Asymptomatic Male Smokers Research Articles

Effect of cigarette smoking on lipid profile, high sensitivity c-reactive protein, and malondialdehyde

Background: One of the most common reasons for preventable mortality is the smoking habit. Cigarette smoke promotes the process of atherogenesis by producing oxygen-derived free radicals which cause damage to the lipids. Cigarette smoking is associated with impaired endothelium-dependent vasodilatation and cardiovascular disease (CVD). Aims and Objectives: The objectives of the study were the following: (i) to compare the levels of total cholesterol (TC), triglyceride (TG), high-density lipoprotein (HDL), low-density lipoprotein (LDL), and very LDL (VLDL) in asymptomatic male smokers and non-smokers of the age group 25–50 years; (ii) to determine and compare the levels of high sensitivity C-reactive protein (hs-CRP) in the above two groups, and (iii) to study and compare the levels of malondialdehyde (MDA) in the above groups. Materials and Methods: The study was conducted on 60 males in which 30 smokers and 30 non-smokers of the age group 25–50 years were incorporated. It was a cross-sectional comparative study, which included the participants who met all the inclusion and exclusion criteria. Before the conduct of the study, informed consent was obtained from all the participants. Moreover, the selection of participants was done in a consecutive manner until the sample size was achieved. TC and TGs were estimated by the enzymatic colorimetric method, HDL cholesterol by the phosphotungstic acid method, and LDL and VLDL by Friedwald’s formula. MDA was determined by spectrophotometry and hs-CRP by the immunoturbidometric method. The data acquired were analyzed by utilizing the Statistical Package for the Social Sciences version 18. Results: Dyslipidemia was seen in smokers as evidenced by significantly elevated levels of TC, TG, LDL, and VLDL; and significantly reduced levels of HDL. The mean values of hs-CRP were significantly elevated in smokers when compared to that of non-smokers. Oxidative stress was increased in subjects who were smokers. The mean values of MDA were significantly elevated in the smokers. Conclusion: The smoking habit is associated with dyslipidemia, oxidative stress, and inflammation which predisposes to the development of endothelial dysfunction and atherosclerosis. The significance of early screening measures to be undertaken in asymptomatic smokers for dyslipidemia, oxidative stress, and hs-CRP is unveiled by the present study. Therefore, early screening can be used to advise smokers to refrain from smoking to avoid complications of CVDs, so that they can upgrade the quality of their life.

Liver function parameters in asymptomatic smokers – A cross-sectional study

Background: Smoking remains the single most common cause of preventable deaths. The liver is affected by the process of smoking through various inflammatory pathways. This will lead to aggravation of pathogenic impact on the liver tissue. The present study was undertaken to determine the liver function parameters in cigarette smokers. Aims and Objectives: The objective was to estimate and compare the parameters of liver function – alanine transaminase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP), total bilirubin, total protein, albumin, and globulin in asymptomatic male smokers and non-smokers of the age group 25–50 years in the above two groups. Materials and Methods: A cross-sectional comparative study was conducted on 60 males with 30 smokers and 30 non-smokers of the age group 25–50 years. All the subjects who have satisfied the inclusion and exclusion criteria were incorporated in the study. Informed consent was taken before the conduct of the study. The participants were selected in a consecutive manner till the sample size was achieved. AST, ALT, ALP, total bilirubin, total protein, and albumin were estimated using ERBA EM 360 fully automatic analyzer. The difference between the total protein and albumin was used to calculate the level of globulin. The Statistical Package for the Social Sciences version 18 was used for data analysis. Results: The mean values of AST, ALT, and ALP were significantly elevated in smokers when compared to non-smokers. The mean values of total bilirubin, total protein, albumin, and globulin were significantly decreased in smokers. Conclusion: Smoking leads to the development of hepatic damage which increases the intensity of complications. The study reveals the importance of screening asymptomatic smokers for liver function parameters to avoid complications of hepatic diseases hence improving the quality of life.

Lung Transfer Factor in Middle Aged Asymptomatic Male Smokers of a City from West India: A Cross-Sectional Study.

Smoking is an increasingly popular indulgence in India. Assessment by routine spirometry falls short of direct functional parameter like Diffusion Lung Capacity (DLC), also known as lung transfer factor (LTF). To measure LTF amongst middle aged male smokers and to study various correlates for it. Total of 45 asymptomatic male current smokers were enrolled for this cross-sectional study conducted at pulmonary function testing lab of Physiology Department of our college. Smoking history was evaluated and smoking index was defined by product of number smoked per day and years smoked. We used instrument Ultima PFX of Medgraphic Company. After pre syringe calibration LTF was measured by Methane mixture using protocols of ATS. Parameters measured were Dlco-uncorrected, corrected and normalized to VA (alveolar volume). Results were compared for statistical significance and significance was set as p <0.05. In case group of 45(25 bidi and 20 cigarette smokers) mean age was 30 years, mean duration was 8 years, mean smoking index was 60. We found small insignificant decline in actual LTF values than predicted which was not significantly different between bidi and cigarette smokers. Duration, age and intensity of smoking were negatively and significantly correlated with LTF value while anthropometric parameters were not. Smoking adversely affects LTF in young asymptomatic current male smoker that further declines with severity of smoking and with duration regardless of type of smoking. With years to come, these alterations can largely be prevented by smoking cessation, at least theoretically.

Prevalence and progression of combined pulmonary fibrosis and emphysema in asymptomatic smokers: A case-control study.

We aimed to estimate the prevalence of combined pulmonary fibrosis and emphysema (CPFE) and describe the follow-up CT results of CPFE in asymptomatic smokers. This study was retrospective, and approved by an institutional review board. CT images of 2,016 current or previous male smokers who underwent low-dose chest CT at our healthcare centre were reviewed. Quantitative CT analysis was used to assess the extent of emphysema, and two radiologists visually analyzed the extent of fibrosis. Changes in fibrosis (no change, improvement, or progression) were evaluated on follow-up CT imaging (n = 42). Kaplan-Meier survival analysis, multivariate logistic regression and its ROC curve were used for survival and progression analysis. The prevalence of CPFE among asymptomatic male smokers was 3.1% (63/2,016). The median follow-up period was 50.4months, and 72.7% (16/22) of continued smoker had progressing fibrosis on follow-up CT. CPFE progressed more rapidly in continuous smokers than in former smokers (p = 0.002). The 3.5-year follow-up period after initial CPFE diagnosis maximized the sum of sensitivity and specificity of CPFE progression prediction in continuous smokers. The prevalence of CPFE turned out not to be inconsiderable in asymptomatic male smokers, but serial CT follow-up would be helpful in recognizing disease progression. • The prevalence of CPFE in asymptomatic smokers is 3.1 % (63/2,016). • Progression of CPFE is associated with smoking status. • 3.5years of follow-up period would be needed to identify CPFE progression.

Histiocitosis de células de Langerhans pulmonar: Caso clínico

Adult pulmonary Langerhans cell histiocytosis (PLCH) is a rare disorder of unknown etiology that occurs predominantly in young smokers, with an incidence peak at 20-40 years of age. In adults, pulmonary involvement with Langerhans cell histiocytosis usually occurs as a single-organ disease and is characterized by focal Langerhans cell granulomas infiltrating and destroying distal bronchioles. We report a 23-year-old asymptomatic male smoker with a non specific interstitial infiltrate found in preventive chest X ray examination. A high resolution chest CT scan showed multiple cystic structures predominating in the upper lobes, with small centrilobular nodules. A transbronchial biopsy showed a lymphocytic lung infiltrate with Langerhans cells. A surgical biopsy confirmed the diagnosis of pulmonary Langerhans cell histiocytosis. After six months of follow up, the patient is in good conditions.

Significantly higher prevalence of cad in asymptomatic male smokers as compared with their female counterparts

Objective: The incidence of coronary artery disease (CAD) as detected by myocardial perfusion imaging (MPI) in asymptomatic smokers is unknown. The objective was to compare the prevalence of CAD among male and female smokers who underwent dobutamine (DBA) stress test with MPI. Methods: We performed a retrospective cohort study on 192 smokers (99 males, mean age 70 + 11 years and 93 females, mean age 72 + 10 years) with severe COPD and no history of CAD, referred for DBA stress MPI for non-vascular elective surgeries. Clinical risks score for CAD were similar in both groups except more women had diabetes and hyperlipidemia than men. There was no significant difference in the number of pack years of cigarettes smoked. All patients achieved > 85% of predicted maximal heart rate with DBA infusion. Results: Overall 64 /192 (33%) had myocardial perfusion defects. The prevalence of defects among males was 53/99 (55%) versus 11/93 (12%) among females, p <0.001. The relative risk of CAD in males was 4.5 times compared to females. The prevalence of multi-vessel disease was higher in men than in women (30% vs 9%), p<0.001. Conclusion: In this study, we found a high prevalence of CAD among male asymptomatic COPD patients with extensive smoking history, compared with age and risk factor matched female asymptomatic COPD patients. Pulmonary limitations in males with severe COPD may mask their CAD.

Development of Barrett's Esophagus after ‘Spontaneous’ Healing of Atrophic Corpus Gastritis

We report here the case of a 58-year-old asymptomatic male smoker who had a gastroscopy performed in 1990 because of a low serum pepsinogen I level (16 microg/l). The patient had severe atrophic corpus gastritis and elevated Helicobacter pylori antibody titers, but no histologic evidence of the bacteria. Additionally, a hiatal hernia without esophagitis was seen. He was followed up endoscopically because of the atypical changes (indefinite for dysplasia) in addition to atrophic gastritis in some of the gastric biopsy samples. During the follow-up period, H. pylori antibody titers declined to normal levels without eradication therapy, and atrophic gastritis healed. The patient developed first erosive esophagitis, and, 5 years later, a 3-cm-long Barrett's esophagus was detected.

Improving coronary heart disease risk assessment in asymptomatic people: role of traditional risk factors and noninvasive cardiovascular tests.

At least 25% of coronary patients have sudden death or nonfatal myocardial infarction without prior symptoms.1 Therefore, the search for coronary patients with subclinical disease who could potentially benefit from intensive primary prevention efforts is critically important. The American Heart Association’s (AHA) Prevention V Conference, “Beyond Secondary Prevention: Identifying the High Risk Patient for Primary Prevention,” addressed ways to identify more patients who are asymptomatic and clinically free of coronary heart disease (CHD) but at sufficiently high risk for a future coronary event to justify more intensive risk reduction efforts.2 In this report, we amplify on key findings and recommendations of the AHA Prevention V conference, highlight new research since the conference, and propose an approach to the use of office-based testing and additional noninvasive procedures in selected patients to better define their coronary event risk. The recommendations are concordant with the recently released approach to risk assessment and management from the third report of the Adult Treatment Panel of the National Cholesterol Education Program (ATP-III).3 Enthusiasm for primary prevention and risk assessment in asymptomatic people has been spurred by recent advances in prevention research. Lipid-lowering trials demonstrated that primary prevention of coronary events is feasible, evidenced by the West of Scotland Coronary Primary Prevention Study (WOSCOPS) trial4 of hypercholesterolemic men and by the Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS) trial5 in average or typical risk men and women with only moderate lipid abnormalities. Aspirin6 or ACE inhibitors7 can also reduce risk in selected asymptomatic, high-risk people. Emerging coronary risk factors have been described including inflammatory, infectious, and thrombotic markers,8 and there has been a steady flow of reports that focus attention on potential new ways of predicting coronary risk.9 In addition, noninvasive tests for subclinical atherosclerotic disease are available …

Screening for Lung Cancer Has No Proven Utility

To the Editor. —Drs Lin and Ihde 1 began their discussion of lung cancer therapeutics with a selected case of a 45-year-old asymptomatic male smoker with a normal physical examination who had a nodule found on a "routine" chest roentgenogram. Although he was staged as T2,N0, he developed metastatic disease soon after lobectomy. If he had been my patient and I had followed the preventive care guidelines of the American College of Physicians, the Canadian Task Force on the Periodic Health Examination, the US Preventive Services Task Force, and the American Cancer Society, 2 a chest roentgenogram would not have been ordered routinely, even though he was at risk based on his smoking history. His cancer would have been discovered when he developed hemoptysis and his outcome would have been no different from what it was in this case. I wonder if Lin and Ihde chose this case for a

Cigarette smoking and density-dependence of maximal expiratory flow in asymptomatic men.

The influence of cigarette smoking on helium response of maximal expiratory flows was studied in 26 asymptomatic male smokers 35 to 55 yr of age. The subjects had smoked 18.0 +/- 10.6 cigarettes/day for 19.2 +/- 6.7 yr (total consumption, 16.1 +/- 9.8 pack/yr) and were selected because they had no history of cardiopulmonary disease, and their physical examination, chest roentgenogram, and spirographic results were normal. Maximal expiratory flow (at the mouth)-volume curves were recorded while the subjects breathed air and a mixture of an 80% helium and 20% oxygen; the helium response (delta He) was expressed as the difference between maximal expiratory flow with helium and maximal expiratory flow with air at 50 and 25% of vital capacity. Current cigarette consumption and total tobacco use were not related to either delta He50% or delta He25%. However, maximal expiratory flows with air and helium were significantly related to current cigarette consumption (for cigarettes/day versus Vmax50% air, r = - 0.587 and p < 0.01; for cigarettes/day versus Vmax25% He+O2, r = - 0.594 and p <0.01) or to lifetime tobacco consumption (for packyr versus Vmax50% air, r = - 0.39 and p < 0.05; for pack-yr versus Vmax25% He + O2, r = - 0.643 and p < 0.001). The result were compatible with a tobacco effect on both central and peripheral airways: increase in upstream resistance due to peripheral airway obstruction, and slight downstream displacement of equal pressure points due to increase in central airway resistance. We concluded that the helium response of maximal expiratory flows is less sensitive than maximal expiratory flows with air in detecting an early effect of tobacco in asymptomatic cigarette smokers.