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The Management of Patients With Chronic Gout vs Acute Gout

James Matera, DO

In this video, James Matera, DO, discusses guidelines for managing patients with chronic gout vs acute gout, hyperuricemia, and the symptom burden and risk factors of gout. This is part two of a three-part video series. 

For more gout content, visit the disease state hub


Watch part one of this three-part series here.

Watch part three of this three-part series here.


 

TRANSCRIPTION:

James Matera, DOGood afternoon. This is Dr. James Matera here. I'm the Senior Vice President for Medical Affairs and Chief Medical Officer at CentraState Medical Center in Freehold, New Jersey, and I'm happy to be talking a little bit about gout and hyperuricemia today for our audience. When we come to gout, we also have to differentiate between what we would consider acute gout or an acute flare or acute gouty arthropathy versus chronic gout. And those can be in the same person. It could be a progression of the disease. Some people are lucky enough just to have one flare of gout. If they go out to the shore and have a little bit of shrimp, they may have a flare, and they may not necessarily need to be treated. But when you have a chronic disease that can also present with acute flares, it has the potential to cause joint destruction.

As far as looking at the numbers, gout can actually affect about 4% of the US population, or almost 9 million people. And despite a good understanding of physiology, we all learned that whole pathway in medical school, and knowing how we can treat it and lower it, lower uric acid, there's still a potential for adverse outcomes. So when we look at our goal of therapy, we still have a lot of gaps in care when it comes to these patients. And that comes right down to how we should best manage this. Part of this is also burdened by the adherence to the medications that we use to treat hyperuricemia and gout. There's a very high level of decreased compliance with these medications, for one reason or another. So it becomes very important to me to understand the burden of the symptoms and how they're going to impact the patient all the way across the spectrum of diseases.

So often, we, as clinicians, have a difficult time separating out the benefits of lowering uric acid, especially in asymptomatic patients, to the benefits of lowering it to help try to prevent adverse outcomes. One of the things that the COVID-19 pandemic also bore out to us was an interesting fact. Gout patients were found to have a higher risk for more serious SARS‑CoV‑2 infections than non-gout patients. This came from a UK database that looked at this, but we have to temper that a little bit. We have to remember that those patients also had higher risk factors that we knew might predispose them to more serious SARS‑CoV‑2 infections, such as hypertension, such as type 2 diabetes. And oftentimes, we'll see hyperuricemia in that. But still, an interesting factor is that, when you looked at gout versus non-gout patients with SARS‑CoV‑2, the gout patients did a little bit worse.

So that's something you always want to look at. When you have a gout patient or someone who suffers from chronic gout, you always worry about an acute flare. Now, acute flare can be debilitating for the patient. It can lead to loss of work and loss of wages. It has a serious economic impact, but they also may sometimes resort to the use of opioids. Now, opioid use in gout is not one of the recommended therapies, but we all know that we've had some very difficult patients that have had to have a little bit more advanced pain management. We certainly are all acutely aware of the opioid crisis in the United States and everywhere else, and we want to try to limit that. And I'll try to give you a little structure around how we treat that. As we look at the overall burden of gout, we may see that it progresses through four different stages.

The first stage would be that asymptomatic phase, where there's no visible effect, no symptoms, no classic symptoms, you're not going to have joint damage, you're not going to have other damage at that point, but that's the early stage. Then you may move into an acute gout. That's where the patient gets that bell rung, where they have a significant issue. And when the patient starts to experience symptoms, they can range from redness or swelling of the joint to the classic podagra, in the great toe that we talk about, and patients will know this. Oftentimes, they can't even put a sheet on their foot when this happens. When this occurs, it's already because the monosodium urate crystals are starting to deposit in the joints. When you do this, you draw in inflammatory cells, you draw in cytokines, and all of this can start to cause joint erosion and joint damage.

So even on the acute flare, while it may be a red light, the siren to the patient, underneath, is already starting to cause some damage. The next phase in the progression of this would be into a more chronic state, where they may have flares. One of our goals is to reduce those flares, but they may not always have those symptoms, but is the underlying joint damage and other issues still occurring if you're not controlling their hyperuricemia? And that's an area that we need a little bit more research into. Finally, once they start to develop chronic tophi, that can almost always indicate two things. Number one, they have significant joint pain and joint damage, and oftentimes, progress to chronic pain. And that's where your opioid use may need to come into play a little bit more. So think of it as a progression through these stages.

As far as most disease states that we know of, it can affect different populations in different ways. And when we look at social determinants and discrepancies in health, this is so important, in every aspect of healthcare now. I always say, and I probably said it in some of my videos before, that the zip code may be as important as the genetic code in some of these patients. So when we want to understand populations at risk, I think we need to see this. Where do we see higher incidences of gout and hyperuricemia? Well, we know it's definitely in underserved communities. And in America, African-American populations in the underserved communities often will have this. Pacific Islanders have a higher predilection for gout, as well as some smaller areas in New Zealand with some of the tribes that are there. But an interesting factor in America is that Japanese Americans also have a predilection for gout, so they may have a higher incidence.

So it's important to understand that. When it comes to healthcare disparities, though, we also see a lot of this. Certainly our underserved. We know that they may not have the access to healthcare that they need, so their gout may go unchecked, untreated, and progress. But an interesting factor also occurs when you compare women to men when it comes to gout. And women may develop gout with other associated conditions, such as hypertension, such as chronic kidney disease, but they may also have atypical joint involvement. And that can lead to delays in diagnosis and therefore, the progression of their disease a little bit faster. They may also not get appropriate treatment for their gout flares, and there are a number of reasons why that may occur. So healthcare disparities continue to play an ever-important role as we go through everything that we have in medicine today. When we look at comorbidities in patients with gout, I think it's very important to distinguish how to manage acute flares.

In 2020, the American College of Rheumatology came out with some basic guidelines on how to treat acute flares. And like I said, opioids are not really up in there. But the way I look at it is, when you have an acute flare, the first line therapies and the recommended therapies are the use of colchicine and nonsteroidal anti-inflammatories, but again, remember in your subgroup of patients with chronic kidney disease, nonsteroidal may not be the best choice or glucocorticoids. And we all know we've had those patients we put on a Medrol dose pack or a declining series of glucocorticoids, that have a very good effect on that. Long-term, not so much. And in my third video, I'll show you a little bit of information about that. There are other agents out there, including IL-1 inhibitors and ACTH, that do play a role.

I don't think they're a first-line therapy. I've never had to use that first line. But in those who don't respond, those who you want to put on glucocorticoid-sparing regimens, or those who can't take nonsteroidal, I certainly think there's room for the IL-2 inhibitors. And there are a few of them out there that are used for this. And there may be other subgroups where we want to use those as well. When we're looking at the chronic management of urate, the use of a treat-to-target strategy is really what I recommend. That includes dose titration. You're not going to have a set dose of your allopurinol or your febuxostat for these patients, because you may not get to that target.

The target level to really prevent a flare is getting those patients under six milligrams per deciliter. And if you remember our definition in women, that's about where it is. So it's a fine line between what would exacerbate a gout attack versus what you want to treat to targets. But I think, if you look at symptomatic improvement and dosing, you have to be very careful when you're looking at those. One dose standard does not fit all. I want to thank you again for listening to this video. As we go to our third video, I'm going to talk a little bit more about the differences of asymptomatic gout and hyperuricemia. Thanks for watching, and please stay tuned for the final verse.

 


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