Severity: Warning
Message: file_get_contents(https://...@pubfacts.com&api_key=b8daa3ad693db53b1410957c26c9a51b4908&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 176
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 176
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 250
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 1034
Function: getPubMedXML
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3152
Function: GetPubMedArticleOutput_2016
File: /var/www/html/application/controllers/Detail.php
Line: 575
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 489
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 316
Function: require_once
Objective: To investigate the role of endogenous hydrogen sulfide (H(2)S) in patients with chronic obstructive pulmonary disease (COPD).
Methods: Levels of serum H(2)S and nitric oxide (NO), lung function and cell differential count in induced sputum were studied in 27 patients with acute exacerbation of COPD (AECOPD), 37 patients with stable COPD and 13 health subjects. Echo-Doppler assessment and arterial blood gas were measured in patients with AECOPD.
Results: (1) The serum H(2)S level was significantly higher in patients with stable COPD [(50.8 +/- 2.5) micromol/L] as compared to those in the controls [(39.8 +/- 1.6) micromol/L] and in patients with AECOPD [(33.5 +/- 2.2) micromol/L, P < 0.01]. (2) The level of serum H(2)S was significantly lower in smokers with AECOPD [(28.1 +/- 1.3) micromol/L] as compared to nonsmokers with AECOPD [(39.4 +/- 3.9) micromol/L, P < 0.05] and healthy nonsmokers [(39.8 +/- 1.6) micromol/L, P < 0.01]. (3) There was significant difference in the serum H(2)S level among stable COPD patients with different severity of airway obstruction (P < 0.05); being lower in patients with stage III [(45.1 +/- 4.1) micromol/L] as compared to stage I obstruction [(70.2 +/- 6.2) micromol/L, P < 0.05]. (4) AECOPD with pulmonary hypertension pulmonary artery systolic pressure (PASP) > or = 35 mm Hg (1 mm Hg = 0.133 kPa) showed a lower serum H(2)S level [(26.3 +/- 2.2), (36.2 +/- 2.5) micromol/L, P < 0.05] than that with a normal resting PASP. (5) H(2)S in serum was positively correlated with NO levels (r = 0.278, P = 0.029), FEV(1)% predicted values (r = 0.533, P = 0.000), percentage of sputum lymphocytes (r = 0.286, P = 0.028) and macrophages (r = 0.334, P = 0.01); and negatively correlated with PASP (r = -0.561, P = 0.011) and the percentage of sputum neutrophils (r = -0.422, P = 0.001) in patients with COPD.
Conclusion: Endogenous H(2)S may be involved in the pathogenesis of airway obstruction in COPD and may be a noninvasive marker of disease activity and severity.
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