Acute and Chronic Gout Treatment

In this video, Robert Terkeltaub, MD, discusses classifying gout as acute or chronic, and how treatment should be tailored for each patient based on disease severity and characteristics as well as other patient-specific factors. 

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Robert Terkeltaub, MD, is a professor of medicine emeritus in the Division of Rheumatology, Allergy and Immunology at the University of California, San Diego. 


Hi, I'm Bob Terkeltaub and I'm a Professor of Medicine Emeritus at UC San Diego and I'm a rheumatologist.  

I am a rheumatologist and a physician-scientist looking at gout inflammation, and I think about it every day when I show up in the clinic. I run a gout clinic, I have a general rheumatology clinic. And seeing all these patients, and reading all the research. I think of gout as a chronic disease with acute flares that are symptomatic and with potential to cause joint damage. Yes, chronic gout is sort of catchall term, a basket term to describe people with very frequent flares. But, if you have a gout flare every two weeks, it's not acute gout every two weeks. It's chronic gout, correct? Yes. Or a flare every month. I mean, that's chronic, correct? 

The time people spend – globally- in flare has a published average of about 10% of the days in a year. That’s the number for those without what we would call chronic gout. That's the all comers. People that spend a hell of a lot more than 10% of the days of the year in flare have chronic gout, whether they have palpable tophi or not. Yet we have only thought of chronic gout patients as people who have chronic symptomatology, often with things that you can see. Swollen, chronically swollen joints. We know that those joints by examining them, by looking at the imaging that they have masses of urate crystals in a mesh of tissue; we call those tophi. They're not rocks of uric acid. Only about up to a third of those tophi are composed of urate crystals. There's a lot of chronic inflammation. There's fibrosis. It's a mixed chronic tissue reaction to the urate crystals present in tophi.  

When people have fibrosis, we think of disease as chronic. And when they have chronic inflammatory cells and tophi, we think of that as chronic gout. Chronic synovitis, big palpable masses that you can feel. They can be huge. They can be very deforming. They can limit the ability to shake somebody's hand. Of interest to me, as a golfer, are so many of my patients who tell me they can't play golf anymore, can't hold the club, or they can't walk because they have chronic pain in their foot, or in their feet, because of joint damage, or they have chronic masses in their feet that are tophaceous that erode into bone and cartilage that limit the mobility in their joints. 

Let’s think about people who have very, very frequent flare activity who have palpable tophi, joint damage, and often both together. A lot of those people have hyperuricemia that is truly refractory to our best oral treatment. So many of those folks have terrible genetics for gout. They have early onset disease.  And we define that as gout coming on before age 40. Often in my clinic I see gout coming on before age 30 and not due to the stereotypic things that we think of re gout and genetics, such as Lesch-Nyhan disease and other inborn errors of purine metabolism. There's actually very common genetic variance of urate transporters that are associated with tophaceous disease, early onset disease, pretty bad disease. And in certain populations, it's predominantly the genetic variants that cause this. And there's one in particular, ABCG2 Q141K is the gene product. That variant impairs gut excretion of urate as well as to, some degree as well, renal excretion of urate. It's very common in East Asian populations, South Asian populations, and Mexican Americans actually. It's more common there than in White patients and much more common than in Black patients. There's some personalization in how we look at patients based on where they're from, what their genetics are, and the age of onset of their disease. And then do they have palpable tophaceous disease? What's their symptom burden? And so, we tailor the treatment and the aggressiveness of the treatment and the target urate of the treatment to all these factors. We mix up a recipe. We try to bake into the cake what comorbidities they have and what drugs we can use.  

For example, it's harder to treat flares in gout patients with chronic kidney disease. You're not going to use NSAIDs if they have stage three chronic kidney disease. And somebody with difficult to control diabetes, you're not going to be too enthusiastic about using prednisone tapers to treat their gout flares. And then many drugs interact with colchicine, which we use to prevent and treat gout flares. So, CKD makes gout a more complex disease to manage. And gout has gotten more complex actually in the last few decades. As we miraculously keep people alive with coronary artery disease, with chronic kidney disease, with other medical conditions including cancers and diabetes, we see a lot more gout.  And we see a lot of older people who are on 15 or 20 medications who have 5, 6, 7 comorbidities and they have terrible gout. And we've got to figure out the safest and best ways to treat them.  

So, I think we need a specialist's outlook to enrich how we look at particular disease and how we try to help the primary care doctors and the nurse practitioners and physician assistants who take care of these people, who have a problem list that's a mile long. So that's why, I would guess, you're talking to me today.