glucose / Q000378:metabolism; D015658:HIV Infections / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D050152:Intra-Abdominal Fat / Q000187:drug effects* / Q000473:pathology*; D050356:Lipid Metabolism; D008297:Male; D008875:Middle Aged; D009929:Organ Size; D010865:Pilot Projects; D012737:Sex Factors; D000077333:Telmisartan
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; D001562:Benzimidazoles; D001565:Benzoates; D018836:Inflammation Mediators; D005947:Glucose; D000077333:Telmisartan