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      Relationship between pain outcomes and smoking history following video-assisted thoracic surgery for lobectomy: a retrospective study

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          The relationship between chronic smoking history and postoperative pain remains controversial. This study aimed to elucidate this relationship in non-small cell lung cancer (NSCLC) patients who underwent video-assisted thoracic surgery (VATS) lobectomy.

          Patients and methods

          This retrospective observational study included NSCLC patients treated with VATS lobectomy between January 2011 and July 2017. Demographic and clinical information, including preoperative smoking history, was collected. The primary goal was to investigate the relationship between smoking history and postoperative pain outcomes (oral morphine equivalent [OME] consumption and pain score). Multivariate linear regression analysis was performed, and P<0.05 was considered as statistically significant.


          A total of 1,785 patients were included in the final analysis. Multivariate linear regression analysis revealed that total smoking amount (in packs), status as current smoker, and cessation time did not have an association with OME consumption (mg) or pain scores on postoperative days 0–2 ( P>0.05). However, patients who had never smoked consumed less morphine equivalent analgesics (mg) on postoperative days 0–2 (coefficient: −17.48, 95% CI [−33.83, −1.13], P=0.036) compared to patients who had a history of smoking.


          Patients who had never smoked had lower opioid analgesics consumption on the days immediately following surgery, while being a current smoker or the total amount of smoking in packs did not affect postoperative pain outcomes after VATS lung lobectomy.

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          Most cited references 23

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          Smoking, smoking cessation, and lung cancer in the UK since 1950: combination of national statistics with two case-control studies.

           R Doll,  R. Peto,  E Whitley (2000)
          To relate UK national trends since 1950 in smoking, in smoking cessation, and in lung cancer to the contrasting results from two large case-control studies centred around 1950 and 1990. United Kingdom. Hospital patients under 75 years of age with and without lung cancer in 1950 and 1990, plus, in 1990, a matched sample of the local population: 1465 case-control pairs in the 1950 study, and 982 cases plus 3185 controls in the 1990 study. Smoking prevalence and lung cancer. For men in early middle age in the United Kingdom the prevalence of smoking halved between 1950 and 1990 but the death rate from lung cancer at ages 35-54 fell even more rapidly, indicating some reduction in the risk among continuing smokers. In contrast, women and older men who were still current smokers in 1990 were more likely than those in 1950 to have been persistent cigarette smokers throughout adult life and so had higher lung cancer rates than current smokers in 1950. The cumulative risk of death from lung cancer by age 75 (in the absence of other causes of death) rose from 6% at 1950 rates to 16% at 1990 rates in male cigarette smokers, and from 1% to 10% in female cigarette smokers. Among both men and women in 1990, however, the former smokers had only a fraction of the lung cancer rate of continuing smokers, and this fraction fell steeply with time since stopping. By 1990 cessation had almost halved the number of lung cancers that would have been expected if the former smokers had continued. For men who stopped at ages 60, 50, 40, and 30 the cumulative risks of lung cancer by age 75 were 10%, 6%, 3%, and 2%. People who stop smoking, even well into middle age, avoid most of their subsequent risk of lung cancer, and stopping before middle age avoids more than 90% of the risk attributable to tobacco. Mortality in the near future and throughout the first half of the 21st century could be substantially reduced by current smokers giving up the habit. In contrast, the extent to which young people henceforth become persistent smokers will affect mortality rates chiefly in the middle or second half of the 21st century.
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            Smoking and pain: pathophysiology and clinical implications.

            Cigarette smoke, which serves as a nicotine delivery vehicle in humans, produces profound changes in physiology. Experimental studies suggest that nicotine has analgesic properties. However, epidemiologic evidence shows that smoking is a risk factor for chronic pain. The complex relationship between smoking and pain not only is of scientific interest, but also has clinical relevance in the practice of anesthesiology and pain medicine. This review will examine current knowledge regarding how acute and chronic exposure to nicotine and cigarette smoke affects acute and chronic painful conditions. It will cover the relevant pharmacology of nicotine and other ligands at the nicotinic acetylcholine receptor as related to pain, explore the association of cigarette smoking with chronic painful conditions and potential mechanisms to explain this association, and examine clinical implications for the care of smokers with pain.
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              Smoking and low back pain. A systematic literature review of 41 journal articles reporting 47 epidemiologic studies.

               Christian Yde (1999)
              A systematic review of the epidemiologic literature on smoking and low back pain. To establish whether smoking causes low back pain and whether cessation of smoking reduces the incidence and/or prevalence of low back pain. It seems to have become increasingly commonly accepted that smoking causes low back pain and that abstinence from smoking is an effective means for its prevention and treatment. Does the evidence in the epidemiologic literature support this concept? Forty-one original research reports reporting 47 studies, published between 1974 and 1996, were systematically reviewed for strength of association, dose-response correlation, temporality, reduction of symptoms with smoke cessation, and consistency of findings. In addition, the presence of positive findings was viewed in light of definition of low back pain, representativeness of the study sample, sample size, and in relation to whether the prime objective had been to study the smoking-low back pain issue. Two reviews were performed by the author, blindly and separated by a 2-month interval. There was no consistency of statistically significant positive associations between smoking and low back pain. The association, when present, was usually weak and clearly apparent only in large study samples. No other study characteristics had an effect on the frequency of positive associations. Additional analyses were therefore performed only on studies with large samples. In general, these did not contain consistent positive findings in relation to dose-response, temporality, or reversibility. Signs of causality were consistently evident only in the study with the largest sample (n > 30,000). Presently, smoking should be considered a weak risk indicator and not a cause of low back pain.

                Author and article information

                J Pain Res
                J Pain Res
                Journal of Pain Research
                Journal of Pain Research
                Dove Medical Press
                06 April 2018
                : 11
                : 667-673
                [1 ]Department of Anesthesiology and Pain Medicine, Seoul National University Bundang Hospital, Seongnam, Korea
                [2 ]Department of Thoracic and Cardiovascular Surgery, Seoul National University Bundang Hospital, Seongnam, Korea
                Author notes
                Correspondence: In-Ae Song, Department of Anesthesiology and Pain Medicine, Seoul National University Bundang Hospital, 166, Gumi-ro, Bundang-gu, Seongnam 463-707, Korea, Tel +82 31 787 7499, Fax +82 31 787 4063, Email songoficu@ 123456outlook.kr
                © 2018 Oh et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                Original Research

                Anesthesiology & Pain management

                anesthesia, analgesia, opioid, postoperative pain, smoking


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