Serum surfactant protein D, lung function decline, and incident chronic obstructive pulmonary disease: a longitudinal study in Beijing.

BACKGROUND: Chronic obstructive pulmonary disease (COPD) has become a major public-health problem in China. Surfactant protein D (SP-D) is a very promising biomarker and therapeutic target for COPD. To assess whether baseline serum SP-D is associated with lung function decline and incident COPD. METHODS: This longitudinal study was initiated in 2009 in a community in Beijing. Data were collected on spirometry, and the baseline level of serum SP-D was measured in 772 non-COPD subjects aged 40-70 years old. In 2012, spirometry was repeated in 364 individuals, 37 of whom subjects had incident COPD. RESULTS: From 2009 to 2012, subjects with incident COPD had a more rapid decline in FEV1 (MD 98.27 vs. MD 43.41 mL) compared with those without COPD. There was no association between baseline serum SP-D and the COPD incidence. Smoking (OR =2.72; P=0.002) and age (OR =1.06; P=0.000) were risk factors for COPD. The rate of FEV1 decline varies widely in the general population, and the univariate analysis showed that baseline serum SP-D levels (R=-0.169; P=0.003), income level, home-road distance, and statin use were inversely correlated with the decline in FEV1. After multivariable analyses, only smoking was consistently associated with the decline in FEV1. CONCLUSIONS: There was no correlation between baseline serum SP-D levels and incident COPD in a general population. Smoking and age were major risk factors for COPD. The effect of serum SP-D levels on the decline in FEV1 needs further investigation.

[Prognostic factors for patients with pulmonary thromboembolism after orthopaedic surgery].

OBJECTIVE: To investigate the changes of serum enzymes and their prognostic value in patients with pulmonary thromboembolism after orthopaedic surgery. METHODS: Clinical data of 134 cases of confirmed pulmonary thromboembolism after orthopaedic surgery from 1997 to 2010 were reviewed.The 134 cases were divided into dead group (n=28) and survival group (n=106). The clinical presentation, electrocardiogram, arterial oxygen pressure (PaO2), chest X-ray, echocardiography,and serum enzymes including alanine transaminase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transpeptidase (γ-GT), lactate dehydrogenase (LDH), creatine kinase (CK) and creatine kinase isoenzyme (CK-MB) were analyzed. And multivariable Logistic regression was conducted to identify the risk factors of in-hospital death. RESULTS: The average age of dead patients was higher than that of survival patients (P=0.043), while the P(O2) of dead patients was much lower than that of survival patients (P=0.035). The percentage of syncope, hypotension, right bundle-branch block and SIQIIITIII, pulmonary hypertension and right ventricular dysfunction in dead patients were higher than those in survival patients (P=0.009, P=0.041, P=0.018, P=0.030, P=0.042 and P=0.038), respectively. There were significant differences of elevated serum ALT, LDH and CK-MB levels between dead patients and survival patients (P=0.042, P=0.035 and P=0.017). Logistic regression indicated that the risk factors for death of patients with PTE after orthopaedic surgery were age (OR, 1.182; 95% CI, 1.010-1.383; P=0.036), hypoxemia (OR, 1.128; 95% CI, 1.018-1.249; P=0.022), hypotension (OR, 3.346; 95% CI, 1.116-10.031; P=0.031), right ventricular dysfunction (OR, 4.083; 95% CI, 1.040- 16.035; P=0.044) and elevated serum CK-MB levels (OR, 3.466; 95% CI, 1.054-11.400; P=0.041). CONCLUSION: The incidence rate of elevated serum ALT, LDH and CK-MB levels in patients who died of pulmonary thromboembolism after orthopaedic surgery was higher than that of survival patients; Age, hypoxemia, hypotension and right ventricular dysfunction were independent risk factors of in-hospital death; The CK-MB might be a useful biomarker for risk stratification of acute PTE.

[The expression and implications of human alpha-defensin 1-3 in serum and induced sputum in patients with chronic obstructive pulmonary disease].

OBJECTIVE: To measure the levels of human alpha-defensin 1-3 (HNP1-3) in the serum and induced sputum in patients with chronic obstructive pulmonary disease (COPD) and therefore to investigate the possible roles of HNP1-3 in COPD. METHODS: Thirty patients with acute exacerbation of COPD, 21 patients with stable COPD, and 22 healthy subjects were recruited. The concentrations of HNP1-3 and interleukin-8 (IL-8) in serum and induced sputum were measured by enzyme-linked immunosorbent assay (ELISA). The correlations among HNP1-3, neutrophils, IL-8, and lung functions were investigated. The data were analyzed using a statistical software package (SPSS 11.5). Variables were compared with One-Way ANOVA or Chi-square test. The correlations between variables were analyzed using Pearson's correlation coefficient or Spearman correlation coefficient. RESULTS: The sputum HNP1-3 level was significantly higher in AECOPD patients [9,652(4,272 -12,576) ng/L] than in healthy subjects [4,194 (700 -10,505) ng/L, chi2 =7.53, P <0.01] and in stable COPD patients [7,011(6,658 -7,319) ng/L, chi2 = 10.24, P <0.01]. There was significant difference among the three groups (chi2 =7.31, P <0.05). There was no significant difference in the serum HNP1-3 level among the three groups: AECOPD group [51(39 - 173) ng/L], stable COPD group [135(113 - 241) ng/L], healthy subjects group [130(13 - 160) ng/ L], chi2 = 5.75, P > 0.05. The sputum HNP1-3 level was positively correlated with the number, percentage of sputum neutrophils, and sputum IL-8 level (r = 0.29 to 0.53, respectively P <0.01). The sputum HNP1-3 level was negatively correlated with FEV1/predicted values, FEV1/FVC, and PaO2 (r= -0.33 to -0.44, respectively P <0.01). CONCLUSIONS: HNP1-3 may be involved in the pathogenesis of airway inflammation in COPD. Sputum HNP1-3 may be a noninvasive marker of severity of COPD.

Living near a Major Road in Beijing: Association with Lower Lung Function, Airway Acidification, and Chronic Cough.

BACKGROUND: The effects of near-road pollution on lung function in China have not been well studied. We aimed to investigate the effects of long-term exposure to traffic-related air pollution on lung function, airway inflammation, and respiratory symptoms. METHODS: We enrolled 1003 residents aged 57.96 ± 8.99 years living in the Shichahai Community in Beijing. Distances between home addresses and the nearest major roads were measured to calculate home-road distance. We used the distance categories 1, 2, and 3, representing <100 m, 100-200 m, and >200 m, respectively, as the dose indicator for traffic-related air pollution exposure. Lung function, exhaled breath condensate (EBC) pH, and interleukin 6 levels were measured. As a follow-up, 398 participants had a second lung function assessment about 3 years later, and lung function decline was also examined as an outcome. We used regression analysis to assess the impacts of home-road distance on lung function and respiratory symptoms. As the EBC biomarker data were not normally distributed, we performed correlation analysis between home-road distance categories and EBC biomarkers. RESULTS: Participants living a shorter distance from major roads had lower percentage of predicted value of forced expiratory volume in 1 s (FEV1% -1.54, 95% confidence interval [CI]: -0.20 to -2.89). The odds ratio for chronic cough was 2.54 (95% CI: 1.57-4.10) for category 1 and 1.97 (95% CI: 1.16-3.37) for category 2, compared with category 3. EBC pH was positively correlated with road distance (rank correlation coefficient of Spearman [rs] = 0.176, P < 0.001). CONCLUSIONS: Long-term exposure to traffic-related air pollution in people who live near major roads in Beijing is associated with lower lung function, airway acidification, and a higher prevalence of chronic cough. EBC pH is a potential useful biomarker for evaluating air pollution exposure.

[The COX regression analysis on the use of corticosteroids in the treatment of SARS].

OBJECTIVE: To explore the effectiveness of corticosteroids (GCS) and to determine how to use it in the treatment of SARS. METHODS: All reported probable cases in Beijing were reviewed. Those who fulfilled the diagnostic criteria with an integrity clinical record were recruited in the study. A database was established and all the clinical data, including patients' personal information, epidemiological history, underlying diseases, clinical manifestations, laboratory tests and therapies after hospitalization, as well as the outcome of the disease, were inputted under a quality control. Unifactor and COX multifactor regression analysis were done. The dose of GCS was all expressed in that of methylprednisolone. RESULTS: 1291 cases were in consistence with the demands mentioned above. Among them, 1084 cases (83.96%) had used GCS and 207 did not in the course of SARS. There was no significant difference of average age (t = -1.08, P = 0.2808) and the time from SARS onset to hospitalization (P = 0.2797) between the two groups. COX regression showed that the risk of fatality in the GCS group was higher than that of those who did not use GCS (RR = 1.334, 95% of CI: 0.588 - 3.026). In the patients with comorbidities, RR was 2.086 (95% of CI: 0.694 - 6.267), and RR was 0.536 (95% of CI: 0.146 - 1.970) in the patients with no comorbidity. In those without any comorbidity, the initial doses, maximal doses, average doses and cumulative doses all showed a 'J' shape change. An appropriate dose could keep RR to be the lowest whereas the doses either higher or lower than it could increase RR. The initial dose with the lowest RR was 80 - 160 mg/d, the maximum 80 - 160 mg/d, the average < 80 mg/d and the cumulative one 1000 - 3000 mg although there was no statistical significance (all P > 0.05). RR was less than 1 in non-comorbidity patients who initiated GCS therapy before the 15th day of the disease. RR was 1.415 (95% of CI: 0.195 - 10.257) in the patients who began to use GCS over this period. Counting from hospitalization, the time of GCS use also showed a 'J' type change of RR. The initiation of GCS from day 5 to 7 had the lowest RR (0.282, 95% of CI: 0.043 - 1.828) and that from day 8 to 14 was 1 (95% of CI: 0.150 - 6.654). CONCLUSION: In the treatment of SARS, GCS seems to be effective. An appropriate dose and a right time of application decrease the risk of death. The use of GCS in SARS patients with comorbidities should be with caution.