Serum hydrogen sulfide as a novel marker predicting bacterial involvement in patients with community‐acquired lower respiratory tract infections

Abstract

Endogenous hydrogen sulfide (H2S) may be involved in the pathogenesis of systemic inflammation. It was investigated whether serum H2S levels differed among patients with community-acquired pneumonia, those with exacerbations of COPD or control subjects, and whether H2S may be used as a surrogate marker of the need for antibiotic treatment. Serum H2S levels were measured in 129 patients with pneumonia or COPD exacerbations and in 72 healthy control subjects. The mean serum H2S concentration was 36% lower in patients with pneumonia (22.7 +/- 14.6 micromol/L) than in control subjects (35.4 +/- 5.3 micromol/L) (P < 0.01). Serum H2S concentration did not differ between patients with acute exacerbations of COPD (33.8 +/- 18.6 micromol/L) and control subjects. Within the COPD group, patients with Anthonisen type 1 exacerbations had a lower serum H(2)S concentration (22.5 +/- 11.6 micromol/L) than control subjects, and those with type 3 exacerbations had a higher serum H2S concentration (54.2 +/- 21.3 micromol/L) than control subjects. There was no difference between patients with type 2 exacerbations (41.7 +/- 8.4 micromol/L) and control subjects. In patients requiring antibiotics, serum H2S concentration was 41% lower than in those not requiring antibiotics. The area under the receiver operating characteristic curve for H(2)S as a surrogate marker of the need for antibiotics was 0.862 (95% confidence interval: 0.805-0.919, P < 0.01). Serum H2S levels were inversely correlated with serum CRP levels (r = -0.337, P < 0.01). Serum H2S levels may be used as a marker in lower respiratory tract infections. Further studies are required to validate the role of serum H2S levels in guiding antibiotic selection.