Objective To systematically assess the correlation between smoking and the risk of endometriosis, so as to offer scientific basis to health education and preventing decision. Methods A literature search was performed in The Cochrane Library, Pubmed, Embase, CBM, CNKI and Wanfang database to collect the case control studies on the correlation between smoking and endometriosis. Two reviewers independently screened the literatures according to the inclusion and exclusion criteria, extracted the data, assessed the quality, and then conducted Meta-analyses on the 13 included RCTs by using RevMan 5.0 software, with calculation of the OR value and 95%CI. Results A total of 13 case control studies involving 14260 cases were included, of which 1900 ones were endometriosis. The quality assessment indicated that 2 studies were in quality of Level A, 4 were Level B, 7 were Level C, totally meant low quality. Meta-analyses showed that compared with non-smokers, there was no increasing possibility of endometriosis in smokers (OR= 0.91, 95%CI 0.82 to 1.02). The geographical subgroup analyses showed there was no significant difference in the incidence of endometriosis between the non-smokers and smokers in North America (OR=0.96, 95%CI 0.84 to 1.08), but a significant difference was found between non-smokers and smokers in Europe (OR=0.72, 95%CI 0.54 to 0.97). Conclusion There is no causative relationship between smoking and incidence of endometriosis. However, more high-quality trials are expected for further study because of the heterogeneity and poor quality of the current included studies.
Objective To explore the anti-inflammatory effects of ambroxol hydrochloride in chronic obstructive pulmonary disease（COPD）.Methods Thirty Wistar rats were randomly divided into three groups，ie.a control group，a smoking group and an ambroxol group.The rats in the smoking and ambroxol groups were exposed to cigarettes smoking for 12 weeks.Ambroxol hydrochloride was administered via intragastric gavage after 4 weeks smoking in the ambroxol group.After 12 weeks，the expiratory airway resistance(Re) and dynamic lung compliance(CLdyn) were measured.The expression levels of nuclear factor kappa B（NF-κB）and intercellular adhesion molecule-1(ICAM-1) in airway epithelium cell were observed by immunohistochemical method.Results Re was increased and CLdyn was decreased significantly in the smoking and ambroxol groups compared with the control group(all Plt;0.01).Re was lower (Plt;0.01) and CLdyn was higher(Plt;0.05) in the ambroxol group than those in the smoking group.B.The level of NF-κB and ICAM-1 in smoking and ambroxol groups were obviously increased compared with the control group (all Plt;0.05)，which was decreased in the ambroxol group compared with the smoking group(both Plt;0.05).C.The expression of NF-κB was positively correlated with ICAM-1 expression in airway epithelial cells（r=0.924，Plt;0.01）.Conclusions Smoking can increase the airway resistance，reduce the lung compliance and increase the expression of NF-κB and ICAM-1 in airway epithelium.Ambroxol hydrochloride can relieve those effects of smoking，which suggested an anti-inflammatory therapeutic role in COPD.
Objective To investigate the relationship between smoking and lung cancer by evidence-based evaluation. Methods Using Meta-analysis method, the results of 29 case-control studies involving the relationship between smoking and lung cancer in recent decade were analyzed by Review Manager 4. 2 software. Results The association between smoking and lung cancer was significant ( Z =12. 16, P lt; 0. 000 01) , and the pooled OR value was 5. 75( 4. 34, 7. 62) . The population attributable risk percentage( PARP) of smoking was 69. 16% . The pooled OR of 1-10 cpd( cigarettes per day) , 10-20 cpd, 20-40 cpd and more than 40 cpd were 1. 97( 1. 69, 2. 30) , 5. 20( 3. 54, 7. 62) , 7. 46( 5. 22, 10. 67) and 15. 14 ( 5. 27, 43. 44) respectively. The pooled OR of less than 20 years of smoking duration, 20-40 years and more than 40 years were 1. 25( 1. 01, 1. 53) , 5. 10( 3. 03, 8. 57) and 10. 77( 7. 30, 15. 89) respectively. While the pooled ORof less than 10 pack-years, 10-20 pack-years, 20-40 pack-years and more than 40 pack-years were 1. 73( 1. 01, 2. 96) , 3. 73 ( 3. 02, 4. 61) , 5. 69 ( 3. 79, 8. 54) and 8. 41 ( 4. 56, 15. 51) respectively. The pooled OR of initial smoking age less than 15 years old, 15-20 years old and more than 20 years old were 13. 31( 7. 09, 24. 97) , 7. 21( 4. 51, 11. 52) and 4. 74( 3. 47, 6. 47) respectively. The pooled OR of quitting smoking for 1-10 years, 10-20 years and more than 20 years were 7. 16( 4. 70, 10. 91) , 2. 12( 1. 16, 3. 86)and 1. 47 ( 0. 67, 3. 20 ) respectively, and more than 20 years of quitting smoking had no significant difference. The pooled OR of light smoking and deep smoking were 3. 26( 1. 24, 8. 58) and 8. 07( 4. 67, 13. 94) respectively. Conclusions Smoking is an important risk factor of lung cancer. Meta-anlalysis revealed cigarettes comsuption per day, smoking duration, total amount of cigarettes ( pack-years) , smoking behaviour( depth) , initial age of smoking and duration of quitting smoking can increase the risk of lung cancer.
Objective To investigate the effects of smoking intensity, duration and cessation on mRNA and protein expressions of matrix metalloproteinase-9 ( MMP-9) in tracheal epitheliumof rats, and the relationship between smoking or smoking cessation and airway remodeling in chronic obstructive pulmonary disease ( COPD) . Methods Forty Wistar rats were randomly divided into 5 groups, ie. a normal control group, a long termheavy smoking group, a short termheavy smoking group, a long termlight smoking group,and a smoking cessation group which was exposed to room air for 10 weeks after long term heavy smoking.The expressions of MMP-9 mRNA and protein in tracheal epithelium of rats were detected by in situ hybridization and munohistochemistry respectively. Results ( 1) The pathological changes of emphysema were observed in the lung tissue of every smoking rat, and were most sever in the long term heavy smoking group. ( 2) Compared with the normal control group [ ( 0. 88 ±0. 88) PU, ( 2. 80 ±1. 66) PU] , the expressions of MMP-9 mRNA and proteins in tracheal epithelium were remarkable elevated in the long term heavy smoking group [ ( 22. 01 ±2. 86) PU, ( 20. 81 ±2. 46) PU] , the short term heavy smoking group [ ( 14. 94 ±3. 46) PU, ( 13. 68 ±2. 00) PU] , the long term light smoking group [ ( 6. 92 ±2. 71) PU,( 8. 84 ±1. 80) PU] and the smoking cessation group [ ( 19. 00 ±3. 36) PU, ( 14. 82 ±1. 74) PU] ( P lt;0. 01) . Compared with the long term heavy smoking group, the expressions of MMP-9 in tracheal epithelium were decreased in other three smoking groups ( P lt; 0. 05) . Conclusions Smoking could increase the expression of MMP-9 in tracheal epithelium and cause trachea damage and remodeling with intensity and duration in rats. Smoking cessation could decrease the MMP-9 expression and alleviate trachea remodeling,suggesting its role in the prevention of COPD.
Objective To investigate the clinical characteristics, short-term therapy outcome and survival in patients of lung cancer with different smoking status. Methods 3751 cases were enrolled and the differences in age, sex, pathological type, stage, treatment modality, efficiency and survival were compared according patients′smoking status. Results 1206 ( 32. 2% ) patients were never smokers and 2545 ( 67. 8% ) were smokers. 80. 3% male patients and 10. 5% female patients were smokers. Among never smoking lung cancer patients, proportion of female gender, adenocarcinoma, second primary neoplasm,advanced stages and non-operative treatment were high. In the smokers, much more COPD and pulmonary tuberculosis, squamous cancer and operative treatmentwere found. No statistical differences were detected in overall outcome and survival. Conclusions The clinical characters and treatmentmodalities of patients with lung cancer of different smoking status were significant different, but had the same survival. Patients’smoking status should be accountted into the diagnosis and treatment of lung cancer.
Objective To explore the ultrastructure characteristics of pulmonary arteries in smokers with normal lung function and with chronic obstructive pulmonary disease ( COPD) . Methods 33 patients who undertook surgery for peripheral lung cancer were collected. According to smoking history and pulmonary function, the patients were divided into three groups, ie. non-smokers with normal pulmonary function ( group A, n = 10) , smokers with normal pulmonary function ( group B, n = 13) , and smokers in stable phase of COPD ( group C, n = 10) . Normal lung tissues without cancer were sampled and observed under light and electric microscope. Results ①Compared with group A, the thickness of intimal layer of intra-acinar pulmonary muscular arteries of group B and C were significantly higher, the area of their lumenwas lower, and the proportion of their muscular arteries was higher( P lt; 0. 01) . ②Ultrastructure of small pulmonary arteries of group A showed that intimal layer was normal, so as to endothelial cells and smooth muscle cells. Collagen fiber was not increased. Ultrastructure observation of group B showed that endothelialcells were distorted, basal membrane was thick, and collagen fiber increased in vessels. Ultrastructure observation of group C showed that endothelial cells degenerated, vascular intima thickness increased, andsynthetic phenotype smooth muscle cells increased. ③ Smoking index was positively correlated with the proportion of muscular arteries and the proportion of intimal area( r =0. 464,0. 635, P lt;0. 05, respectively) ,and negatively correlated with the proportion of lumen area( r= - 0. 603, P lt;0. 05) . Conclusions Smokers with normal lung fuction and with COPD show the similar ultrastructural characterizations in endothelial cells, smooth muscle cells, and pulmonary arterial remodeling, which related closely to smoking.
Objective To investigate the role of inflammatory factors like serumleptin, adiponectin,interleukin-6( IL-6) , and C-reactive protein ( CRP) in the systemic inflammatory response of smokinginduced COPD. Methods Thirty male Wistar rats were randomly divided into three groups, ie. a high-dose smoking group, a low-dose smoking group, and a control group. Serum leptin, adiponectin, IL-6, and CRP levels were measured by ABC-ELISA. Results The serum leptin and adiponectin levels in both smoking groups decreased significantly compared with the control group( P lt; 0. 05) , while the difference was not significant between the two smoking groups ( P gt; 0. 05) . The serum IL-6 and CRP levels in both smoking groups increased significantly compared with the control group( P lt; 0. 05) , which were higher in the highdosesmoking group than those in the low-dose smoking group( P lt;0. 05) . Conclusions Smoking increases the serum levels of IL-6 and CRP, but reduces the serum levels of leptin and adiponectin in rats. These results suggest that leptin, adiponectin, IL-6, and CRP may be involved in the systemic inflammatory response of smoking-induced COPD.
Objective To determine if the therapeutic response to an inhaled corticosteroid is attenuated in individuals with asthma who smoke.Methods 38 outpatients with chronic stable asthma who visited during March 2008 and January 2009 were enrolled in the study. 23 cases were nonsmokers and 15 cases were smokers. All of them were treated by daily inhaled budesonide, and β2 agonist when necessary.They were required to record symptoms and peak expiratory flow every day on an asthmatic diary card. Thepatients were followed 28 days. ACT score, asthma-symptom score, Asthma Control Test ( ACT) score,pulmonary function, and peak expiratory flow were compared between the non-smoking and the smoking asthmatic patients. Results All of the patients had statistically significant increases in ACT score, mean morning and night PEF, mean forced expiratory volume in 1 second, and a significant decrease in asthmasymptom score after budesonide treatment compared with before. There were significantly greater changes inany of these parameters in the non-smokers than in the smokers. Conclusions Active cigarette smoking impairs the efficacy of short term inhaled corticosteroid treatment in asthma. This finding has important implications for the management of patients with asthma who smoke.
Objective To investigate the effects of smoking on β-defensin-2 ( BD-2) expression in induced sputumand lung tissue, and its role in chronic obstructive pulmonary disease ( COPD) . Methods Patients suffering with early peripheral squamous celled lung cancer and underwent lobectomy were divided into a smoking COPD group ( COPD group) , a non-COPD smoking group ( smoker group) , and a nonsmoking group ( control group) . Preoperative induced sputumsamples were collected after hypertonic saline induction. Lung tissue samples were intraoperatively collected far from the tumor site. The sputum samples were prepared for total and differential cell count, while the lung tissue samples for pathology examination. The BD-2 concentration in sputumand lung homogenate were measured by ELISA. Correlation were analyzed between BD-2 concentration and smoking index, airway inflammation, and lung function. Results The lung pathology were highly consistent with the experimental grouping. The total cell count and neutrophils proportion in sputum and BD-2 concentration in lung homogenate were ( 2. 32 ±0. 51) ×106 / g, ( 35. 7 ±9. 8) % , and ( 14. 5 ±5. 7) ng/L in the control group respectively, while increased in the smoker group [ ( 4. 57 ±0. 87) ×106 / g, ( 52. 5 ±10. 9) % , and ( 78. 3 ±13. 1) ng/L, P lt;0. 05] , and further increased in the COPD group [ ( 6. 61 ±1. 03) ×106 / g, ( 65. 5 ±12. 3) % , and ( 127. 0 ±35. 0) ng/L, P lt; 0. 05] . The lymphocytes proportion and BD-2 concentration in sputum increased in the COPD group [ ( 3. 2 ±1. 7) % and ( 298. 0 ±135. 0) ng/L] as well as in the smoker group [ ( 2. 5 ±1. 2) % and ( 315. 0 ±124. 0) ng/L] ,as compared with the control group [ ( 1. 1 ±0. 3) % and ( 132. 0 ±48. 0) ng/L] ( P lt; 0. 05) . Linear correlation analysis revealed that BD-2 concentration in sputumwas positively correlated with smoking index,sputum total cell count and neutrophils proportion, whereas BD-2 concentration in lung homogenate wasreversely correlated with pulmonary ventilation function ( P lt; 0. 05) . Conclusions Smoking up-regulates the BD-2 level in sputum and lung tissues. Further more, the BD-2 expression status in lung tissue of smoking individuals might be associated with COPD susceptibility.
Objective To observe the levels of malonaldehyde (MDA) , interleukin-8 (IL-8) and tumor necrosis factor-α(TNF-α) in lung tissues of subjects with or without chronic obstructive pulmonary disease (COPD) , and investigate their roles in the the pathogenesis of COPD. Methods The content of MDA, IL-8 and TNF-αin lung tissues of smokers with COPD (n=9) , ex-smokers with COPD (n=8) , non-smokers with COPD (n=7) , healthy smokers (n=9) , healthy ex-smokers (n=8) and healthy nonsmokers (n=6) was measured with enzyme-linked immunosorbent assay ( ELISA) and corrected by creatinine. Results The levels of MDA, IL-8 and TNF-α in lung tissues of the COPD patients were significantly higher than those in the healthy subjects (Plt;0.05) , which were also significantly higher in the smokers when compared with the non-smokers (Plt;0.05) , whether suffering from COPD or not. In the COPD patients, not the levels of IL-8 but MDA and TNF-αin lung tissues of the smokers were significantly higher than those in the ex-smokers (Plt;0.05) ; whereas in the healthy cases, no statistical significance was revealed between the smokers and the ex-smokers on the levels of MDA and IL-8 in lung tissues except TNF-α( Pgt;0.05) . Conclusion The abnormal increase of MDA, IL-8 and TNF-αin lung tissues caused by chronic smoking may play an important role in the the pathogenesis of COPD.