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Saag et al 1 reported that smokers were more often rheumatoid factor (RF) positive, had more often rheumatoid nodules and more radiographic erosions compared with non-smokers. Their report questions whether smoking stimulates RF production and thus affects the disease progression in RA. Their findings relate to previous reports that smoking increases the risk of RA,2-8 although not all studies agree.9 As raised RF, in particular IgA RF, is associated with poor prognosis in RA,10 we report a positive correlation between smoking and IgA RF.
We studied 59 RA patients participating in a prospective study on RA. They comprised 47 female patients and 12 male patients of mean age 57.0 years and mean disease duration 12 years. They were attending the rheumatology clinic at King’s College Hospital, London and fulfilled the 1987 ACR criteria for RA. Forty six patients (78%) were taking one or more disease modifying drugs (DMARDs), most often methotrexate, gold or salazopyrine. RA was assessed by Disease Activity Score (DAS) using 28 tender and swollen joints, health assessment questionnaire (HAQ), Larsen score for erosions, and C reactive protein (CRP). RF was measured by nephelometry and IgA RF and IgM RF by enzyme linked immunosorbent assay (ELISA). The results are presented as medians (25th and 75th centiles). Findings were evaluated with the Mann-Whitney U test and Fisher’s exact test when appropriate. The level of significance was set at 5%.
Only 12 (20%) patients were active smokers at the time of study. They had significantly higher RF levels by nephelometry (p=0.023) and higher IgA RF by ELISA (p=0.017) compared with non-smokers (table 1). IgM RF also tended to be higher among smokers (p=0.073). Of the smokers 67% had an increase in both IgA RF and IgM RF compared with only 26% of the non-smokers (p=0.014). DAS, HAQ, Larsen score, and rheumatoid nodules were similar between groups.
Our findings that smoking has a strongest association with IgA RF supports the findings of Saag et al.1 They used a latex fixation test to measure RF, which will preferentially detect IgM RF and does not discriminate between RF isotypes.
Although we found no significant differences between smokers and non-smokers regarding clinical features and this contrasts with the results of Saag et al,1 the prevalence of smoking in our study was low (20%) and the study cohort was also heterogenous in respect to both age and disease duration. Therefore, negative results must be treated with caution.
The association of smoking with IgA RF is interesting as IgA antibodies are important for mucosal immunity. Thus, it is tempting to speculate that smoking may activate or stimulate the mucosal immune system of the respiratory tract leading to increased production of IgA RF. A similar mechanism has previously been suggested for other diseases where mucosal immunity is important and IgA RF is occasionally raised, such as dermatitis herpetiformis and coeliac disease.11
We recommend that larger studies are established to evaluate the association between smoking, RF, and disease progression in RA as stopping smoking may have important advantages for RA patients.