All About: Gout

Being so common, gout is one of the diseases we’ve all heard of. Either we’ve had it ourselves or a family member, friend has at some point. For most of us, it isn’t an everyday problem; the attacks come and go leaving sometimes months, or even years between where you won’t give it much thought, if any at all. But we can’t sleep on gout… it’s a unique, destructive disease but we’re fortunate to have treatment at our fingertips for it if you know where to look. Today, we’re talking about exactly that.

What is gout?

Gout is a common disease within this small group of crystalline diseases. These occur when crystals, composed of various substances (something called uric acid, in gout’s case), accumulates inside joints and other tissues when there’s an excess. Even with high uric acid levels where we’ve got some deposits inside joints, usually your body just ignores these! The deposits don’t cause any issues… until one day, they do. And when they do, they really do. When the conditions are right, your body might suddenly recognize these clumps of crystals as something that should be there and decide to start a wildly active inflammatory reaction inside the joint (or joints!).

How does that manifest? The common story goes you’d have zero symptoms when you go to bed one night only to wake up the next morning with your big toe, knee, possibly even multiple joints, feeling like they are absolutely on fire. The pain can be astronomical, leaping out of your skin-kind of pain. Even the sensation of your sheets rubbing against a joint might be enough to make you yelp in pain. That’s your gout “attack”.

What happens next? If we do nothing, most gout attacks naturally run their course and dissipate over about two or three weeks, some longer. That means without any specific treatment, injections, or otherwise, it eventually settles and goes away. However, 2-3 weeks is an average; I’ve seen cases where gout attacks smolder and linger for more than two or three months. Fortunately that’s the exception, not the rule.

Why do we get gout?

This is the most common question I am asked, whether it’s about gout or practically any rheumatic disease: “How did this happen?” In the case of gout, you can most squarely place blame on genetics more than anything else. Genetics, meaning what our parents gifted us in terms of how well we clear uric acid from the body, tends to be the single biggest factor that increases or decreases our chance of having gout in our lifetimes regardless of what we eat or how our kidneys function. The other factors here, diet and kidney function, are still important but not always the driving ones.

Diving into diet, you might be surprised to hear what we eat doesn’t make as significant a difference for gout as we might like to think. Imagine you have a pair of 65-year-old identical twin men with the same genetics, but different lifestyles. One twin frequents the all-you-can-eat seafood buffet, enjoying his favorite fish and lobster with a cold beer—something many gout sufferers might recognize as a gout “bomb” waiting to explode. On the other hand, you have the other twin who adheres to the strict purine-limited diet, avoiding seafood, shellfish, red meats, beer and even other forms of alcohol, and goes further by consuming the most beneficial gout/uric acid foods like dairy/milk, tart cherries, etc., all in excess. He’s living the perfect gout diet!

What does it amount to?

The reality is, there’s going to be just a tiny, approximately 1 milligram per deciliter (mg/dL) difference in uric acid level between those two twins. That’s hardly anything in the grand scheme!

To give context to that number, uric acid starts landing into tissue around a level of 6.8 mg/dL. Most of us without gout will average a bit lower level at around 4-6 mg/dL whereas on the other end of things the highest I’ve ever seen is about 13 mg/dL. A 1 mg/dL difference is barely enough to shift that number meaningfully one way or the other unless they’re already at the cusp of that danger range, say at the 6-7 mg/dL range. If someone is right at that border, sure, take it easy on the shellfish and let’s see what we can get away with! If we’re in the 7.5+ mg/dL range, we’re really just not going to avoid gout attacks by diet alone at least most the time (there are ALWAYS exceptions). Like many other things, we just can’t beat the genetics we’re working against.

What can sometimes be underappreciated in this context is the contribution of our kidneys (kidney doctors hear that line often). Naturally, kidneys force out uric acid through the urine, taking that excess from our bodies. Some individuals, even with perfectly healthy kidneys, have kidneys that are just a bit less efficient at expelling uric acid than others. Add to that, as we age, our kidneys slowly wear out so regardless how they functioned at perfect health, they’ll work even less efficiently with chronic kidney disease. Indeed, as we approach the need for dialysis, our uric acid levels tend to float quite high.

How do we treat it?

It depends! The reality is, it very much depends on what we’re treating.

We’re really talking about treating two different things:

• How do you treat an attack once it starts? i.e. “breaking an attack”
• How do you lower the uric acid level so you prevent future attacks?

These aren’t the same: dropping one’s uric acid levels won’t stop an attack that’s already in-progress, and treating the inflammation of an attack won’t do anything to lower uric acid levels to prevent the next attack.

We call stopping an attack “breaking” it. There’s a self-sustaining fire that burns inside of a gouty joint for 2-3 weeks before finally burning itself out and settling back to normal if we do nothing. We can break that attack far sooner, putting that fire out nearly immediately and allowing things to settle back to normal much, much more quickly. The treatments here vary a bit and what’s right for you depends on your medical history, your preferences, and your doctor:

• Non-steroidal anti-inflammatory drugs (NSAIDs) like ibuprofen or indomethacin
• Corticosteroids (“cortisone”, steroid) either given in pill form (prednisone, methylprednisolone) or the usually preferred injectable form into the joint or muscle (injecting a single or couple joints greatly limits how much steroid the rest of your body is exposed to compared to taking a pill version or muscular injection of the same)
• Colchicine (only when taken at the absolute onset of an attack – these aren’t considered effective after 24 hours of an attack!)
• Adrenocorticotropin hormone (ACTH) injection (“Purified Cortrophin Gel”), a very promising recent approval by the FDA specifically for gout, a muscle injection that has a tremendous steroid-like anti-inflammatory effect to the whole body with far fewer side effects than the equivalent injected steroid dose would have.
• Canukinumab (“Ilaris”), also another very recent FDA approval for gout (although it’s been in use for gout in the EU since 2013), is a type of biologic therapy hitting one of the underpinnings of the gout inflammation, IL-1. This is generally used when other options fail or can’t be used, and gives a more effective pain response more quickly than a steroid injection would.

How do you prevent the attacks?

The goal here is lowering uric acid. When you’re near the threshold uric acid level, say around 6-7 mg/dL, I recommend to most a “gout diet”, a diet low in purines and processed foods so that your body produces a bit less uric acid. I included a link to two Arthritis Foundation articles containing lists of these foods:

• https://www.arthritis.org/health-wellness/healthy-living/nutrition/healthy-eating/fight-gout-with-food
• https://www.arthritis.org/health-wellness/healthy-living/nutrition/healthy-eating/which-foods-are-safe-for-gout

My general advice with low-purine diets is that they’re restrictive – unless you’re near the threshold, you’re again better off with a combination of lifestyle and medication rather than diet alone since the diet just won’t cut it – and you’re leaving out foods that many of us really enjoy. You have to live life at the end of the day, right?

When it comes to medications, we largely rely on four options to lower uric acid.

• Xanthine oxidase inhibitors, i.e. allopurinol and febuxostat (“Uloric”). These work to reduce how much uric acid is produced in your liver. These are both highly effective and can do wonders for many of us with high uric acid. Febuxostat is a bit newer and can be pricey on some insurance plans but can be had cheaply with discount programs and with independent pharmacies. Mark Cuban’s CostPlus Drugs also has this for a very reasonable price, about $10/mo when viewing it in March 2024.
• Drugs that encourage your kidneys to expel more, i.e. probenecid – these are not generally in common use anymore since they tend to only work in those folks who have “lazy” kidneys to begin with, meaning kidneys that just naturally don’t kick out as much uric acid as others do. In other folks with more efficient kidneys, or in those where the kidneys have become partially damaged (chronic kidney disease), these tend to not do anything at all.
• Pegloticase (“Krystexxa”), an infusion of a protein that directly destroys uric acid, one that humans don’t naturally produce. This is a wildly effective means to drop someone’s uric acid from nearly any range down to 1-2 mg/dL in as quick as one infusion. This one is a fantastic option for those who’ve had gout for long enough that it’s produced tophi, these large off-white-colored chunks of uric acid that can erode into bone and tendons. We’ll use this occasionally when the other options can’t be used or didn’t work.

When it comes to choosing whether to take these, you have to ask how often you’re having an attack to begin with. If you have a gout attack once a year or maybe once every other year, does it make sense to take a daily medication to prevent those one or two gout attacks every couple of years? No way – common sense says you might better off having a plan in place to break an attack and then deal with the rare events as they come. If you’re having attacks more than twice a year, most rheumatologists, myself included, would generally recommend it’s time to consider a maintenance option like the above or else risk the eventual development of gouty deposits, like this:

Do we have to take these medications… forever? This is a common question too – none of us wants to take anything we don’t have to, and if we do, we want the shortest possible duration. The simple answer for most is… yes, you do. The treatments available are great, both for breaking and preventing attacks – but the uric acid-lowering medications are all hamstrung by the fact that if we stop taking them, the uric acid just comes right back. They work when the medications are in our body, but the underlying problem i.e. high uric acid, is never fixed (unless we’re talking about kidney replacement or other odd cases).

The high uric acid is a disease we can’t currently cure – it’ll keeps coming back to bite you if you don’t control it and tends to bite just as hard as it did in the first attack you ever had.

Do you think you have gout?

Ask your doctor for advice or reach out to a local rheumatologist since we specialize in gout, particularly the tricky or complicated kinds. In very typical cases, like an attack in a toe, we can diagnose this with blood work alone. Any other case should go through a bit more thorough investigation like taking a small amount of fluid from an involved joint with a needle or. Rheumatologists trained in ultrasound, including myself, may also be able to find enough evidence with a simple ultrasound examination of your joints without resorting to the needle drainage. Most would rather a non-invasive look with ultrasound than the dreaded needle poke any day!

Don’t wait though – if you’re having attacks despite any treatment you might be on (or not on treatment), talk to your doctor or ask to see a rheumatologist – recurrent episodes of gout won’t just be painful and disruptive to your life, the repeated attacks can cause permanent damage to your joints and even lead to deformities that can be stopped if the right treatment can be started.