Bariatric Surgery and the Incidence of Rheumatoid Arthritis

A Swedish Obese Subjects Study

Cristina Maglio; Yuan Zhang; Markku Peltonen; Johanna Andersson-Assarsson; Per-Arne Svensson; Christian Herder; Anna Rudin; Lena Carlsson


Rheumatology. 2020;59(2):303-309. 

In This Article


Obesity is one of the described risk factors for the development of RA and it negatively affects disease activity and treatment outcomes.[3,4,7–9] Although it has been shown that bariatric surgery–induced weight loss results in decreased disease activity and improved response to treatment, the effect of bariatric surgery on the incidence of RA is not known.[14] In this study we could not detect any association between bariatric surgery and the incidence of RA in subjects with obesity followed up for up to 29 years. Baseline CRP levels and smoking, but not ESR, were associated with a greater risk of developing RA during follow-up.

In the same cohort of >4000 subjects with obesity, we have recently shown that bariatric surgery prevented the development of gouty arthritis and psoriasis, but it did not affect the incidence of PsA.[17,18] RA and PsA are both inflammatory joint disorders that are very different at a clinical, immunological and pathogenic level, although they share some features and common risk factors, such as obesity.[24] In our previous article, the incidence of PsA was similar in the control and bariatric surgery groups, although there was a non-significant trend for a lower incidence in the surgery group. Our current results show no trends for a lower incidence of RA in the bariatric surgery group either in the intention-to-treat analysis or the per-protocol analysis.

Previous studies have shown that obesity augments RA disease activity and decreases the likelihood to achieve a sustained remission despite treatment.[7–9] Although the negative effect of excess weight on RA disease activity and response to treatment is widely known, the impact of obesity per se as a risk factor for the development of RA is still debated. Some studies show no increased risk for RA in subjects with obesity.[25–27] Conversely, several studies, including large meta-analyses, have shown that a higher BMI increases the risk of developing RA, although often the increased risk due to obesity was rather modest and possibly only limited to women.[3–6,28–30] In our analyses, we could not detect any significant association between bariatric surgery as well as change in BMI 2 years after surgery and the incidence of RA in subjects with obesity. Moreover, no interaction was observed between bariatric surgery and sex. However, it is important to point out that our results do not necessarily rule out that obesity is a risk factor for RA. It is possible to speculate that long-term obesity, associated with a mild inflammatory state,[31] has triggered the development of asymptomatic preclinical RA and that such changes could not be counterbalanced by the subsequent weight loss. On the other hand, our results show that obesity duration did not affect the incidence of RA. Another possible explanation is that the role of obesity in the pathogenesis of RA is rather marginal, as also suggested by the HRs for the risk of RA that in most studies, including meta-analyses, were <1.5.[4,5,32] It is also important to note that many study participants from the surgery group still remain affected by obesity even after profound weight loss following bariatric surgery (about −23% of the original BMI), and this allows for speculations about the possibility that an even greater degree of weight loss might be needed to provide protection from the development of RA.

Serum from patients with preclinical RA shows signs of activation of the immune system, as suggested by the presence of ACPAs, chemokines and cytokines up to 10 years before the onset of the disease.[33,34] CRP is also known to be elevated years before the diagnosis of RA.[34–36] Our results show that elevated CRP levels at baseline preceded RA in subjects with obesity followed-up for up to 29 years. This association was independent of bariatric surgery as well as other risk factors for RA, including smoking.

RA was not among the primary nor secondary aims of the SOS trial, hence the study was not designed for this outcome. As expected, the number of subjects who developed RA during follow-up was limited, suggesting that our study might be underpowered to detect a difference in the incidence of RA between the surgery and the control group. Moreover, compared with the surgery group, the control group had a less severe risk profile for RA at baseline, including lower BMI, lower serum CRP and lower prevalence of smokers, and to a certain extent this might have smoothed the effect of bariatric surgery on the development of RA. Another limitation of the study is that the diagnosis of RA was retrieved only through the Swedish National Patient Register by screening ICD codes and therefore we may have missed some patients diagnosed with RA. However, it is important to point out that the National Patient Register is a record of all the diagnoses made in public hospitals all over Sweden and private practices are still uncommon in the country.[37] Moreover, in Sweden, the diagnosis of RA can be only made by a rheumatologist, thus increasing the chances that the record of RA diagnoses that we have is accurate. We also have to acknowledge that the information about serostatus is missing for 17 subjects. This limits the possibility of a more detailed analysis.

In this study we did not observe any association between bariatric surgery and the incidence of RA in subjects with obesity during a long follow-up. Further longitudinal studies in larger cohorts are needed to confirm this finding.