© 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
Summary
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.
Introduction
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).
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Piśmiennictwo
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