3.12 Gastro-intestinal diseases

Last updated: May 2021

Suggested citation: Purcell, K. Winnall, W, Hurly, S and Greenhalgh E 3.12 Gastro-intestinal diseases. In Greenhalgh EM, Scollo, MM and Winstanley, MH [editors].  Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2021. Available from  http://www.tobaccoinaustralia.org.au/3-12-gastrointestinal-diseases

3.12.1 Peptic ulcer disease

Peptic ulcer disease involves the formation of ulcers in either the lining of the stomach (gastric ulcers) or the duodenum (duodenal ulcers), in the section of the small intestine closest to the stomach. Sometimes the lower oesophagus is also affected. Mucus and other secretions line the gastrointestinal tract, protecting it from gastric acid. If this protective mechanism is impaired, or if there is an increase in gastric acid or other damaging agents, then ulceration may occur.

The presence of Helicobacter pylori in the stomach causes damage to the gastrointestinal wall, greatly increasing the risk of developing peptic ulcers. Helicobacter pylori is present in all people with duodenal ulcers and 70–90% of people with gastric ulcers. The risk of developing peptic ulcers is also increased among people who take non-steroidal anti-inflammatory drugs (NSAIDS).

Peptic ulcers were the eleventh most common cause of hospital admissions in Australia in 2007–2008,1 and almost 3% of Australians reported having some sort of peptic ulcer in 2001.2

Smoking increases the risk of peptic ulcer disease in people who are infected with Helicobacter pylori.3 Smokers in the US have almost twice the risk of a peptic ulcer compared to non-smokers.4 In Australia, about 13% of peptic ulcer disease in men and 9% in women has been attributed to smoking.5

Smoking affects the gastrointestinal tract in several ways: it reduces the production of gastric mucus and other protective secretions, promotes duodenal reflux and reduces blood flow to the lining of the tract. In this compromised environment, Helicobacter pylori may be better able to spread and cause damage.3 Smoking may also be related to an increased risk of developing complications of peptic ulcer disease, such as ulcer perforation or bleeding, but this effect may be confined to people who are not taking NSAIDS. 3

The increased risk of peptic ulcer disease consequential to smoking appears to reverse with smoking cessation.3

The higher prevalence of peptic ulcer disease in people with mental illness may be due to smoking and alcohol dependence in this population.6

3.12.2 Inflammatory bowel disease

Inflammatory bowel disease (IBD) is a group of conditions in which the intestines are inflamed. The two major types of IBD are Crohn’s disease and ulcerative colitis. Crohn’s disease can involve any part of the gastrointestinal tract, but most commonly affects the small intestine or the colon. Ulcerative colitis is restricted to the colon and the rectum. The presenting symptoms of these two IBDs are often similar (abdominal pain, vomiting, diarrhoea), but the pathophysiology differs. Crohn’s disease is thought to be an autoimmune disease but ulcerative colitis is not. Tissue inflammation tends to be deeper with Crohn’s disease than with ulcerative colitis. Both conditions are treated with drugs and/or surgery.7, 8

A complex interaction between genetic factors and environmental factors, including smoking, influences the risk and prognosis of inflammatory bowel disease.9-11

The 2014 US Surgeon General’s report found that smoking at or before diagnosis was associated with a 1.8-fold increased risk of this disease. The report concluded that smoking is a likely cause of Crohn’s disease; however, while smokers had a higher risk of Crohn’s disease, more research is needed to determine whether smoking is a definitive cause of this increased risk.12 Smoking affects the immune system in a variety of ways and it is unclear which of its immunologic effects are relevant to Crohn’s disease.8

At the time of diagnosis, smokers with Crohn’s disease report a greater use and greater dependency on corticosteroids compared with non-smokers.13 People with Crohn’s disease who continue to smoke also have a worse prognosis and their symptoms are exacerbated compared with non-smokers.14 A 2016 systematic review and meta-analysis of the effects of smoking on the disease course in Crohn's disease confirmed that smokers had increased risks of a recurrence of disease activity.15 Smokers also have a greater risk of needing intestinal surgery.11, 13, 15 After surgery, they are more than twice as likely as non-smokers to have a disease recurrence, and a 2.5-fold increased risk of repeat surgery within 10 years.14 A meta-analysis found that smokers had a lower chance of success for specific treatments for Crohn’s disease. Smokers were less likely than non-smokers to have a clinical response or remission after anti-TNF therapy.16 Quitting smoking has a beneficial impact on disease related outcomes.15

Smokers with both main types of irritable bowel disease appear to be at greater risk of manifesting symptoms of the disease in other parts of the body, including chronic skin disorders and joint problems.17 Following cessation, the risk reduced to that of never smokers between 1 and 2 years after quitting.17

In contrast to its impact on Crohn’s disease, smokers seem to have a decreased risk of ulcerative colitis by about 40% and quitting increases the risk18 (see also Section 3.28). The 2014 Surgeon General’s report concluded that smoking may have a protective effect.12 Ex-smokers have an almost 80% higher risk of ulcerative colitis compared with never smokers.18 The reason or reasons for the apparent contradictory effect of smoking on the two main IBDs is unknown.8

Microscopic colitis is also a type of inflammatory bowel disease characterised by watery diarrhoea. It affects the large bowel and can only be diagnosed from a biopsy examined under the microscope. Two large prospective cohort studies of women in the United Kingdom found an association between current smoking and increased risk of microscopic colitis. The risk of microscopic colitis was greatest for heavier smokers (higher pack-years). The risk was reduced following sustained smoking cessation of five years or more.19 A meta-analysis found that smoking in both males and females was associated with an increased risk of microscopic colitis.20 Smokers had over 3 times the risk for both main types of the disease compared to non-smokers.20 Further research is required to determine if smoking is causally associated with microscopic colitis and the mechanisms involved.

3.12.3 Disorders of the liver and gallbladder

Smoking adversely affects the hepatobiliary system.

The ‘Million Women Study’ in the UK found that smokers had a two- to three-fold increased risk of liver cirrhosis and a small increased risk of gallbladder disease (symptomatic gallstones or cholecystitis), by about 10–30%.21 Ex-smokers were found to have elevated risks for these conditions compared with never smokers, but lower risks than current smokers.

A 2019 meta-analysis of data from 26 prospective studies found that smoking appears to increase the risk of developing all biliary tract cancers except gallbladder cancer.22

A 2016 systematic review and meta-analysis of 59,530 gallbladder disease among 4,213,482 participants found an increased risk of gallbladder disease associated with tobacco smoking. There was a dose-dependent positive association with increasing number of cigarettes smoked per day.23

Large case-control studies in the UK and US have found that smoking increases the risk of primary biliary cirrhosis (now referred to as primary biliary cholangitis) by about 50–60%.24, 25 Primary biliary cholangitis is an autoimmune disease that results in the destruction of hepatic bile ducts A 2011 meta-analysis of five published studies, that together included almost 2,000 cases of primary biliary cirrhosis, confirmed the association and found that smoking increases risk by almost 70%.26 A 2019 systematic review and meta-analysis of nine case controlled studies with 21,577 participants also confirmed that smokers were at greater risk of primary biliary cholangitis than never smokers. The effect of smoking on the immune system and the cytotoxic effect of cigarettes are potential mechanisms underlying this elevated risk.27 The severity of disease is associated with greater intensity of smoking. For every pack-year increase in smoking intensity, there was a 3.2 times higher likelihood of advanced fibrosis. Smokers with advanced primary biliary cholangitis also had increased mortality rates compared with never smokers.28

Non-alcoholic fatty liver disease (NAFLD) is another important liver disease often associated with obesity and metabolic syndrome. While some large studies have found that smoking is an independent risk factor for NAFLD,29, 30 others have reported that the association between smoking and risk of NAFLD only occurred among those who did not drink alcohol.31 There appears to be a dose–response association and the incidence of fatty liver disease increases significantly as the number of cigarettes smoked increased.31, 32 Smoking also appears to increase the severity of NAFLD, and smokers have a higher risk of liver fibrosis compared with non-smokers.33-36 People with NAFLD may also be more likely to die with this disease if they are smokers.37 There also appears to be an increased risk of NAFLD associated with exposure to secondhand smoke.38

 See Section 3.17 for a discussion of autoimmune disease of the liver.

3.12.4 Disorders of the pancreas

Pancreatitis is inflammation of the pancreas. It can be acute or chronic. The most common symptom is severe abdominal pain. Gallstones are a cause of acute pancreatitis and high alcohol intake is a risk factor for chronic pancreatitis. Smoking may increase the risk of gallstones and is also strongly associated with drinking alcohol. It was initially difficult to determine whether smoking per se increases the risk of pancreatitis independently of other risk factors. However, the association between smoking and pancreatitis is now well-established.39-42

Smoking is associated with an increased risk of acute pancreatitis, an earlier age of onset, and more frequent recurrences of acute pancreatitis.43 Dual use of tobacco and high-risk drinking are associated with increased risk.41, 44 Male smokers who consumed more than four drinks per day had a higher risk of developing pancreatitis compared with never smokers and former smokers. 41 The mechanisms by which smoking increases the risk of pancreatitis are not well understood, although two components of cigarette smoke, (nicotine and NNK) have been shown to induce changes in the pancreas consistent with those seen in pancreatitis.45, 46 A genetic study found evidence supporting a role for smoking and other risk factors (gallstone disease, type 2 diabetes and elevated calcium and triglyceride levels) in the causation of acute and chronic pancreatitis.47

A cohort study of over 18,000 residents of Copenhagen found that smoking increases the risk of pancreatitis, independently of its effect on gallstones and its association with alcohol consumption. In fact about 46% of cases of pancreatitis in this group of people were attributed to smoking.48 A 2015 meta-analysis of twenty-two studies also identified a positive association between cigarette smoking with the development of pancreatitis.40

A large population-based prospective study in the United States confirmed that smoking was an independent risk factor for non-gallstone related pancreatitis, recurrent acute pancreatitis and chronic pancreatitis. Smoking was not associated with gallstone acute pancreatitis.41 Another meta-analysis of 12 observational studies had similar findings—that smokers were at greater risk of developing acute pancreatitis but not gallstone related pancreatitis.42 A dose–response effect was observed, with current smokers having a 40% increased risk of acute pancreatitis for every additional 10 cigarettes per day they smoked.42

Another meta-analysis of twelve studies confirmed an association between smoking and increased risk of acute pancreatitis. The risk is strongest for current smokers, but former smokers had a higher risk compared with never smokers.49 A 2019 systematic review and meta-analysis found that current smoking was associated with 49%, 93% and 62% increases in the relative risk of acute pancreatitis, chronic pancreatitis and acute/chronic pancreatitis combined, respectively, compared to never smokers. Former smokers showed 24%, 30% and 29% increases in the relative risk compared to never smokers. There was a dose–response effect, with an increasing risk for every 10 cigarettes smoked per day and an increased risk for every 10 pack-years of smoking.50

Note that pancreatitis may increase the risk of pancreatic cancer, which is one of the malignancies caused by smoking (see Section 3.5.2).3

3.12.5 Other gastrointestinal disorders

Data from an Australian twin study suggest that smoking increases the risk of appendectomy by about 65%, but that this risk decreases by 15% every year after quitting.51 A retrospective survey of more than 6,000 male British construction workers who underwent appendicectomy over a 33-year period found that smoking increased the risk of perforated appendix and also increased the risk of post-operative consultations in non-perforated appendicitis (see Section 3.15).52

The microbiota refers to a community of microbes residing in a location comprising of bacteria, archaea, viruses, fungi, and protozoa.53 The gut microbiota has a critical role in the development of healthy immune responses.53 Smoking is associated with changes in the gut microbiota.54, 55 However, the ways in which smoking might alter the microbiota are still being examined.53 A 2018 study of people undergoing an upper GI endoscopy found that mucosa-associated microbiota (MAM) of current smokers has reduced bacterial diversity compared with never smokers.56 A population based cross-sectional study of 758 males, also found the bacterial composition of gut microbiota among smokers was different to that of never smokers.57 Smoking cessation has some benefits, with bacterial diversity at least partially or fully restored in ex-smokers.56,57

Sessile serrated polyps (SSPs) are associated with the development of colorectal cancer.58,59 A large cross-sectional study from Korea of more than 30,000 adults undergoing colonoscopy included both younger (30–49 years) and older (50–75 years) adults. Current smokers in both age groups had an increased risk of SSPs. Heavier smokers (those with the greatest pack-years) were at greater risk of developing SSPs than lighter smokers and never smokers and also had an elevated risk of larger or multiple SSPs.59

A 2016 systematic review and meta-analysis found that tobacco smoking is associated with an increased incidence of diverticular disease and related complications.60 This disease includes three conditions: diverticulosis (formation of pockets in the lining of the bowel), diverticulitis (inflammation and infection of these pockets) and diverticular bleeding. There was a dose-dependent effect, with increasing number of cigarettes smoked per day associated with higher risk of diverticular disease. There is also some evidence that smoking increases the risk of diverticular disease complications, but the number of relevant studies was small.60 A later study showed that smoking was associated with increased incidence of complications in diverticulitis, with a higher length of hospital stay but no difference in in-hospital mortality.61

For information about anal fistula, see Section 3.17.2


Relevant news and research

For recent news items and research on this topic, click  here. ( Last updated  June 2024)



1. Australian Institute of Health and Welfare, Australia's health 2010. Australia's health series no. 12. AIHW cat. no. AUS 122. Canberra: AIHW; 2010. Available from: https://www.aihw.gov.au/reports/australias-health/australias-health-2010/contents/table-of-contents.

2. Australian Institute of Health and Welfare, Australia's health 2004. Australia's health series no. 9. AIHW cat. no. AUS 44. Canberra: AIHW; 2004. Available from: https://www.aihw.gov.au/reports/australias-health/australias-health-2004/contents/table-of-contents.

3. US Department of Health and Human Services. The health consequences of smoking: a report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. Available from: http://www.cdc.gov/tobacco/data_statistics/sgr/index.htm.

4. Garrow D and Delegge MH. Risk factors for gastrointestinal ulcer disease in the US population. Digestive Diseases and Sciences, 2010; 55(1):66-72. Available from: https://www.ncbi.nlm.nih.gov/pubmed/19160043

5. Whetton S, Tait RJ, Scollo M, Banks E, Chapman J, et al. Identifying the social costs of tobacco use to Australia in 2015/16. National Drug Research Institute, Curtin University, 2019. Available from: https://ndri.curtin.edu.au/NDRI/media/documents/publications/T273.pdf.

6. Goodwin R, Keyes K, Stein M, and Talley N. Peptic ulcer and mental disorders among adults in the community: the role of nicotine and alcohol use disorders. Psychosomatic Medicine, 2009; 71(4):463–8. Available from: https://pubmed.ncbi.nlm.nih.gov/19443694/

7. Langholz E. Current trends in inflammatory bowel disease: the natural history. Therapeutic Advances in Gastroenterology, 2010; 3(2):77-86. Available from: https://www.ncbi.nlm.nih.gov/pubmed/21180592

8. El-Tawil AM. Smoking and inflammatory bowel diseases: what in smoking alters the course? International Journal of Colorectal Disease, 2010; 25(6):671-80. Available from: https://www.ncbi.nlm.nih.gov/pubmed/20333390

9. Allais L, De Smet R, Verschuere S, Talavera K, Cuvelier CA, et al. Transient receptor potential channels in intestinal inflammation: what is the impact of cigarette smoking? Pathobiology, 2017; 84(1):1-15. Available from: https://www.ncbi.nlm.nih.gov/pubmed/27388890

10. Adams A, Kalla R, and Satsangi J. Editorial: the influence of genetic factors in mediating the effects of tobacco smoke in IBD. Alimentary Pharmacology and Therapeutics, 2018; 47(2):306-7. Available from: https://www.ncbi.nlm.nih.gov/pubmed/29265462

11. Lang BM, Biedermann L, van Haaften WT, de Valliere C, Schuurmans M, et al. Genetic polymorphisms associated with smoking behaviour predict the risk of surgery in patients with Crohn's disease. Alimentary Pharmacology and Therapeutics, 2018; 47(1):55-66. Available from: https://www.ncbi.nlm.nih.gov/pubmed/29052254

12. US Department of Health and Human Services. The Health Consequences of Smoking: 50 Years of Progress. A Report of the Surgeon General. Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014. Available from: http://www.surgeongeneral.gov/library/reports/50-years-of-progress/full-report.pdf.

13. Alexakis C, Saxena S, Chhaya V, Cecil E, Majeed A, et al. Smoking status at diagnosis and subsequent smoking cessation: associations with corticosteroid use and intestinal resection in Crohn's disease. American Journal of Gastroenterology, 2018; 113(11):1689-700. Available from: https://www.ncbi.nlm.nih.gov/pubmed/30323269

14. Reese GE, Nanidis T, Borysiewicz C, Yamamoto T, Orchard T, et al. The effect of smoking after surgery for Crohn's disease: a meta-analysis of observational studies. International Journal of Colorectal Disease, 2008; 23(12):1213-21. Available from: https://www.ncbi.nlm.nih.gov/pubmed/18762954

15. To N, Gracie DJ, and Ford AC. Systematic review with meta-analysis: the adverse effects of tobacco smoking on the natural history of Crohn's disease. Alimentary Pharmacology and Therapeutics, 2016; 43(5):549-61. Available from: https://www.ncbi.nlm.nih.gov/pubmed/26749371

16. Lee S, Kuenzig ME, Ricciuto A, Zhang Z, Shim HH, et al. Smoking may reduce the effectiveness of anti-TNF therapies to induce clinical response and remission in Crohn's disease: A systematic review and meta-analysis. Journal of Crohn's and Colitis, 2021; 15(1):74-87. Available from: https://www.ncbi.nlm.nih.gov/pubmed/32621742

17. Severs M, van Erp SJ, van der Valk ME, Mangen MJ, Fidder HH, et al. Smoking is associated with extra-intestinal manifestations in inflammatory bowel disease. Journal of Crohn's and Colitis, 2016; 10(4):455-61. Available from: https://www.ncbi.nlm.nih.gov/pubmed/26721937

18. Mahid SS, Minor KS, Soto RE, Hornung CA, and Galandiuk S. Smoking and inflammatory bowel disease: a meta-analysis. Mayo Clinic Proceedings, 2006; 81(11):1462-71. Available from: https://www.ncbi.nlm.nih.gov/pubmed/17120402

19. Burke KE, Ananthakrishnan AN, Lochhead P, Olen O, Ludvigsson JF, et al. Smoking is associated with an increased risk of microscopic colitis: results from two large prospective cohort studies of US women. Journal of Crohn's and Colitis, 2018; 12(5):559-67. Available from: https://www.ncbi.nlm.nih.gov/pubmed/29370359

20. Al Momani L, Balagoni H, Alomari M, Gaddam S, Boonpherg B, et al. The association between smoking and both types of microscopic colitis: A systematic review and meta-analysis. Arab Journal of Gastroenterology, 2020; 21(1):9-18. Available from: https://www.ncbi.nlm.nih.gov/pubmed/32241698

21. Liu B, Balkwill A, Roddam A, Brown A, Beral V, et al. Separate and joint effects of alcohol and smoking on the risks of cirrhosis and gallbladder disease in middle-aged women. American Journal of Epidemiology, 2009; 169(2):153-60. Available from: https://www.ncbi.nlm.nih.gov/pubmed/19033524

22. McGee EE, Jackson SS, Petrick JL, Van Dyke AL, Adami HO, et al. Smoking, alcohol, and biliary tract cancer risk: A pooling project of 26 prospective studies. Journal of the National Cancer Institute, 2019; 111(12):1263-78. Available from: https://www.ncbi.nlm.nih.gov/pubmed/31127946

23. Aune D, Vatten LJ, and Boffetta P. Tobacco smoking and the risk of gallbladder disease. European Journal of Epidemiology, 2016; 31(7):643-53. Available from: https://www.ncbi.nlm.nih.gov/pubmed/26898907

24. Prince MI, Ducker SJ, and James OF. Case-control studies of risk factors for primary biliary cirrhosis in two United Kingdom populations. Gut, 2010; 59(4):508-12. Available from: https://www.ncbi.nlm.nih.gov/pubmed/20332522

25. Gershwin ME, Selmi C, Worman HJ, Gold EB, Watnik M, et al. Risk factors and comorbidities in primary biliary cirrhosis: a controlled interview-based study of 1032 patients. Hepatology, 2005; 42(5):1194-202. Available from: https://www.ncbi.nlm.nih.gov/pubmed/16250040

26. Liang Y, Yang Z, and Zhong R. Smoking, family history and urinary tract infection are associated with primary biliary cirrhosis: A meta-analysis. Hepatology Research, 2011; 41(6):572-8. Available from: https://www.ncbi.nlm.nih.gov/pubmed/21615644

27. Wijarnpreecha K, Werlang M, Panjawatanan P, Kroner PT, Mousa OY, et al. Association between smoking and risk of primary biliary cholangitis: A systematic review and meta-analysis. Journal of Gastrointestinal and Liver Diseases, 2019; 28:197-203. Available from: https://www.ncbi.nlm.nih.gov/pubmed/31204401

28. Mantaka A, Koulentaki M, Samonakis D, Sifaki-Pistolla D, Voumvouraki A, et al. Association of smoking with liver fibrosis and mortality in primary biliary cholangitis. European Journal of Gastroenterology and Hepatology, 2018; 30(12):1461-9. Available from: https://www.ncbi.nlm.nih.gov/pubmed/30106760

29. Kim BJ, Kang JG, Han JM, Kim JH, Lee SJ, et al. Association of self-reported and cotinine-verified smoking status with incidence of metabolic syndrome in 47 379 Korean adults. Journal of Diabetes, 2019; 11(5):402-9. Available from: https://www.ncbi.nlm.nih.gov/pubmed/30306721

30. Jung HS, Chang Y, Kwon MJ, Sung E, Yun KE, et al. Smoking and the risk of non-alcoholic fatty liver disease: A cohort study. American Journal of Gastroenterology, 2019; 114(3):453-63. Available from: https://www.ncbi.nlm.nih.gov/pubmed/30353055

31. Okamoto M, Miyake T, Kitai K, Furukawa S, Yamamoto S, et al. Cigarette smoking is a risk factor for the onset of fatty liver disease in nondrinkers: A longitudinal cohort study. PLoS ONE, 2018; 13(4):e0195147. Available from: https://www.ncbi.nlm.nih.gov/pubmed/29664906

32. Kim BJ, Han JM, Kang JG, Rhee EJ, Kim BS, et al. Relationship of cotinine-verified and self-reported smoking status with metabolic syndrome in 116,094 Korean adults. Journal of Clinical Lipidology, 2017; 11(3):638-45 e2. Available from: https://www.ncbi.nlm.nih.gov/pubmed/28431854

33. Munsterman ID, Smits MM, Andriessen R, van Nieuwkerk CMJ, Bloemena E, et al. Smoking is associated with severity of liver fibrosis but not with histological severity in nonalcoholic fatty liver disease. Results from a cross-sectional study. Scandinavian Journal of Gastroenterology, 2017; 52(8):881-5. Available from: https://www.ncbi.nlm.nih.gov/pubmed/28446050

34. Ou H, Fu Y, Liao W, Zheng C, and Wu X. Association between smoking and liver fibrosis among patients with nonalcoholic fatty liver disease. Canadian Journal of Gastroenterology and Hepatology, 2019; 2019:6028952. Available from: https://www.ncbi.nlm.nih.gov/pubmed/31737583

35. Zein CO, Unalp A, Colvin R, Liu YC, McCullough AJ, et al. Smoking and severity of hepatic fibrosis in nonalcoholic fatty liver disease. Journal of Hepatology, 2011; 54(4):753-9. Available from: https://www.ncbi.nlm.nih.gov/pubmed/21126792

36. Takenaka H, Fujita T, Masuda A, Yano Y, Watanabe A, et al. Non-alcoholic fatty liver disease is strongly associated with smoking status and is improved by smoking cessation in Japanese males: A retrospective study. Kobe Journal of Medical Sciences, 2020; 66(3):E102-E12. Available from: https://www.ncbi.nlm.nih.gov/pubmed/33431783

37. Charatcharoenwitthaya P, Karaketklang K, and Aekplakorn W. Cigarette smoking increased risk of overall mortality in patients with non-alcoholic fatty liver disease: A nationwide population-based cohort study. Frontiers in Medicine, 2020; 7:604919. Available from: https://www.ncbi.nlm.nih.gov/pubmed/33365321

38. Akhavan Rezayat A, Dadgar Moghadam M, Ghasemi Nour M, Shirazinia M, Ghodsi H, et al. Association between smoking and non-alcoholic fatty liver disease: A systematic review and meta-analysis. SAGE Open Medicine, 2018; 6:2050312117745223. Available from: https://www.ncbi.nlm.nih.gov/pubmed/29399359

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