title: Impact of protease inhibitor therapy on HIV-related oropharyngeal candidiasis.
abstract: OBJECTIVE
  To determine the relationship between antiretroviral therapy and changes in prevalence and amount of oropharyngeal candidiasis (OPC) and skin test reactivity for delayed type hypersensitivity.
  
  
  METHODS
  Observational cohort.
  
  
  METHODS
  University-based public hospital AIDS clinic.
  
  
  METHODS
  Adults with advanced HIV infection who had been taking nucleoside transcriptase inhibitor drugs but had not taken a protease inhibitor and who started antiretroviral treatment with ritonavir.
  
  
  METHODS
  OPC lesions score, oral candidal colonization, oral candidal quantification, skin test reactivity for delayed type hypersensitivity (purified protein derivative, candidal and streptokinase antigens), plasma HIV RNA and CD4 cell count at weeks 8, 16 and 48 weeks.
  
  
  RESULTS
  In the 99 patients who entered the study, there was a significant reduction in the HIV plasma RNA (mean log decrease from baseline at 48 weeks 0.88) and a significant increase in CD4 cell counts (mean CD4 cell increase from baseline at 48 weeks 128 x 10(6) cells/l). Only 17% of patients had < 200 copies/ml HIV RNA at 48 weeks. There were significant decreases in the prevalence of OPC lesions (31% at baseline to 1% at 48 weeks; P < 0.001), and in oral candidal loads [2226 to 811 colony-forming units (CFU)/ml; P = 0.0171]. The percentage of patients with at least one positive skin test increased significantly (6 to 28%; P < 0.05). Patients whose CD4 lymphocyte count was > 200 x 10(6) cells/l at 48 weeks had significantly lower oral candidal loads and were more likely to have a positive skin test than patients whose CD4 cell count was < 200 x 10(6) cells/l.
  
  
  CONCLUSIONS
  In patients with advanced HIV infection, antiretroviral treatment including a protease inhibitor has a positive impact in the natural history of OPC. This positive impact appears to be correlated with a better immunological function and occurs despite continuous HIV replication.
authors.affiliation: Internal Medicine Service, La Paz Hospital, Autonoma University School of Medicine, Madrid, Spain.
authors.forename: J R
authors.initials: JR
authors.lastname: Arribas
authors.forename: S
authors.initials: S
authors.lastname: Hernández-Albujar
authors.forename: J J
authors.initials: JJ
authors.lastname: González-García
authors.forename: J M
authors.initials: JM
authors.lastname: Peña
authors.forename: A
authors.initials: A
authors.lastname: Gonzalez
authors.forename: T
authors.initials: T
authors.lastname: Cañedo
authors.forename: R
authors.initials: R
authors.lastname: Madero
authors.forename: J J
authors.initials: JJ
authors.lastname: Vazquez
authors.forename: W G
authors.initials: WG
authors.lastname: Powderly
mesh_terms: D017088:AIDS-Related Opportunistic Infections / Q000188:drug therapy* / Q000276:immunology / Q000382:microbiology; D000328:Adult; D000368:Aged; D019380:Anti-HIV Agents / Q000627:therapeutic use; D018791:CD4 Lymphocyte Count; D002175:Candida / Q000302:isolation & purification; D002180:Candidiasis, Oral / Q000188:drug therapy* / Q000453:epidemiology / Q000382:microbiology; D004359:Drug Therapy, Combination; D005260:Female; D015658:HIV Infections / Q000188:drug therapy / Q000276:immunology / Q000821:virology; D017320:HIV Protease Inhibitors / Q000627:therapeutic use*; D015497:HIV-1 / Q000502:physiology; D006801:Humans; D006968:Hypersensitivity, Delayed; D008297:Male; D008875:Middle Aged; D009960:Oropharynx / Q000382:microbiology; D012367:RNA, Viral / Q000097:blood; D018894:Reverse Transcriptase Inhibitors / Q000627:therapeutic use; D019438:Ritonavir / Q000627:therapeutic use*
chemical_list: D019380:Anti-HIV Agents; D017320:HIV Protease Inhibitors; D012367:RNA, Viral; D018894:Reverse Transcriptase Inhibitors; D019438:Ritonavir