title: Prediction of imminent complications in HIV-1-infected patients by markers of lymphocyte apoptosis.
abstract: OBJECTIVE
  The aim of the study was to compare accepted surrogate markers of HIV disease progression with markers of lymphocyte apoptosis in their ability to predict short-term disease progression.
  
  
  METHODS
  In all, 40 HIV-positive patients were studied prospectively and observed during follow-up for HIV-related adverse clinical events. Ex vivo apoptosis was measured with the markers CD95 expression, annexin V binding, and Apostain dye uptake by flow cytometry at baseline. Established markers of disease progression (CD4 count, HIV-RNA level, and CD8/38 count), CD8, B-cell, and natural killer (NK) cell counts were determined by standard procedures at baseline and after 6 months.
  
  
  RESULTS
  In HIV-infected patients, CD95 expression and annexin V binding showed significantly elevated apoptosis in peripheral blood lymphocytes and all lymphocyte subsets at baseline compared with HIV-negative, healthy controls. Apostain failed to differentiate between HIV-infected patients and healthy controls. HIV-related complications could be predicted by CD4 and CD8/38 counts, but not HIV viral load as assessed by relative operating characteristic (ROC) analysis (CD4, p = .003; CD8/38, p = .031). A similar or even better diagnostic accuracy was found for CD95 expression in total lymphocytes (p<.001), the CD4+ (p = .003) and CD8+ (p = .005) T-cell subsets and for annexin V binding in CD4+ T cells (p = .005). When patients with CD4 counts <200 cells/microl were analyzed separately, only annexin V binding in CD4+ T cells, but none of the other prognostic markers could predict complications (p = .001).
  
  
  CONCLUSIONS
  Determination of annexin V binding on CD4+ T cells may be a useful tool to monitor HIV-infected patients with low (<200 cells/microl) CD4 counts, as it can reliably assess the risk for imminent complications in such patients.
authors.affiliation: Department of General Internal Medicine, University of Bonn, Germany. j-c.wasmuth@uni-bonn.de
authors.forename: J C
authors.initials: JC
authors.lastname: Wasmuth
authors.forename: K H
authors.initials: KH
authors.lastname: Klein
authors.forename: F
authors.initials: F
authors.lastname: Hackbarth
authors.forename: J K
authors.initials: JK
authors.lastname: Rockstroh
authors.forename: T
authors.initials: T
authors.lastname: Sauerbruch
authors.forename: U
authors.initials: U
authors.lastname: Spengler
mesh_terms: D017088:AIDS-Related Opportunistic Infections / Q000209:etiology*; D000328:Adult; D017304:Annexin A5 / Q000378:metabolism; D018941:Antigens, CD19; D000943:Antigens, Differentiation / Q000302:isolation & purification*; D000944:Antigens, Differentiation, B-Lymphocyte / Q000302:isolation & purification; D000945:Antigens, Differentiation, T-Lymphocyte / Q000302:isolation & purification; D017209:Apoptosis; D005260:Female; D005544:Forecasting; D015658:HIV Infections / Q000150:complications* / Q000209:etiology; D015497:HIV-1; D006801:Humans; D007694:Killer Cells, Natural; D008297:Male; D008875:Middle Aged; D011485:Protein Binding; D012307:Risk Factors; D019014:fas Receptor / Q000302:isolation & purification
chemical_list: D017304:Annexin A5; D018941:Antigens, CD19; D000943:Antigens, Differentiation; D000944:Antigens, Differentiation, B-Lymphocyte; D000945:Antigens, Differentiation, T-Lymphocyte; D019014:fas Receptor