gender disparities

The Role of Gender in Rheumatoid Arthritis and Mortality Outcomes

In this podcast, Sri Banerjee, MD, PhD, MPH, MAS, speaks about how gender modifies the effect of rheumatoid arthritis on all-cause mortality and why rheumatoid arthritis is underdiagnosed. 

Additional Resource:

Sri Banerjee, MD, PhD, MPH, MAS, is a faculty member at Walden University in the School of Health Sciences. He is a clinical biostatistician and an epidemiologist in Leola, Pennsylvania. 

 

TRANSCRIPTION:

Jessica Bard: Hello everyone. And welcome to another installment of Podcast 360, your go-to resource for medical news and clinical updates. I'm your moderator, Jessica Bard with Consultant 360 Specialty Network. According to the Centers for Disease Control and Prevention, the risk of stroke for women aged 55 to 75 years in the United States is one in five. And one in four women will get rheumatoid arthritis. Dr Sri Banerjee is here to speak with us about his team's research, inflammatory biomarkers of mortality in female patients with stroke. He'll also speak about how it relates to rheumatoid arthritis. Dr Banerjee is a faculty member at Walden University in the School of Health Sciences. He's also a clinical biostatistician and an epidemiologist in Leola, Pennsylvania. Thank you for joining us today, Dr Banerjee. Can you please tell us more about how this study came about and an overview of this study?

Dr Sri Banerjee: Jessica, when I was first starting off in my journey thinking about disease and everything, I wanted to first understand it from a pathological perspective. So looking at some of the basic principles of pathology. When I first opened a pathology book, one of the first principles that was taught was the idea of inflammation. And there's actually, depending on who you ask, four or five original cardinal signs, some of which are rubor, which is redness, dolor, which is pain, calor, which is heat, and there are others. So these are the basic cardinal signs. And this never left me.

When I later on furthered my education, this idea that inflammation is at the root of much of the pathology that is going on at the cellular level, that never left me. Later on when I wanted to explore deeper into certain subject area, decided that inflammation and cardiovascular disease, that's where I was going to put a little bit more focus and emphasis on. So I developed that idea and then collaborated with others. And this led to understanding not only inflammation, but in the context of what is going on with people that have autoimmune disorders. So this is where the idea came about.

Jessica Bard: Talk to us about how your idea and how the findings of the study really connect to rheumatoid arthritis?

Dr Sri Banerjee: Thanks for that question, Jessica. And that is a very important question as well. In general, if you're thinking about the principle of autoimmune, so the idea is that you have an immune system which has been developed, in fact since childhood, and what your immune system is doing is trying to take what is out there, all of the types of viruses, bacteria, and creating an immunological kind of profile as we develop. Sometimes what happens is, whether it's environmental factors or diseases, something a lot of times that goes awry. And so a lot of it is genetics too. So when we're talking about rheumatoid arthritis, we're talking about this same immune system that is for several reasons, is rampantly going after our joints.

This is a process which when you actually combine with other disease conditions, for instance, in this topic we're talking about stroke. When you combine this additive effect, this can potentially really have detrimental effects on the body. In a nutshell, when you're combining major autoimmune condition that causes inflammation, like rheumatoid arthritis on one hand, and then when you're combining that with a major cardiovascular event, stroke is considered a type of cardiovascular event, then the combination effect is potentially way more detrimental.

Jessica Bard: Now give us a summary of the results of this study.

Dr Sri Banerjee: Certainly. And this study, one thing that we ended up doing is actually going back to a familiar secondary data set, which looks at multiple biomarkers, multiple types of disease conditions, all simultaneously. And National Health and Nutrition Examination Survey is perfect for studying phenomena like that. So what we did is we went in there and looked at, of course not only the mortality outcomes in 2015, but also looking at kind of individuals that had already experienced stroke, if inflammation was resulting in poor mortality outcomes. I already introduced the idea that when you have inflammation and when you have a preexisting disease condition, this principle that this has poor outcomes.

So what we did is we were testing that theory. When you had stroke and then when you had something that is a common autoimmune, inflammatory biomarker, like C-reactive protein, what is the end result? And surely enough, in our results we found not only significance, but also poor outcomes through Cox regression. And in the multi varied Cox regression model, we actually found that individuals that have both a positive stroke history and increased C-reactive protein are 87% more likely to experience mortality. The hazard ratio was actually 1.87, and this was statistically significant. You had a P that was less than 0.05 here. Very important findings.

Jessica Bard: Now, some critics might say that this might be part of pop science or self-help without any scientific backing. What would you say to those critics and those people?

Dr Sri Banerjee: Jessica, a very good question. Very insightful in thinking about this. Because you're right, there is individuals, there's people that are talking about this, and rightfully so. For instance, Dr Oz did a special last year to try to talk about an increase awareness on inflammatory biomarkers, talking about it being in epidemic proportions. The problem a lot of times is that it becomes so confusing, because sometimes the facts and what is being promoted in social media where the evidence is not all that processed, sometimes there's mixtures in that, there's levels of evidence. So we have to be careful that we actually can differentiate fact from fiction and are able to say firmly that these are in fact scientists saying these are the mechanisms of inflammation versus something that person is making a claim about a supplement, a vitamin supplement, which may or may not address inflammation.

But there is key studies out there, seminal studies. One of them is Ridker, et al. This was a study that came out in the New England Journal of Medicine. And so far, there are thousands of citations from this study. And this study showed, in fact that biologic agents that address inflammation in cardiovascular disease actually make a difference. This is taking this a step further. This is not only saying that inflammation is actually the agent, but also saying that we can address this and certain cardiovascular diseases can be addressed. The hope is if we can connect this to stroke, and then if we can be thinking about kind of individuals that may have autoimmune disease, like rheumatoid arthritis, if we can think about that, then potentially we can do something about that.

Jessica Bard: And we'll include a link to that study in the additional resources section on our page. How will this study impact clinical practice going forward?

Dr Sri Banerjee: Right there, Jessica, is the important question. We've talked about all this theory. We've talked about all this research. But how do we let it take flight? How do we make sure that what we have found is actually something that people are using? Here's my advice from this, this information is important. And one of the potential things is we're creating risk prediction scores for patients. We're trying to understand what are factors and variables that we can address so that people can have better outcomes, lower mortality. And if we can start to address this inflammatory bio mark, imagine the difference that this can make. If we can start to monitor, bio monitor C-reactive protein at critical junctures, especially after individuals, females that have experienced stroke, then maybe we can actually start to address some of these mortality outcomes, some of these poor outcomes that are coming about from people that have experienced stroke or other severe cardiovascular diseases. I think there's a lot of promise from these findings.

Jessica Bard: I think that was well said. What would you say are the overall take home messages from our conversation today?

Dr Sri Banerjee: Good question. So let's go back to the basic principle of inflammation. I think one takeaway message is that we really need to be understanding inflammation, but not only at a whole body systemic level, but also kind of at connecting it to different diseases. Certain disease processes we know, we know for a fact physiologically is causing inflammation. We know for a fact when you have ischemia, the parenchyma, the brain parenchyma is getting damaged. And when it's getting damaged, there's inflammatory cascades, there's selections, there's complement cascade. There's all of these things that are getting released, just amplifying this inflammation. So we know what is going on at a cellular level. Let's translate some of these cellular level observations and start to implement these in clinical practice.

Jessica Bard: Well, Dr Banerjee, thank you so much for your time today. Is there anything else that you'd like to add?

Dr Sri Banerjee: No, that will be all. Thank you.

Jessica Bard: Thank you joining us. Thank you