Exhaled hydrogen sulfide in patients with chronic obstructive pulmonary disease and its correlation with exhaled nitric oxide.

BACKGROUND: Exhaled nitric oxide (NO) is a noninvasive biomarker of airway inflammation in pulmonary diseases. Hydrogen sulfide (H2S), as the third member of the gasotransmitter family, is involved in the pathophysiological process in lung diseases. H2S also exists in exhaled breath and can be sampled non-invasively. The study investigated the level of exhaled H2S in patients with chronic obstructive pulmonary disease (COPD) and its correlation with exhaled NO. METHODS: Levels of exhaled NO and H2S, lung function, and cell differential counts in induced sputum were studied in 19 patients with acute exacerbation of COPD (AECOPD), 19 patients with stable COPD and seven healthy smoke controls. RESULTS: Exhaled H2S levels were similar in patients with AECOPD (10.0 parts per billion (ppb), 8.0-13.0 ppb), stable COPD (10.0 ppb, 9.0-12.0 ppb), and healthy controls (9.0 ppb, 8.0-16.0 ppb) (P > 0.05). Exhaled NO levels were similar in patients with AECOPD (155.0 ppb, 129.0-190.0 ppb), stable COPD (154.0 ppb, 133.0-175.0 ppb) and healthy controls (165.0 ppb, 112.0-188.0 ppb) (P > 0.05). Exhaled H2S levels correlated positively with exhaled NO in all healthy controls and patients with COPD (r=0.467, P < 0.01). No significant correlation was found between the exhaled H2S level and percentage of predicted FEV1 (P > 0.05) and proportion of different cell types in induced sputum (P > 0.05). CONCLUSIONS: There is a correlation between exhaled H2S and exhaled NO. The role of exhaled H2S in airway inflammation in COPD still needs further investigation.

Involvement of endogenous hydrogen sulfide in cigarette smoke-induced changes in airway responsiveness and inflammation of rat lung.

Hydrogen sulfide (H2S), recently considered the third endogenous gaseous transmitter, may have an important role in systemic inflammation. We investigated whether endogenous H2S may be a crucial mediator in airway responsiveness and airway inflammation in a rat model of chronic exposure to cigarette smoke (CS). Rats randomly divided into control and CS-exposed groups were treated with or without sodium hydrosulfide (NaHS, donor of H2S) or propargylglycine (PPG, inhibitor of cystathionine-γ-lyase [CSE], an H2S-synthesizing enzyme) for 4-month exposure. Serum H2S level and CSE protein expression in lung tissue were higher, by 2.04- and 2.33-fold, respectively, in CS-exposed rats than in controls (P<0.05). Exogenous administration of NaHS to CS-exposed rats alleviated airway reactivity induced by acetylcholine (Ach) or potassium chloride (KCl) by 17.4% and 13.8%, respectively, decreased lung pathology score by 32.7%, inhibited IL-8 and TNF- α concentrations in lung tissue by 34.2% and 31.4%, respectively, as compared with CS-exposed rats (all P<0.05). However, blocking endogenous CSE with PPG in CS-exposed rats increased airway reactivity induced by Ach or KCl, by 24.1% and 24.5%, respectively, and aggravated lung pathology score, by 44.8%, as compared with CS-exposed rats (all P<0.01). Incubation in vitro with NaHS, 1-3 mmol/L, relaxed rat tracheal smooth muscle precontracted by Ach or KCl. However, the NaHS-induced relaxation was not blocked by glibenclamide (10⁻4 mol/L), L-NAME (10⁻4 mol/L), or ODQ (1 µmol/L) or denudation of epithelium. Endogenous H2S may have a protective role of anti-inflammation and bronchodilation in chronic CS-induced pulmonary injury.

Economic analysis in admitted patients with acute exacerbation of chronic obstructive pulmonary disease.

BACKGROUND: The socio-economic burden of acute exacerbation of chronic obstructive pulmonary disease (AECOPD) in Beijing is not fully understood. The study investigated the hospitalization cost in patients with AECOPD and the associated factors. METHODS: A multi-center, retrospective study was conducted in the four hospitals in Beijing including two level III hospitals and two level II hospitals. Patients with AECOPD admitted to the hospitals between January and December in 2006 were enrolled. The hospitalization cost and its relationship with disease severity and treatment were analyzed. RESULTS: Totally 439 patients were enrolled with 294 men (67.0%) and a mean age 73.4 years. The mean hospital stay was 20.7 days. A total of 204 patients (46.5%) had respiratory failure, 153 (34.9%) with cor pulmonale, 123 (28.0%) with coronary artery disease, 231 (52.6%) with hypertension, 70 (15.9%) with cerebrovascular disease and 32 (7.3%) with renal failure. The percentage of drug cost to total cost was the highest (71.2%), followed by laboratory cost (16.7%), therapy cost (9.7%), oxygen cost (7.3%), radiology cost (4.5%), examination cost (4.5%), bed cost (4.1%). Correlation analysis showed that cost was positively correlated with age, hospitalization days, co-morbidities such as respiratory failure and cor pulmonale, hypertension. Three hundred and twenty-one patients were further analyzed. The hospitalization cost increased in patients with non-invasive ventilation (P < 0.01), invasive mechanical ventilation (P < 0.01), ICU stay (P < 0.01), antibiotics (P < 0.05), systemic steroids (P < 0.01), and poor prognosis (P < 0.05). Correlation analysis showed that the hospitalization cost was negatively correlated with percentage forced expiratory volume in 1 second (FEV(1)%) (r = -0.149, P < 0.05), pH (r = -0.258, P < 0.01), and PaO(2) (r = -0.131, P < 0.05), positively correlated with PaCO2 (r = 0.319, P < 0.01), non-invasive positive pressure ventilation (r = 0.375, P < 0.01) and duration (r = 0.463, P < 0.01), invasive mechanical ventilation (r = 0.416, P < 0.01) and duration (r = 0.511, P < 0.01), ICU stay (r = 0.390, P < 0.01) and duration (r = 0.650, P < 0.01), antibiotics (r = 0.140, P < 0.05) and systemic steroids (r = 0.202, P < 0.01). CONCLUSIONS: AECOPD had a great impact on healthcare resources utilization. Disease severity, use of non-invasive or invasive ventilation, ICU stay and usage of antibiotics and systemic steroids were the major determinants of hospitalization cost. Long-term regular treatment aimed at reducing the frequency of acute exacerbation will lower the social and economic burden of chronic obstructive pulmonary disease (COPD).