title: HIV infection and glycemic response to newly initiated diabetic medical therapy.
abstract: OBJECTIVE
  Type 2 diabetes (DM2) is increasingly common in HIV-infected individuals. Antiretroviral agents and chronic inflammation may adversely affect glycemic control. However, little is known about the effectiveness of diabetic medical therapy in HIV-infected patients. The objective of this study was to compare the effectiveness of initial diabetic medical therapy in patients with and without HIV infection.
  
  
  METHODS
  A retrospective cohort study was conducted among adults with DM2 initiating diabetic medications within the Centers for AIDS Research Network of Integrated Clinical Systems cohort.
  
  
  METHODS
  Generalized estimating equations were used to compare changes in hemoglobin A1c (HbA1c) through the year after initiation of therapy, controlling for baseline HbA1c and demographic and clinical covariates.
  
  
  RESULTS
  Two hundred and eighty-six HIV-infected patients and 858 age and sex-matched HIV-uninfected patients initiated diabetic medications during the study period. Overall, patients had an adjusted absolute mean reduction in HbA1c of 1.04% [95% confidence interval (CI) -0.87 to -1.22] during the first year of therapy. HIV-infected patients achieved significantly smaller reductions in HbA1c, with an absolute mean difference of -0.17% (95% CI -0.28 to -0.06; P = 0.003). On subanalyses, HIV-infected patients on a protease inhibitor-based regimen had significantly smaller reductions in HbA1c compared to HIV-uninfected patients (adjusted absolute difference -0.21%, 95% CI -0.35 to -0.08; P = 0.002).
  
  
  CONCLUSIONS
  Patients with HIV infection who initiate diabetic medical therapy achieve smaller reductions in HbA1c than patients without HIV infection in the course of routine clinical care. This less robust response may in part be related to use of antiretrovirals that exacerbate insulin resistance, specifically protease inhibitors.
authors.affiliation: Division of Infectious Diseases, Department of Medicine, Hospital of the University of Pennsylvania, 3400 Spruce Street, 3rd Floor, Silverstein Building, Ste. E, Philadelphia, PA 19104, USA. jennifer.han@uphs.upenn.edu
authors.forename: Jennifer H
authors.initials: JH
authors.lastname: Han
authors.forename: Heidi M
authors.initials: HM
authors.lastname: Crane
authors.forename: Scarlett L
authors.initials: SL
authors.lastname: Bellamy
authors.forename: Ian
authors.initials: I
authors.lastname: Frank
authors.forename: Serena
authors.initials: S
authors.lastname: Cardillo
authors.forename: Gregory P
authors.initials: GP
authors.lastname: Bisson
mesh_terms: D000328:Adult; D000368:Aged; D019380:Anti-HIV Agents / Q000494:pharmacology*; D015415:Biomarkers / Q000378:metabolism; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism*; D002097:C-Reactive Protein / Q000187:drug effects / Q000378:metabolism*; D015331:Cohort Studies; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000188:drug therapy; D005260:Female; D006442:Glycated Hemoglobin / Q000187:drug effects / Q000378:metabolism*; D015658:HIV Infections / Q000188:drug therapy / Q000378:metabolism*; D017320:HIV Protease Inhibitors / Q000494:pharmacology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies; D016896:Treatment Outcome
chemical_list: D019380:Anti-HIV Agents; D015415:Biomarkers; D001786:Blood Glucose; D002097:C-Reactive Protein; D006442:Glycated Hemoglobin; D017320:HIV Protease Inhibitors; C517652:hemoglobin A1c protein, human