Respirology (Carlton, Vic.) · 2009
Serum hydrogen sulfide as a novel marker predicting bacterial involvement in patients with community-acquired lower respiratory tract infections.
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Chen Ya-Hong, Yao Wan-Zhen, Gao Jing-Zhen, Geng Bin, Wang Pei-Pei, Tang Chao-Shu
Аннотация
BACKGROUND AND OBJECTIVE: 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.
METHODS: Serum H2S levels were measured in 129 patients with pneumonia or COPD exacerbations and in 72 healthy control subjects.
RESULTS: 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).
CONCLUSIONS: 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.
METHODS: Serum H2S levels were measured in 129 patients with pneumonia or COPD exacerbations and in 72 healthy control subjects.
RESULTS: 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).
CONCLUSIONS: 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.