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Serum hydrogen sulfide as a novel marker predicting bacterial involvement in patients with community‐acquired lower respiratory tract infections
Author(s) -
CHEN YaHong,
YAO WanZhen,
GAO JingZhen,
GENG Bin,
WANG PeiPei,
TANG ChaoShu
Publication year - 2009
Publication title -
respirology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 85
eISSN - 1440-1843
pISSN - 1323-7799
DOI - 10.1111/j.1440-1843.2009.01550.x
Subject(s) - medicine , gastroenterology , copd , antibiotics , confidence interval , pneumonia , receiver operating characteristic , hydrogen sulfide , pathogenesis , respiratory system , surrogate endpoint , community acquired pneumonia , respiratory tract , microbiology and biotechnology , sulfur , chemistry , organic chemistry , biology
Background and objective: Endogenous hydrogen sulfide (H 2 S) may be involved in the pathogenesis of systemic inflammation. It was investigated whether serum H 2 S levels differed among patients with community‐acquired pneumonia, those with exacerbations of COPD or control subjects, and whether H 2 S may be used as a surrogate marker of the need for antibiotic treatment. Methods: Serum H 2 S levels were measured in 129 patients with pneumonia or COPD exacerbations and in 72 healthy control subjects. Results: The mean serum H 2 S concentration was 36% lower in patients with pneumonia (22.7 ± 14.6 µmol/L) than in control subjects (35.4 ± 5.3 µmol/L) ( P < 0.01). Serum H 2 S concentration did not differ between patients with acute exacerbations of COPD (33.8 ± 18.6 µmol/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 µmol/L) than control subjects, and those with type 3 exacerbations had a higher serum H 2 S concentration (54.2 ± 21.3 µmol/L) than control subjects. There was no difference between patients with type 2 exacerbations (41.7 ± 8.4 µmol/L) and control subjects. In patients requiring antibiotics, serum H 2 S 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 H 2 S levels were inversely correlated with serum CRP levels ( r = −0.337, P < 0.01). Conclusions: Serum H 2 S levels may be used as a marker in lower respiratory tract infections. Further studies are required to validate the role of serum H 2 S levels in guiding antibiotic selection.