Dr Baker reviews research he and colleagues conducted into responses to different therapeutic strategies for rheumatoid arthritis according to patients' body mass index and adiposity.

Joshua Baker, MD, is associate professor of medicine (Rheumatology) at the Hospital of the University of Pennsylvania and the Veteran's Administration Medical Center and associate professor of epidemiology in biostatistics and epidemiology.

TRANSCRIPT:

Hi, my name is Josh Baker from the University of Pennsylvania, and I'm here to talk to you about our study that we presented on Tuesday, entitled “Low Body Mass and Low Adiposity Predict Differential Responses to Two Different Treatment Strategies for Rheumatoid Arthritis.”

So in this study, we looked at two different clinical trials that studied the effect of TNF plus methotrexate versus triple therapy, which is methotrexate plus sulfasalazine plus hydroxychloroquine. So this is the RACAT and TEAR clinical trials. And the hypothesis was that people with lower BMI would have a greater response to TNF drugs by identifying a more severe phenotype of disease. So we studied the RACAT study and stratified patients according to their BMI. So it could either be low or normal, less than 25 kilograms per meter squared, or overweight or obese. And we looked at the change in outcomes between TNF and triple therapy.

Among those that were overweight and obese, there was no difference between triple therapy and TNF therapy. However, among those that were low and normal BMI, there was a greater response to the TNF therapy. And that was true for the change in DAS28, but also for multiple different ACR responses and low disease activity. In the TEAR study, we saw a similar pattern, but it was only significant for ACR20 responses, where we saw a greater response to the TNF in the low and normal BMI patients.

The other thing that we did in the study was we measured adipokines. So adipokines are associated with total and visceral adiposity. And we created an adipokine score that represented the number of adipokines above or below the median in a pattern consistent with greater adiposity. So what this allowed us to do was to stratify the patients according to high adiposity and low adiposity, and we looked at the same treatment responses.

And what we saw was that those with high adiposity or a pattern of adipokines consistent with high adiposity had no difference in the response to the TNF versus triple therapy, whereas among those with a low adipokine score or low adiposity, there was a greater response to the TNF therapy.

So overall, these results of the study suggest that those with low BMI and low adiposity may have better responses to TNF therapies. And the adipokine data suggests that we can identify a greater number of people that are potentially likely to benefit from the TNF therapy by screening using adipokine scores. It may be that the difference that we're seeing here is related to phenotypic differences in disease due to weight loss in people that have severe RA, although more evidence would be needed to support that.

With that, I'll just say thank you for your attention, and see you around.