Journal of AIDS & Clinical Research

Increased Exhaled Hydrogen Peroxide in Human Immunodeficiency Virus- Infected Patients without Clinical Signs and Symptoms of Opportunistic Lung Disease

Abstract

Maciej Krol, Arkadiusz Balcerowski, Maria Luczynska, Urszula Szkudlarek and Dariusz Nowak

Background: HIV-infected subjects present with decreased antioxidant defense and increased activation of inflammatory cells which may lead to overproduction of oxidants. This study determined whether HIV-infected patients without clinical signs and symptoms of opportunistic lung disease (OLD-negative) exhaled more H2O2 than healthy controls and whether there was association between the exhalation of H2O2 and whole blood chemiluminescence (CL) and clinical variables. Methods: A cross-sectional study was conducted. H2O2 in exhaled breath condensate and CL, resting and agonist-induced with N-formyl-methionyl-leucyl-phenylalanine (fMLP) were measured in 36 OLD-negative patients and 14 healthy controls. Univariate linear regression was used to summarize the average relationship and quantile regression analyzed the relationship at different points of the exhaled H2O2 distribution. Multivariate analyses were carried out using multiple linear regressions. Results: The fold increase of the geometric mean exhaled H2O2 against healthy controls was 3.76-times higher in OLD-negative patients than in controls (95% CI: 2.65-5.33, p<0.001), whereas that of either resting or fMLPinduced CL was 1.46 or 1.63, respectively (95%: 1.17-1.83 and 1.27-2.08, p<0.01). Exhaled H2O2 was not associated with CL, either resting or fMLP-induced. Linear regression detected positive relationship between the exhalation of H2O2 and viral load (R-squared 0.23, p<0.05). The effects of viral load were best revealed at a higher exhalation of H2O2 (quantiles 0.6 and 0.7; both Pseudo R-squared 0.21, p<0.05). In a multivariate model, the main independent contributors to the exhalation of H2O2 were viral load and highly active antiretroviral therapy (HAART), which together accounted for 35% of the variance in exhaled H2O2. If the analysis was limited exclusively to HAART-treated, a better model fit was obtained (R-squared 0.79), confirming that viral load is the main contributor to the exhaled H2O2. Conclusion: Inordinate increase in exhaled H2O2 may reflect airway oxidative stress in HIV-1 infection which may be related to viral load.