3.17 Inflammatory conditions and autoimmune disease

Last updated: February 2024 
Suggested citation: Kalitsis, L, Winnall, WR, Hurley, S, & Greenhalgh, EM 3.17 Inflammatory conditions and autoimmune disease. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2024. Available from https://www.tobaccoinaustralia.org.au/chapter-3-health-effects/3-17-inflammatory-conditions-and-autoimmune-disease


Along with its widely recognised role in cancer, lung diseases and cardiovascular diseases, smoking also has wide-ranging and severe impacts on the immune system. It increases inflammation levels, increases the risk of allergic conditions, increases the incidence of autoimmune diseases, decreases immune responses to infectious diseases and increases infection rates.1 The 2014 US Surgeon General’s report concluded that components of cigarette smoke have both immune activating and immune-suppressive effects.2

This section describes the effects of smoking on chronic inflammation and autoimmune diseases. See Section 3.9 for a description of how cigarette smoke increases the susceptibility to infection of smokers.


Inflammation is a response of the immune system to a range of stimuli. These include infections, injuries, damage from heat or chemical burns, poisoning, as well as conditions such as autoimmune diseases and atherosclerosis (hardening of the arteries). Inflammation involves an influx of immune cells, usually white blood cells, into an area of damage or infection. Inflammation is a process used to fight infections, clear damage, and heal wounds. Counterintuitively, inflammation itself can cause damage, particularly if it continues unresolved for a long period of time.2,3

Acute (short-term) inflammation usually last for a few days. Causes include injuries and bacterial infections. Chronic inflammation refers to long-term conditions. Often chronic inflammation occurs as an aberration of the immune system, where it inadvertently attacks the body rather than responding to a pathogen or clearing damage. This section discusses chronic inflammatory conditions affected by smoking, particularly autoimmune diseases.

Cigarette smoke has pro-inflammatory effects that trigger an inflammatory response. This occurs both in the lungs and in the rest of the body. The chemicals present in cigarette smoke interact with various different cell types of the immune system, increasing the numbers of cells that accumulate at site of inflammation and changing the levels of cytokines (signalling molecules released by immune cells)1 and other biological molecules that regulate inflammation.2

Autoimmune diseases

Autoimmune diseases are a range of at least 80 conditions in which the immune system attacks the body. In these diseases, an immune response is raised to a healthy part of the person’s own body, rather than to an invading pathogen or an injury. Chronic inflammation is a common symptom for people with autoimmune diseases and leads to damage that causes problems specific to each separate disease. Autoimmune diseases are usually long-term conditions without a cure, however treatments that reduce inflammation can improve quality of life for people suffering many of these conditions. The exact causes—that is, the reasons why the immune system attacks the body—are usually unknown. Many autoimmune diseases involve production of antibodies that recognise parts of the body rather than pathogens.4 These auto-antibodies direct immune responses to damage normal tissues. Another feature of some autoimmune diseases are white blood cells called T-cells that recognise and attack normal cells rather than virally infected cells, their standard target.2

3.17.1 Rheumatoid arthritis

Rheumatoid arthritis is an autoimmune disease characterised by joint inflammation, pain, swelling, stiffness and loss of function. Rheumatoid arthritis most commonly affects synovial joints, such as those in the hands, arms, knees and feet. Many people with rheumatoid arthritis suffer debilitating fatigue which makes it difficult to participate fully in life.5,6About 456,000 Australians (1.9% of the total population) have rheumatoid arthritis, based on self-reported data from 2017–18, with the prevalence being higher for women (2.3%) than for men (1.5%).6

Several auto-antibodies are involved in the pathophysiology of rheumatoid arthritis, of which rheumatoid factor (RF) and anti-citrullinated protein antibodies (ACPA) are the most common.7 The presence of RF and/or ACPA antibodies in a joint activates and attracts immune cells. Pro-inflammatory signaling molecules are subsequently released by these cells, which can amplify the immune response and contribute to chronic inflammation of and damage to the joint.7,8  

The 2014 US Surgeon General’s report concluded that cigarette smoking is a cause of rheumatoid arthritis.2 The risk of developing rheumatoid arthritis is between 1.4 and 4 times higher for people who smoke compared to those who have never smoked, with evidence suggesting that there is a dose-response relationship between smoking and the risk of disease development.2 Rheumatoid arthritis patients who smoke have been shown to have higher levels of RF antibodies compared to patients who have never smoked.9-11 The interaction between smoking and genetic factors may explain this association. However, further research is warranted to clarify the exact mechanism.12  Observational studies have found that current smoking is associated with greater disease activity and lower health-related quality of life among rheumatoid arthritis patients.13,14

Immunosuppressant and anti-inflammatory drugs are effective treatment options for rheumatoid arthritis.15 However, smoking reduces the efficacy of and response to many drug treatments.2,16,17 One example is methotrexate, a common immunosuppressant used in the treatment of rheumatoid arthritis. A 2023 systematic review and meta-analysis found that patients with rheumatoid arthritis who smoked were 2.69 times more likely to have no benefit from methotrexate compared to patients who did not smoke.17 Similarly, tumour necrosis factor alpha (TNFα) inhibitors reduce inflammation associated with rheumatoid arthritis by blocking the effects of TNFα, a pro-inflammatory signalling molecule.18 An observational study found that rheumatoid arthritis patients who smoked were less likely to benefit from TNFα inhibitors compared to those who did not smoke.16

A 2022 systematic review and meta-analysis assessing smoking cessation interventions used among rheumatoid arthritis patients found that cessation rates ranged between 4% and 43% depending on the intervention, duration of follow-up period, and quality of the study.19 Further research is necessary to determine whether smoking cessation reduces the risk, severity, and progression of the disease.19,20 For more information on cessation interventions for people with health conditions see Section 7.12.

3.17.2 Anal abscess and fistula

Anal abscess is an inflammatory disease of the skin around the anus. Inflammation causes sores, or ulcers, to form on the inside wall of the bowel. Those ulcers can extend through the entire thickness of the bowel wall, creating a tunnel (or ‘fistula’) to drain the pus from the infected area through an abscess on the skin on or near the anus. The fistula remains even if the abscess is successfully treated with antibiotics and this is prone to constant inflammation and re-infection.21 A small case–control study of 74 patients with anal abscess/fistula found that smoking within the previous year doubled the risk of this condition.22 Further evidence resulted from a case–control study in 2018. This study of a Chinese population found people with an anal abscess had a 12.3-fold higher odds of a history of smoking compared to people without the condition.23  

3.17.3 Graves’ disease

Graves’ disease is an autoimmune disease that affects the thyroid gland, usually leading to an enlargement of the gland and increased production of thyroid hormones. Some symptoms, such as insomnia, weight-loss, and sweating, result from the changes in thyroid hormones, whereas symptoms such as swelling and complications affecting the eyes are a result of autoimmune inflammation.24  

Genetic factors account for most of the risk for Graves’s disease, with environmental risk factors accounting for approximately 21% of the risk.25 Smoking is a risk factor for Graves’ disease, but there is currently insufficient evidence to conclude that smoking is a cause. A case–control study from 1993 found that smokers had a 1.9-fold higher odds of developing Grave’s disease than non-smokers.26 In addition, a 2023 population-based study found that smoking exacerbated the risk of developing Grave’s disease among those who already had a family history of the disease.27

Smoking is also a risk factor for a rare complication of Grave’s disease called Graves’ ophthalmopathy.28 For more details, see Section 3.10.4.

3.17.4 Psoriasis (see Skin 3.14.4)

3.17.5 Systemic lupus erythematosus (see Skin 3.14.5)

3.17.6 Diabetes (see Smoking and Diabetes in Section 3.16)

3.17.7 Multiple Sclerosis

Multiple sclerosis is an autoimmune disease of the central nervous system (the brain, spinal cord, and optic nerves).29 This disease occurs when the immune system attacks the myelin sheath, a protective covering surrounding nerve cells. This results in the development of lesions and demyelination, which subsequently disrupt nerve cell signaling.29 The clinical presentation of multiple sclerosis depends on the location and severity of lesions and demyelination. Disease progression also varies, with some patients experiencing relapsing and/or progressive symptoms.30 For information about other neurological diseases, see section 3.18.2.

Smoking is considered to be a risk factor for multiple sclerosis.2,31,32 However, there is evolving research that suggests smoking may have a causative role in the development of this disease. A 2017 systematic review and meta-analysis exploring the association between smoking and multiple sclerosis pooled data from 36 studies, of which 28 case-control, four cross-sectional, and four cohort studies were included. The meta-analysis demonstrated that people who smoke had around a 50% higher risk of developing multiple sclerosis compared to people who did not smoke.33 The authors utilised the “Bradford Hill” criteria to assess causality, and concluded that there was strong evidence of a causal relationship between smoking and the risk of developing multiple sclerosis, and moderate evidence of a causal role of smoking in disease progression.33

Numerous studies have found that multiple sclerosis patients who smoke may have a higher risk of greater disease severity and complications, including increased respiratory symptoms,34 greater brain atrophy,35-37 worse cognitive function,36,38 higher disability burden,39,40 and higher frequency of relapse.41 Some of these disease outcomes have been found to be reversible with cessation.31

The biological mechanisms that underpin the association between smoking and multiple sclerosis are unclear, however several potential mechanisms have been suggested. Cigarette smoke contains nitric oxide, which may play a role in the degradation of nerve tissue.40,42,43 Free radicals, cyanates, and carbon monoxide in cigarette smoke may also be toxic to nerve cells.31 People who smoke experience long-term inflammation and changes to the regulation of inflammatory cells that may play a role in causing autoimmune diseases such as multiple sclerosis.40 People who smoke also have a higher risk of cardiovascular diseases which also increases their risk of multiple sclerosis progression.40,44

3.17.8 Primary biliary cirrhosis

Primary biliary cirrhosis is a rare autoimmune disease of the liver. Numerous studies have shown that smokers are more likely to develop this disease compared to non-smokers.45-47 A systematic review and meta-analysis from 2019 found that the odds of primary biliary cirrhosis for ever smokers was significantly higher than non-smokers (odds ratio of 1.31). Smoking was also associated with an increased risk of more severe disease46,48 and mortality from this condition.49 For more details, see Section 3.12.3.

3.17.9 Inflammatory Bowel Disease (see Section 3.12.2)

3.17.10 Other autoimmune diseases

There is some evidence of an effect of smoking on other chronic inflammatory and autoimmune diseases. However, the evidence is insufficient for making specific conclusions about smoking being an independent risk factor or a cause.

Smoking may be a risk factor for a rare disease called chronic periaortitis (inflammation surrounding the aorta).50 Smoking may also be a risk factor for microscopic colitis, a common cause of chronic, non-bloody diarrhoea.51


Relevant news and research

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



1. Arnson Y, Shoenfeld Y, and Amital H. Effects of tobacco smoke on immunity, inflammation and autoimmunity. Journal of Autoimmunity, 2010; 34(3):J258-65. Available from: https://www.ncbi.nlm.nih.gov/pubmed/20042314

2. 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: https://www.ncbi.nlm.nih.gov/books/NBK179276/pdf/Bookshelf_NBK179276.pdf.

3. Duan L, Rao X, and Sigdel KR. Regulation of Inflammation in Autoimmune Disease. Journal of Immunology Research, 2019; 2019:7403796. Available from: https://www.ncbi.nlm.nih.gov/pubmed/30944837

4. Office on Women's Health. Autoimmune diseases. US Department of Health & Human Services 2019. Last update: Viewed Available from: https://www.womenshealth.gov/a-z-topics/autoimmune-diseases.

5. Aletaha D and Smolen JS. Diagnosis and Management of Rheumatoid Arthritis: A Review. Journal of the American Medical Association, 2018; 320(13):1360-72. Available from: https://doi.org/10.1001/jama.2018.13103

6. Australian Institute of Health and Welfare. Rheumatoid arthritis.  Canberra: AIHW, 2023. Available from: https://www.aihw.gov.au/reports/chronic-musculoskeletal-conditions/rheumatoid-arthritis.

7. Derksen V, Huizinga TWJ, and van der Woude D. The role of autoantibodies in the pathophysiology of rheumatoid arthritis. Seminars in Immunopathology, 2017; 39(4):437-46. Available from: https://www.ncbi.nlm.nih.gov/pubmed/28451788

8. van Delft MAM and Huizinga TWJ. An overview of autoantibodies in rheumatoid arthritis. Journal of Autoimmunity, 2020; 110:102392. Available from: https://www.sciencedirect.com/science/article/pii/S0896841119308194

9. Elzorkany B, Mokbel A, Gamal SM, Hmamouchi I, and Dougados M. Does smoking affect level of seropositivity in RA? A post-HOC global and inter-country analysis of COMORA cohort. Rheumatology International, 2021. Available from: https://www.ncbi.nlm.nih.gov/pubmed/33625544

10. Sugiyama D, Nishimura K, Tamaki K, Tsuji G, Nakazawa T, et al. Impact of smoking as a risk factor for developing rheumatoid arthritis: a meta-analysis of observational studies Annals of the Rheumatic Diseases, 2010; 69(1):70–81. Available from: http://ard.bmj.com/cgi/rapidpdf/ard.2008.096487v2

11. Regueiro C, Rodriguez-Rodriguez L, Lopez-Mejias R, Nuno L, Triguero-Martinez A, et al. A predominant involvement of the triple seropositive patients and others with rheumatoid factor in the association of smoking with rheumatoid arthritis. Science Reports, 2020; 10(1):3355. Available from: https://www.ncbi.nlm.nih.gov/pubmed/32098994

12. Ishikawa Y and Terao C. The Impact of Cigarette Smoking on Risk of Rheumatoid Arthritis: A Narrative Review. Cells, 2020; 9(2). Available from: https://www.ncbi.nlm.nih.gov/pubmed/32092988

13. Alfredsson L, Klareskog L, and Hedstrom AK. Influence of smoking on disease activity and quality of life in patients with rheumatoid arthritis: results from a Swedish case-control study with longitudinal follow-up. Arthritis Care and Research, 2022. Available from: https://www.ncbi.nlm.nih.gov/pubmed/36149365

14. Gianfrancesco MA, Trupin L, Shiboski S, van der Laan M, Graf J, et al. Smoking Is Associated with Higher Disease Activity in Rheumatoid Arthritis: A Longitudinal Study Controlling for Time-varying Covariates. Journal of Rheumatology, 2018. Available from: https://www.ncbi.nlm.nih.gov/pubmed/30504507

15. Di Matteo A, Bathon JM, and Emery P. Rheumatoid arthritis. The Lancet, 2023; 402(10416):2019-33. Available from: https://www.sciencedirect.com/science/article/pii/S0140673623015258

16. Saevarsdottir S, Wedren S, Seddighzadeh M, Bengtsson C, Wesley A, et al. Patients with early rheumatoid arthritis who smoke are less likely to respond to treatment with methotrexate and tumor necrosis factor inhibitors: observations from the Epidemiological Investigation of Rheumatoid Arthritis and the Swedish Rheumatology Register cohorts. Arthritis and Rheumitism, 2011; 63(1):26-36. Available from: https://www.ncbi.nlm.nih.gov/pubmed/20862678

17. Nayebirad S, Javinani A, Javadi M, Yousefi-Koma H, Farahmand K, et al. The effect of smoking on response to methotrexate in rheumatoid arthritis patients: A systematic review and meta-analysis. Modern Rheumatology, 2023. Available from: https://www.ncbi.nlm.nih.gov/pubmed/36688574

18. Ma X and Xu S. TNF inhibitor therapy for rheumatoid arthritis. Biomed Reports, 2013; 1(2):177-84. Available from: https://www.ncbi.nlm.nih.gov/pubmed/24648915

19. Lopez-Olivo MA, Sharma G, Singh G, James J, Krause KJ, et al. A systematic review with meta-analysis of the effects of smoking cessation strategies in patients with rheumatoid arthritis. PLoS ONE, 2022; 17(12):e0279065. Available from: https://www.ncbi.nlm.nih.gov/pubmed/36520847

20. Roelsgaard IK, Esbensen BA, Ostergaard M, Rollefstad S, Semb AG, et al. Smoking cessation intervention for reducing disease activity in chronic autoimmune inflammatory joint diseases. Cochrane Database of Systematic Reviews, 2019; 9:CD012958. Available from: https://www.ncbi.nlm.nih.gov/pubmed/31476270

21. Colorectal Surgical Society of Australia and New Zealand. Anal Abscess / Anal Fistula.  2013. Last update: Viewed Available from: https://cssanz.org/index.php/patients/anal-abscess-anal-fistula.

22. Devaraj B, Khabassi S, and Cosman BC. Recent smoking is a risk factor for anal abscess and fistula. Diseases of the Colon and Rectum, 2011; 54(6):681-5. Available from: https://www.ncbi.nlm.nih.gov/pubmed/21552051

23. Zheng LH, Zhang AZ, Shi YY, Li X, Jia LS, et al. Impact of Smoking on Anal Abscess and Anal Fistula Diseases. Chinese Medical Journal, 2018; 131(9):1034-7. Available from: https://www.ncbi.nlm.nih.gov/pubmed/29692373

24. Smith TJ and Hegedüs L. Graves’ disease. New England Journal of Medicine, 2016; 375(16):1552-65.

25. Antonelli A, Ferrari SM, Ragusa F, Elia G, Paparo SR, et al. Graves' disease: Epidemiology, genetic and environmental risk factors and viruses. Best Practice & Research Clinical Endocrinology & Metabolism, 2020; 34(1):101387. Available from: https://www.ncbi.nlm.nih.gov/pubmed/32107168

26. Prummel MF and Wiersinga WM. Smoking and risk of Graves' disease. Journal of the American Medical Association, 1993; 269(4):479-82. Available from: https://www.ncbi.nlm.nih.gov/pubmed/8419666

27. Kim HJ, Hong G, Hwang J, Kazmi SZ, Kim KH, et al. Familial Risk of Graves' Disease among First-Degree Relatives and Interaction with Smoking: A Population-Based Study. Journal of Clinical Endocrinology and Metabolism, 2023. Available from: https://www.ncbi.nlm.nih.gov/pubmed/36808421

28. 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: https://www.cdc.gov/tobacco/data_statistics/sgr/2004/complete_report/index.htm.

29. Thompson AJ, Baranzini SE, Geurts J, Hemmer B, and Ciccarelli O. Multiple sclerosis. The Lancet, 2018; 391(10130):1622-36. Available from: https://www.sciencedirect.com/science/article/pii/S0140673618304811

30. Brownlee WJ, Hardy TA, Fazekas F, and Miller DH. Diagnosis of multiple sclerosis: progress and challenges. The Lancet, 2017; 389(10076):1336-46. Available from: https://www.sciencedirect.com/science/article/pii/S014067361630959X

31. Rosso M and Chitnis T. Association between cigarette smoking and multiple sclerosis: A review. Journal of the American Medical Association Neurology, 2020; 77(2):245-53. Available from: https://www.ncbi.nlm.nih.gov/pubmed/31841592

32. Handel AE, Williamson AJ, Disanto G, Dobson R, Giovannoni G, et al. Smoking and multiple sclerosis: an updated meta-analysis. PLoS ONE, 2011; 6(1):e16149. Available from: https://www.ncbi.nlm.nih.gov/pubmed/21249154

33. Degelman ML and Herman KM. Smoking and multiple sclerosis: A systematic review and meta-analysis using the Bradford Hill criteria for causation. Multiple Sclerosis and Related Disorders, 2017; 17:207-16. Available from: https://www.ncbi.nlm.nih.gov/pubmed/29055459

34. Aktan R, Ozalevli S, and Ozakbas S. Effects of cigarette smoking on respiratory problems and functional levels in multiple sclerosis patients. Multiple Sclerosis and Related Disorders, 2018; 25:271-5. Available from: https://www.ncbi.nlm.nih.gov/pubmed/30153625

35. Graetz C, Groger A, Luessi F, Salmen A, Zoller D, et al. Association of smoking but not HLA-DRB1*15:01, APOE or body mass index with brain atrophy in early multiple sclerosis. Multiple Sclerosis, 2019; 25(5):661-8. Available from: https://www.ncbi.nlm.nih.gov/pubmed/29532745

36. Alshehri E, Cohen JA, Ontaneda D, Nakamura K, Husak S, et al. The impact of cigarette smoking on cognitive processing speed and brain atrophy in multiple sclerosis. Multiple Sclerosis, 2023:13524585231172490. Available from: https://www.ncbi.nlm.nih.gov/pubmed/37204214

37. Lie IA, Wesnes K, Kvistad SS, Brouwer I, Wergeland S, et al. The Effect of Smoking on Long-term Gray Matter Atrophy and Clinical Disability in Patients with Relapsing-Remitting Multiple Sclerosis. Neurology Neuroimmunology & Neuroinflammation, 2022; 9(5). Available from: https://www.ncbi.nlm.nih.gov/pubmed/35738901

38. Cortese M, Munger KL, Martinez-Lapiscina EH, Barro C, Edan G, et al. Vitamin D, smoking, EBV, and long-term cognitive performance in MS: 11-year follow-up of BENEFIT. Neurology, 2020; 94(18):e1950-e60. Available from: https://www.ncbi.nlm.nih.gov/pubmed/32300060

39. Heydarpour P, Manouchehrinia A, Beiki O, Mousavi SE, Abdolalizadeh A, et al. Smoking and worsening disability in multiple sclerosis: A meta-analysis. Acta Neurologica Scandinavica, 2018; 138(1):62-9. Available from: https://www.ncbi.nlm.nih.gov/pubmed/29542102

40. Hedstrom AK. Smoking and disability progression in multiple sclerosis. Expert Reviews of Neurotherapeutics, 2020; 20(8):739-41. Available from: https://www.ncbi.nlm.nih.gov/pubmed/32208034

41. Jasielski P, Piedel F, Rocka A, Petit V, and Rejdak K. Smoking as a risk factor of onset and relapse of Multiple Sclerosis - a review. Neurologica i Neurochirurgia Polska, 2020; 54(3):243-51. Available from: https://www.ncbi.nlm.nih.gov/pubmed/32285433

42. Smith KJ, Kapoor R, Hall SM, and Davies M. Electrically active axons degenerate when exposed to nitric oxide. Annals of Neurology, 2001; 49(4):470-6. Available from: https://www.ncbi.nlm.nih.gov/pubmed/11310624

43. Rejdak K, Eikelenboom MJ, Petzold A, Thompson EJ, Stelmasiak Z, et al. CSF nitric oxide metabolites are associated with activity and progression of multiple sclerosis. Neurology, 2004; 63(8):1439-45. Available from: https://www.ncbi.nlm.nih.gov/pubmed/15505162

44. Marrie RA, Rudick R, Horwitz R, Cutter G, Tyry T, et al. Vascular comorbidity is associated with more rapid disability progression in multiple sclerosis. Neurology, 2010; 74(13):1041-7. Available from: https://www.ncbi.nlm.nih.gov/pubmed/20350978

45. Juran BD and Lazaridis KN. Environmental factors in primary biliary cirrhosis. Seminars in Liver Disease, 2014; 34(3):265-72. Available from: https://www.ncbi.nlm.nih.gov/pubmed/25057950

46. Smyk DS, Rigopoulou EI, Muratori L, Burroughs AK, and Bogdanos DP. Smoking as a risk factor for autoimmune liver disease: what we can learn from primary biliary cirrhosis. Annals of Hepatology, 2012; 11(1):7-14. Available from: https://www.ncbi.nlm.nih.gov/pubmed/22166556

47. Lammert C, Nguyen DL, Juran BD, Schlicht E, Larson JJ, et al. Questionnaire based assessment of risk factors for primary biliary cirrhosis. Digestive and Liver Disease, 2013; 45(7):589-94. Available from: https://www.ncbi.nlm.nih.gov/pubmed/23490343

48. Corpechot C, Gaouar F, Chretien Y, Johanet C, Chazouilleres O, et al. Smoking as an independent risk factor of liver fibrosis in primary biliary cirrhosis. Journal of Hepatology, 2012; 56(1):218-24. Available from: https://www.ncbi.nlm.nih.gov/pubmed/21703179

49. 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

50. Palmisano A, Maritati F, and Vaglio A. Chronic Periaortitis: an Update. Current Rheumatology Reports, 2018; 20(12):80. Available from: https://www.ncbi.nlm.nih.gov/pubmed/30397845

51. Park T, Cave D, and Marshall C. Microscopic colitis: A review of etiology, treatment and refractory disease. World Journal of Gastroenterology, 2015; 21(29):8804-10. Available from: https://www.ncbi.nlm.nih.gov/pubmed/26269669