Smoking, Overweight, and the Likelihood of Developing RA
Smoking, Overweight, and the Likelihood of Developing RA
Objectives Rheumatoid arthritis (RA) is a prototypic chronic inflammatory disease with a debilitating course if untreated. A genetic predisposition for RA is known, and its occurrence is associated with the presence of autoantibodies in the serum and with environmental factors. It is unknown if smoking and overweight are contributory factors for developing RA in individuals with RA-specific autoantibodies in the serum.
Methods Fifty-five individuals at risk for developing RA, based on the presence of RA-specific autoantibodies in the serum, who never had any evidence of arthritis upon physical examination, were followed over time. Smoking was assessed as being never or ever smoker and body mass index as <25 (normal) or ≥25 kg/m (overweight). Clinical endpoint was the occurrence of arthritis. Proportional hazard regression analysis was performed to investigate the potential of (combinations of) variables in predicting the onset of arthritis over time.
Results After a median follow up time of 13 (IQR 6–27) months, 15 individuals (27%) developed arthritis. Smoking was associated with the development of arthritis (HR (95% CI): 9.6 (1.3 to 73.0); p=0.029). Overweight was, independently of smoking, associated with arthritis (HR (95% CI): 5.6 (1.3 to 25.0); p=0.023). The overall arthritis risk of 28% after a median of 27 months follow up increased to 60% in individuals with a smoking history combined with overweight.
Conclusions This is the first prospective study showing that smoking and overweight increase the risk of development of arthritis in a cohort of autoantibody-positive individuals at risk for developing RA. These results show the importance of life style factors in development of RA and should be critically evaluated in future clinical research aimed at disease prevention.
Rheumatoid arthritis (RA) is an immune-mediated inflammatory disease characterised by inflammation of synovial joints, often resulting in degradation of articular cartilage and bone, ultimately leading to joint deformities. If untreated, RA leads to disability, loss of quality of life and work loss. RA causes premature death due to cardiovascular disease, analogous to diabetes mellitus and the impact of RA on costs for society is huge. The treatment of established RA is promising but expensive; therefore the need for prevention of RA, if possible, is obvious.
The aetiology of RA, though largely unknown, is considered multifactorial: a family history of RA and the presence of MHC class II genes and PTPN22 increase the susceptibility of RA; the presence of rheumatoid factor (RF) and anti-citrullinated protein-antibodies (ACPA) point to a contribution of autoimmunity mechanisms and environmental factors such as smoking and obesity, and their interactions with genetic factors, have been considered important.
Recent research has discovered that circulating autoantibodies and increased acute phase reactants can precede the clinical onset of RA, but only a minority of individuals with RA-specific autoantibodies actually develops clinically manifest RA. However, the detection of these autoantibodies may define patients with systemic autoimmunity associated with RA without clinical evidence of arthritis, who are at risk of developing RA.
In this prospective observational study the contributory role of the modifiable factors smoking and overweight on the development of arthritis in autoantibody-positive individuals at risk for developing RA was investigated.
Abstract and Introduction
Abstract
Objectives Rheumatoid arthritis (RA) is a prototypic chronic inflammatory disease with a debilitating course if untreated. A genetic predisposition for RA is known, and its occurrence is associated with the presence of autoantibodies in the serum and with environmental factors. It is unknown if smoking and overweight are contributory factors for developing RA in individuals with RA-specific autoantibodies in the serum.
Methods Fifty-five individuals at risk for developing RA, based on the presence of RA-specific autoantibodies in the serum, who never had any evidence of arthritis upon physical examination, were followed over time. Smoking was assessed as being never or ever smoker and body mass index as <25 (normal) or ≥25 kg/m (overweight). Clinical endpoint was the occurrence of arthritis. Proportional hazard regression analysis was performed to investigate the potential of (combinations of) variables in predicting the onset of arthritis over time.
Results After a median follow up time of 13 (IQR 6–27) months, 15 individuals (27%) developed arthritis. Smoking was associated with the development of arthritis (HR (95% CI): 9.6 (1.3 to 73.0); p=0.029). Overweight was, independently of smoking, associated with arthritis (HR (95% CI): 5.6 (1.3 to 25.0); p=0.023). The overall arthritis risk of 28% after a median of 27 months follow up increased to 60% in individuals with a smoking history combined with overweight.
Conclusions This is the first prospective study showing that smoking and overweight increase the risk of development of arthritis in a cohort of autoantibody-positive individuals at risk for developing RA. These results show the importance of life style factors in development of RA and should be critically evaluated in future clinical research aimed at disease prevention.
Introduction
Rheumatoid arthritis (RA) is an immune-mediated inflammatory disease characterised by inflammation of synovial joints, often resulting in degradation of articular cartilage and bone, ultimately leading to joint deformities. If untreated, RA leads to disability, loss of quality of life and work loss. RA causes premature death due to cardiovascular disease, analogous to diabetes mellitus and the impact of RA on costs for society is huge. The treatment of established RA is promising but expensive; therefore the need for prevention of RA, if possible, is obvious.
The aetiology of RA, though largely unknown, is considered multifactorial: a family history of RA and the presence of MHC class II genes and PTPN22 increase the susceptibility of RA; the presence of rheumatoid factor (RF) and anti-citrullinated protein-antibodies (ACPA) point to a contribution of autoimmunity mechanisms and environmental factors such as smoking and obesity, and their interactions with genetic factors, have been considered important.
Recent research has discovered that circulating autoantibodies and increased acute phase reactants can precede the clinical onset of RA, but only a minority of individuals with RA-specific autoantibodies actually develops clinically manifest RA. However, the detection of these autoantibodies may define patients with systemic autoimmunity associated with RA without clinical evidence of arthritis, who are at risk of developing RA.
In this prospective observational study the contributory role of the modifiable factors smoking and overweight on the development of arthritis in autoantibody-positive individuals at risk for developing RA was investigated.
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