Ponad 7000 publikacji medycznych!
Statystyki za 2021 rok:
odsłony: 8 805 378
Artykuły w Czytelni Medycznej o SARS-CoV-2/Covid-19

Poniżej zamieściliśmy fragment artykułu. Informacja nt. dostępu do pełnej treści artykułu
© Borgis - Medycyna Rodzinna 1/2015, s. 12-17
Krzysztof Kanecki, Piotr Tyszko
Środowiskowe i indywidualne czynniki ryzyka rozwoju reumatoidalnego zapalenia stawów
Environmental and personal risk factors for the development of rheumatoid arthritis
Department of Health Care, Medical University of Warsaw
Rheumatoid arthritis (RA) is a systemic, autoimmune, inflammatory disease of unknown etiology, characterized as a progressive disease, leading to joint destruction, physical activity limitation, disability, premature death, and imposes a significant economic burden on patients, family members, and society. While etiology of rheumatoid arthritis is unknown, medical evidences suggest that RA develops more often in individuals with inherited genetic and individual risk factors or exposed to environmental triggers.
The aims of this paper are the present the latest medical data on these risk factors, the identification of the groups of high risk for RA development and the presentation of suggestions for health related, preventive activities in primary health care.
There are many environmental factors, including exposure to tobacco smoke, infections, hormones, dietary factors that, as well as gene-environment interactions have been associated with increased risk for RA. This article presents latest data on the most important environmental, serological and personal risk factors for RA development.
Early identification of risk factors is important part of health care since it provides opportunity for earlier preventive activities, health promotion in individuals at risk of RA development. Presented data on environmental and personal risk factors could be helpful for primary health care doctors, specialists and other people involved in diseases prevention, treatment and promotion of health.

Rheumatoid arthritis (RA) is a systemic, autoimmune, inflammatory disease of unknown etiology, characterized as a progressive disease, leading to joint destruction, physical activity limitation, disability, premature death, and imposes a significant economic burden on patients, family members, and society. RA is considered to appear when genetic and environmental factors interact and trigger immunological changes leading to an inflammatory arthritis. The onset of clinical disease occurs when the cumulative action of genetic and environmental factors trigger an auto-aggressive immune response. This asymptomatic period with immune activation phase, in which autoantibodies and inflammatory markers may be found, could evolve to an unclassifiable or undifferentiated arthritis or an arthritis that fulfills the criteria for RA diagnosis.
There has been limited success defining the environmental factors important in developing RA. The immune pathology in adult RA begins many years before clinical symptom. The RA associated autoantibodies as rheumatoid factor (RF) or anti-citrullinated protein antibody (ACPA) may be present many years before the clinical onset of the disease (1). The search for environmental factors is important because RA was reported to be associated with significantly increased mortality. Moreover, in a cohort of older women, the association appeared to be restricted to those with RF positive disease (2).
Environmental risk factors may be divided in modifiable and non-modifiable factors. All of them are identifying individuals with elevated risk of RA, although all preventive activities are mainly focused on eliminating or limiting the impact of the modifiable factors.
Identification of environmental or familial risk factors for development of rheumatoid arthritis could be helpful in early RA diagnosis. Early diagnosis, referral to rheumatologists and early treatment of RA are recommended by European League against Rheumatism (EULAR) (3). These recommendations help to improve long-term outcomes. Presence of RF or ACPA associates with cardiovascular disease (CVD) and mortality among RA onset before 65 years (4). RA is leading to increased mortality as it was shown in literature in longitudinal observational study (5). Cardiovascular mortality could be associated with chronic inflammation determined by C-reactive protein and erythrocyte sedimentation rate (6).
RA incurs high individual, societal and medical costs, all of which should be considered in its management by the treating rheumatologist (EULAR) or other medical professionals involved in RA treatment. According to EULAR recommendations, treatment should be aimed at reaching a target of remission or low disease activity in every patient and methotrexate should be part of the first treatment strategy in patients with active RA. It was known that successful control of disease activity by treatment with methotrexate reduces mortality in RA (7). Patients with long-standing high disease activity are at substantially increased risk of mortality. In patients responding insufficiently to methotrexate and/or other conventional synthetic disease-modifying antirheumatic drugs strategies, biological disease-modifying antirheumatic drugs should be commenced with methotrexate (EULAR). Comparative analysis suggested also that tumor necrosis alpha inhibitors and rituximab seem to be superior to conventional disease-modifying antirheumatic drugs in reducing this risk (8). All these treatment options could be more cost-effective if the RA diagnosis is made in early stage of this disease. Therefore, Information about risk factors for RA development may be helpful for medical professionals involved in RA diagnosis, treatment and comprehensive care.
The aims of this paper are the presentation the latest medical data on environmental and personal risk factors for the development of rheumatoid arthritis, the identification of the groups of high risk for RA development and the presentation of suggestions for health related, preventive activities in primary health care.
Description of the state of knowledge
Cigarette smoking
Case-control study have demonstrated that cigarette smoking is the strongest environmental factor linked with RA (9). Attributable population risk for smoking is reported to be 25% for all RA and 35% for RA with presence of RF or ACPA (10). The association is more stronger for men than for women (11). A dose-response is reported to be between smoking and RA, particularly in people with seropositive RA with persistence of RA risk for many years after smoking cessation (12). In addition, the risk of seropositive RA associated with smoking has been reported to be highest in those who carry the HLA-DRB1 shared epitope (SE) (13). Other recent data suggested decreased responsiveness to therapy in patients with established RA who were smokers and suggested some relationship between disease development and smoking (14).
Strong combined gene-environment effects were observed, with markedly increased risks of ACPA-positive RA in SE homozygotes who were heavy smokers, heavy coffee drinkers or oral contraceptive users compared with SE noncarriers who were not exposed to these environmental risk factors (15).

Powyżej zamieściliśmy fragment artykułu, do którego możesz uzyskać pełny dostęp.
Mam kod dostępu
  • Aby uzyskać płatny dostęp do pełnej treści powyższego artykułu albo wszystkich artykułów (w zależności od wybranej opcji), należy wprowadzić kod.
  • Wprowadzając kod, akceptują Państwo treść Regulaminu oraz potwierdzają zapoznanie się z nim.
  • Aby kupić kod proszę skorzystać z jednej z poniższych opcji.

Opcja #1


  • dostęp do tego artykułu
  • dostęp na 7 dni

uzyskany kod musi być wprowadzony na stronie artykułu, do którego został wykupiony

Opcja #2


  • dostęp do tego i pozostałych ponad 7000 artykułów
  • dostęp na 30 dni
  • najpopularniejsza opcja

Opcja #3


  • dostęp do tego i pozostałych ponad 7000 artykułów
  • dostęp na 90 dni
  • oszczędzasz 28 zł
1. Nielen MM, van Schaardenburg D, Reesink HW et al.: Specific autoantibodies precede the symptoms of rheumatoid arthritis: a study of serial measurements in blood donors. Arthritis Rheum 2004; 50: 380-386. 2. Mikuls TR, Saag KG, Criswell LA et al.: Mortality risk associated with rheumatoid arthritis in a prospective cohort of older women: results from the Iowa Women’s Health Study. Ann Rheum Dis 2002; 61: 994-999. 3. Smolen JS, Landewè R, Breedveld FC et al.: EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2013 update. Ann Rheum. Dis doi:10.1136/annrheumdis-2013-204573. Accessed: March 26, 2014. 4. Ajeganova S, Andersson ML, Frostegård J et al.: Disease factors in early rheumatoid arthritis are associated with differential risks for cardiovascular events and mortality depending on age at onset: a 10-year observational cohort study. J Rheumatol 2013 Dec; 40(12): 1958-1966. doi: 10.3899/jrheum.130365. Epub 2013 Aug 15. 5. Gonzalez A, Maradit KH, Crowson CS et al.: The widening mortality gap between rheumatoid arthritis patients and the general population. Arthritis Rheum 2007; 56: 3583-3587. 6. Gonzalez-Gay MA, Gonzalez-Juanatey C, Lopez-Diaz MJ et al.: HLA-DRB1 and persistent chronic inflammation contribute to cardiovascular events and cardiovascular mortality in patients with rheumatoid arthritis. Arthritis Rheum 2007; 57: 125-132. 7. Choi HK, Hernan MA, Seeger JD et al.: Methotrexate and mortality in patients with rheumatoid arthritis: a prospective study. Lancet 2002; 359: 1173-1177. 8. Listing J, Kekow J, Manger B et al.: Mortality in rheumatoid arthritis: the impact of disease activity, treatment with glucocorticoids, TNFα inhibitors and rituximab. Ann Rheum Dis. doi:10.1136/annrheumdis-2013-204021. 9. Stolt P, Bengtsson C, Nordmark B et al.: Quantification of the influence of cigarette smoking on rheumatoid arthritis: results from a population based case-control study, using incident cases. Ann Rheum Dis 2003; 62: 835-841. 10. Kallberg H, Ding B, Padyukov L et al.: Smoking is a major preventable risk factor for rheumatoid arthritis: estimations of risks after various exposures to cigarette smoke. Ann Rheum Dis 2011; 70: 508-511. 11. Krishnan E, Sokka T, Hannonen P: Smoking-gender interaction and risk for rheumatoid arthritis. Arthritis Res Ther 2003; 5: 158-162. 12. Costenbader KH, Feskanich D, Mandl LA et al.: Smoking intensity, duration, and cessation, and the risk of rheumatoid arthritis in women. Am J Med 2006; 119: 503-511. 13. Klareskog L, Stolt P, Lundberg K et al.: A new model for an etiology of rheumatoid arthritis: Smoking may trigger HLA-DR (shared epitope)-restricted immune reactions to autoantigens modified by citrullination. Arthritis Rheum 2006; 54: 38-46. 14. Saevarsdottir S, Wedren S, Seddighzadeh M 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 Rheum 2011; 63: 26-36. 15. Pedersen M, Jacobsen S, Garred P et al.: Strong combined gene-environment effects in anti-cyclic citrullinated peptide-positive rheumatoid arthritis: a nationwide case-control study in Denmark. Arthritis Rheum 2007; 56: 1446-1453. 16. Arnson Y, Shoenfeld Y, Amital H: Effects of tobacco smoke on immunity, inflammation and autoimmunity. J Autoimmunity 2010; 34: J258-J265. 17. de Hair MJ, Landewè RB, van de Sande MG et al.: Smoking and overweight determine the likelihood of developing rheumatoid arthritis. Ann Rheum Dis 2013 Oct 1; 72(10): 1654-1658. 18. Lahiri M, Luben RN, Morgan C et al.: Using lifestyle factors to identify individuals at higher risk of inflammatory polyarthritis (results from the European Prospective Investigation of Cancer-Norfolk and the Norfolk Arthritis Register – the EPIC-2-NOAR Study). Ann Rheum Dis 2014 Jan; 73(1): 219-226. doi: 10.1136/annrheumdis-2012-202481. Epub 2013 Mar 16. 19. van de Sande MG, de Hair MJ, van der Leij C et al.: Different stages of rheumatoid arthritis: features of the synovium in the preclinical phase. Ann Rheum Dis 2011; 70: 772-777. 20. Lundberg K, Wegner N, Yucel-Lindberg T et al.: Periodontitis in RA-the citrullinated enolase connection. Nat Rev Rheumatol 2010; 6: 727-730. 21. Wegner N, Wait R, Sroka A et al.: Peptidylarginine deiminase from Porphyromonas gingivalis citrullinates human fibrinogen and alpha-enolase: implications for autoimmunity in rheumatoid arthritis. Arthritis Rheum 2010; 62: 2662-2672. 22. Costenbader KH, Feskanich D, Holmes M et al.: Vitamin D intake and risks of systemic lupus erythematosus and rheumatoid arthritis in women. Ann Rheum Dis 2008; 67: 530-535. 23. Merlino LA, Curtis J, Mikuls TR et al.: Vitamin D intake is inversely associated with rheumatoid arthritis: results from the Iowa Women’s Health Study. Arthritis Rheum 2004; 50: 72-77. 24. Zakeri Z, Sandoughi M, Mashhadi MA et al.: Serum vitamin D level and disease activity in patients with recent onset rheumatoid arthritis. Int J Rheum Dis 2013 Oct 18. doi: 10.1111/1756-185X.12181. (abstract) http://www.ncbi.nlm.nih.gov/pubmed/24134402. Accessed: May 04, 2014. 25. Song GG, Bae SC, Lee YH: Association between vitamin D intake and the risk of rheumatoid arthritis: a meta-analysis. Clin Rheumatol 2012 Dec; 31(12): 1733-1739. doi: 10.1007/s10067-012-2080-7. Epub 2012 Sep 2. 26. Crowson CS, Matteson EL, Davis J et al.: Contribution of obesity to the rise in incidence of rheumatoid arthritis. Arthritis Care Res 3013; 65: 71-77. doi: 10.1002/acr.21660. 27. Pikwer M, Bergstrom U, Nilsson JA et al.: Early menopause is an independent predictor of rheumatoid arthritis. Ann Rheum Dis 2012; 71: 378-381. 28. Doran MF, Pond GR, Crowson CS et al.: Trends in incidence and mortality in rheumatoid arthritis in Rochester, Minnesota, over a forty-year period. Arthritis Rheum 2002; 46: 625-631. 29. Walitt B, Pettinger M, Weinstein A et al.: Effects of postmenopausal hormone therapy on rheumatoid arthritis: the women’s health initiative randomized controlled trials. Arthritis Rheum 2008; 59: 302-310. 30. Doran MF, Crowson CS, O’Fallon WM et al.: The effect of oral contraceptives and estrogen replacement therapy on the risk of rheumatoid arthritis: a population based study. J Rheumatol 2004; 31: 207-213. 31. Bhatia SS, Majka DS, Kittelson JM et al.: Rheumatoid factor seropositivity is inversely associated with oral contraceptive use in women without rheumatoid arthritis. Ann Rheum Dis 2007; 66: 267-269. 32. Jacobsson LT, Jacobsson ME, Askling J et al.: Perinatal characteristics and risk of rheumatoid arthritis. Brit Med J 2003; 326: 1068-1069. 33. Mandl LA, Costenbader KH, Simard JF et al.: Is birthweight associated with risk of rheumatoid arthritis? Data from a large cohort study. Ann Rheum Dis 2009; 68: 514-518. 34. Pikwer M, Bergstrom U, Nilsson JA et al.: Breast feeding, but not use of oral contraceptives, is associated with a reduced risk of rheumatoid arthritis. Ann Rheum Dis 2009; 68: 526-530. 35. Karlson EW, Mandl LA, Hankinson SE et al.: Do breast-feeding and other reproductive factors influence future risk of rheumatoid arthritis? Results from the Nurses’ Health Study. Arthritis Rheum 2004; 50: 3458-3467. 36. Berglin E, Kokkonen H, Einarsdottir E et al.: Influence of female hormonal factors, in relation to autoantibodies and genetic markers, on the development of rheumatoid arthritis in northern Sweden: a case-control study. Scand J Rheumatol 2010; 39: 454-460. 37. Hemminki K, Li X, Sundquist J et al.: Familial associations of rheumatoid arthritis with autoimmune diseases and related conditions. Arthritis Rheum 2009; 60: 661-668. 38. Kolfenbach JR, Deane KD, Derber LA et al.: A prospective approach to investigating the natural history of preclinical rheumatoid arthritis (RA) using first-degree relatives of probands with RA. Arthritis Rheum 2009; 61: 1735-1742. 39. El-Gabalawy HS, Robinson DB, Hart D et al.: Immunogenetic risks of anti-cyclical citrullinated peptide antibodies in a North American Native population with rheumatoid arthritis and their first-degree relatives. J Rheumatol 2009; 36: 1130-1135. 40. Stolt P, Kallberg H, Lundberg I et al.: Silica exposure is associated with increased risk of developing rheumatoid arthritis: results from the Swedish EIRA study. Ann Rheum Dis 2005; 64: 582-586. 41. Turner S, Cherry N: Rheumatoid arthritis in workers exposed to silica in the pottery industry. Occup Environ Med 2000; 57: 443-447. 42. Sverdrup B, Kallberg H, Bengtsson C et al.: Association between occupational exposure to mineral oil and rheumatoid arthritis: results from the Swedish EIRA case-control study. Arthritis Res Ther 2005; 7: 1296-1303. 43. Hart JE, Laden F, Puett RC et al.: Exposure to traffic pollution and increased risk of rheumatoid arthritis. Environ Health Perspect 2009; 117: 1065-1069. 44. Cerhan JR, Saag KG, Merlino LA et al.: Antioxidant micronutrients and risk of rheumatoid arthritis in a cohort of older women. Am J Epidemiol 2003; 157: 345-354. 45. Rosell M, Wesley AM, Rydin K et al.: Dietary fish and fish oil and the risk of rheumatoid arthritis. Epidemiology 2009; 20: 896-901. 46. Benito-Garcia E, Feskanich D, Hu FB et al.: Protein, iron, and meat consumption and risk for rheumatoid arthritis: a prospective cohort study. Arthritis Res Ther 2007; 9: 16. 47. Bengtsson C, Nordmark B, Klareskog L et al.: Socioeconomic status and the risk of developing rheumatoid arthritis: results from the Swedish EIRA study. Ann Rheum Dis 2005; 64: 1588-1594. 48. Pedersen M, Jacobsen S, Klarlund M et al.: Socioeconomic status and risk of rheumatoid arthritis: a Danish case-control study. J Rheumatol 2006; 33: 1069-1074. 49. Di GD, Alfredsson L, Bottai M et al.: Long term alcohol intake and risk of rheumatoid arthritis in women: a population based cohort study. BMJ 2012; 345: 4230. 50. Jin Z, Xiang C, Cai Q et al.: Alcohol consumption as a preventive factor for developing rheumatoid arthritis: a dose-response meta-analysis of prospective studies Ann Rheum Dis. doi:10.1136/annrheumdis-2013-203323.
otrzymano: 2015-02-11
zaakceptowano do druku: 2015-03-02

Adres do korespondencji:
Krzysztof Kanecki
Department of Health Care Medical University of Warsaw
ul. Oczki 3, 02-097 Warszawa
tel. +48 501-929-235,
fax +48 (22) 621-52-56

Medycyna Rodzinna 1/2015
Strona internetowa czasopisma Medycyna Rodzinna