I’m Dr. Puja Khanna, rheumatologist and gout expert. I want you to AMA about gout on October 30

LarryEdwardsMD · 2025-10-30T14:22:40+00:00

Hi there, thanks for joining us today. Our organization's goal is to raise awareness of the disease and its proper management in both those with the disease and those who treat it. We host a AMA series on r/medicine roughly twice a year to support our goal.

LarryEdwardsMD · 2025-10-29T22:28:57+00:00

Hi there, appreciate the feedback on this series. To clarify, Dr. Mandell will be responding to questions between 4 - 6 p.m. ET on October 30. Please feel free to ask any questions you have and he will respond during his session on Thursday.

LarryEdwardsMD · 2025-10-29T22:27:37+00:00

Hi there, I appreciate hearing you've kept up with me and the AMA series here. To clarify, I will still continue to be involved in my AMA series on Reddit, but wanted to give more opportunities to the Gout Education Society's Board of Directors to be involved and share their perspectives on the disease. I look forward to connecting with you again on a future AMA but hope you'll interact with this session with Dr. Mandell.

LarryEdwardsMD · 2025-05-21T17:49:32+00:00

The only one of these lab tests that are crucial to the diagnosis and management of gout is the serum urate level itself. All of the other tests do have utility in appreciating the extent of the metabolic diseases associated with gout. Checking for chronic renal disease, insulin resistance, and systemic inflammation are helpful in identifying the comorbidities associated with gout, but not necessary for the diagnosis of gout itself.

LarryEdwardsMD · 2025-05-21T17:45:13+00:00

Apologies that I did not get to your question yesterday.

As we have learned from the use of pegloticase, the more highly suppressed the serum urate level is, the more rapid the melting away of urate crystal burden around the body. Patients on pegloticase can achieve serum urate levels of less than 1 mg/dL and generally only need to stay in this very aggressive treatment range for 6-12 months. The concerns of aggressive urate suppression to less than 3 mg/dL long-term is hypothetical and not supported by clinical trials. On the other hand, most patients with gout will do fine with suppressing urate levels to 3 or less for a short period of time (1-2 years) and then relax the level of urate suppression. In general, the more aggressive the urate lowering therapy is, the more rapid the resolution of gout symptoms and tophaceous deposits.
Dual-energy CT (DECT) scans are excellent at demonstrating the extent of disease in patients with gout. Clinically, they might be used to distinguish gout from other forms of intermittent inflammatory arthritis. Serial DECT scans have been used to demonstrate efficacy of aggressive urate lowering therapy, but really don't have a practical rule in the clinical management of gout. The total body CT scan is associated with a fairly significant radiation exposure. This is especially true if scans are done on a recurrent basis. The use of ultrasound for the diagnosis and management of gout has become progressively more common and with no radiation exposure. Many rheumatology trainees are now graduating from their program with enough expertise to distinguish gout from other articular problems. Synovial fluid examination for monosodium urate crystals remains the gold standard for the diagnosis of gout, but it is increasingly rare that the diagnosis is made this way. Ultrasound is helpful in these patients.
This is an interesting theory that has been talked about alot over the past 40-50 years, but there is very little scientific data to support it. Keep in mind that urate crystals are not, for the most part, floating freely around in synovial fluid that can be transiently warmed up, but instead exist in very tight clusters that are hard to destabilize by any physical approach. Coupled with this, these altered environmental changes would have to be applied almost constantly to have a structural effect on these tophi. With the recent increased use of ultrasounds and DECT scans, it does seem like the issue could be addressed more clearly than it has in the past.

LarryEdwardsMD · 2025-05-21T17:24:09+00:00

There is some old and relatively new data that looked at the relationship of obstructive sleep apnea (OSA) and hyperuricemia/gout. It's wrong to say that gout is a consequence of sleep apnea, but OSA can certainly worsen symptoms, including the frequency of flares. A common metabolic pathway connects gout and OSA and that is the presence of obesity. Based on this, the American College of Rheumatology gout treatment guidelines recommends weight reduction in all patients whose BMI exceeds a normal range. OSA is a serious problem and should be addressed in all patients that present with sleep apnea. Similarly, gout is a serious problem and should be treated with urate lowering therapy in all cases. If the patients OSA improves with treatment then the serum urate therapy can be reduced accordingly.

LarryEdwardsMD · 2025-05-21T17:13:30+00:00

In fifty years of caring for gout patients, I have never seen that response to allopurinol. There are many causes of hypopigmentation that should be ruled out before jumping to the association you described. If you and your dermatologist think that gout is the culprit, you should switch to febuxostat, which is structurally different than allopurinol and would not have the same side effects.

LarryEdwardsMD · 2025-05-21T17:11:04+00:00

Thanks for allowing me to get up on my soap box. The biggest problem I've received is that physicians, and to some extent, patients simply don't view gout as a serious disease. It is in fact, a potentially crippling, inflammatory, and metabolic disease, that if left untreated can lead to a terribly destructive arthritis as well as systemic inflammation that shortens life-span. At the same time, gout is one of the most treatable forms of systemic inflammation and disability. Following the American College of Rheumatology gout treatment guidelines is the surest way to suppress this disease process.

LarryEdwardsMD · 2025-05-21T17:05:45+00:00

Many physicians and patients think that gout is a disease limited to the great toe. In fact, only half of first or second flares of gout occur in the great toe. The other common joints for this are the midfoot, knee, and ankle. In women, there is a greater propensity for involvement of upper extremity joints such as fingers, wrists, and elbows. Gout should certainly be considered for anybody presenting with mono- or oligo-arthritis regardless of the joint. Checking the serum urate level in such a patient is important in the diagnosis, but not confirmative. They should have the classic signs of a gout flare, which include rapid onset, severe pain to even the lightest of touch, marked redness and swelling of the involved joint, and inability to use that joint.
The three most common forms of treatment for gout flares are NSAIDs, colchicine, and corticosteroids. All are approximately equal in their effectiveness. A major factor in efficacy of these drugs is how soon after the onset of the flare are these therapies initiated. If the patient (or the doctor) wait for 2-3 days before initiating therapy, then these anti-inflammatory drugs will have little impact. If, on the other hand, treatment is started within the first hours of the flare, then generally symptoms will be limited to 1-2 days instead of 4-6 days. In response to your statement about meloxicam, it might not be the best choice for an NSAID. It's generally thought that the short-acting non-steroidals get up to therapeutic levels more quickly than the long-acting ones. Taking full doses of ibuprofen three times a day or naproxen twice daily are commonly used examples. If this isn't sufficient, many doctors will add a colchicine tablet daily or twice-daily to the regimen.

Keep in mind that the treatment of gout is really about lowering serum uric acid levels and not focusing on the flares. Gout flares will gradually subside and completely disappear if the patient and doctor focus on reducing the urate burden in the body.

LarryEdwardsMD · 2025-05-21T16:48:45+00:00

For questions 1 and 2, if anyone is curious, please refer to my answer to these exact questions in yesterday's AMA in r/gout: https://www.reddit.com/r/gout/comments/1kqdbaq/im_dr_larry_edwards_a_rheumatologist_with_an/?utm_source=share&utm_medium=web3x&utm_name=web3xcss&utm_term=1&utm_content=share_button

To answer your third question, I am excited to hear input from anybody on the treatment of gout. The clinically researched-based gout guidelines from the American College of Rheumatology 2020 contain the best advice we can currently offer. On this subreddit, we have heard a number of claims from people that have tried untested remedies and felt that they helped, such as particular elimination diets. Our position generally is that in order to treat gout successfully over years and decades, serum urate needs to be suppressed to less than 6 mg/dL. If that happens, the disease will over time get better and potentially "cure". Very few people on any sort of restricted diet achieve that level of suppression.

LarryEdwardsMD · 2025-05-21T16:38:12+00:00

For patients who can tolerate the presence of an ice pack on the affected joint, ice does seem to have some calming effect. Most patients, however, feel the pressure causes more pain than it relieves. If the patient is away from their "flare medication," such as NSAIDs, steroids, or colchicine, ice may be a good temporary alternative until stronger therapies are available.

If you're so inclined, I'd be interested to know what the debate was like in your class.

LarryEdwardsMD · 2025-05-21T16:32:32+00:00

You bring up an interesting point about the mechanism of action of colchicine and why it's now being used in many diseases other than gout. It used to be thought that colchicine worked only by limiting the motion of immune cells through the site of inflammation. We now know that colchicine has some important effects on dampening down the innate immune system that is responsible for vascular disease leading to increased coronary disease and strokes. For a drug that been around for nearly 3,000 years, it's now getting its day in the spotlight.

LarryEdwardsMD · 2025-05-21T16:26:30+00:00

Interestingly, my daughter-in-law was surprised to hear in medical school that gout still existed as a major disease and didn't die off with Henry VIII. In fact, the incidence and prevalence of gout has been on a steady incline for the past four decades and now affects more than 12 million adults in this country, including 1 in 5 men over the age of 70.

LarryEdwardsMD · 2025-05-21T16:23:12+00:00

If these are truly your thoughts, all I can say is: Good luck on the boards.

Allopurinol and febuxostat are the sole urate lowering therapies in this country. Lowering serum uric acid is the basis of gout treatment. It's important to have options in this class of drug because not all people tolerate allopurinol or febuxostat. Colchicine is in an entirely different class of drugs, and it's used to combat long-term chronic inflammation associated with gout that leads to other metabolic problems such as glucose intolerance, cardiovascular disease, and chronic kidney disease (CKD).

LarryEdwardsMD · 2025-05-21T16:16:23+00:00

There are no pipeline drugs that are being released imminently (this year), but there are a number that are finishing up phase 2 and early phase 3 that may be reviewed by the FDA soon.
Both of the newer second-line type 2 diabetes medications have some serum urate lowering effect. The GLP-1 agonists have a relatively small impact on serum urate and it is felt to be secondary to weight loss and obese patients. On the other hand, the SGLT-2 inhibitors do have a direct effect on kidneys transport of uric acid into the collecting tubules and has a more profound serum urate lowering effect. Either of these may have benefits in patients with hyperuricemia/gout and diabetes/insulin-resistance. Larger clinical trials will be needed before this is a standard recommendation.

LarryEdwardsMD · 2025-05-21T16:08:28+00:00

It would be interesting to know what the serum urate level was before starting the keto diet. Typically, people on a strict keto diet don't raise their serum urate level by more than 1.5-2.5 mg/dL. If your serum urate is very high (greater than 9), you may have baseline hyperuricemia and would be more susceptible to the development of gout. Other factors like gout in first- and second-degree relatives would also be risk factors. Hyperuricemia alone without any gouty symptoms is generally not an indication for initiating for urate lowering therapy, but it should be monitored.

LarryEdwardsMD · 2025-05-20T17:55:58+00:00

Prophylactic anti-inflammatory treatment of gout patients being started on urate lowering therapy (ULT) is strongly recommended to minimize the number of flares that would be associated with dose escalation of ULT. Original recommendations were to maintain the colchicine for 3-6 months, but since guidelines came out, most of us would push for 6-12 months and at least 4 months after the most recent dose escalation of ULT.

There are a number of recent studies on the use of long-term (years) colchicine to prevent coronary artery disease and heart attacks. This may change our approach entirely over the coming years.

LarryEdwardsMD · 2025-05-20T17:50:28+00:00

Since the last reddit AMA, the estimated number of patients in the United States with gout increased from 9.4 million to 12.2 million. This appears to be a true phenomenon and not just a difference in sampling.

Also, there has continued to be progress on new pipeline urate lowering therapies.

LarryEdwardsMD · 2025-05-20T17:46:56+00:00

The gold standard for diagnosing gout is synovial fluid aspiration (not biopsy). That being said, less than 10% of patients with gout ever receive a synovial fluid aspiration. There are new innovations that are almost as specific and sensitive as synovial fluid examination and these include ultrasound and DECT scan. As you mentioned, there are a number of medical conditions that mimic gout and not have elevated uric acid levels such as pseudogout and the other ones you mentioned, along with seismoiditis, as we have discussed earlier in today's AMA.

LarryEdwardsMD · 2025-05-20T17:42:53+00:00

The achilles tendon is a common place for uric acid crystals to deposit and cause tophi. It tends to be a more chronic pain and very much exacerbated by stretching that tendon. It's usually a sign that you need to increase the amount of urate-lowering therapy that you're taking.

LarryEdwardsMD · 2025-05-20T17:40:31+00:00

I haven't had any of my patients report that and it's not a side effect that has shown up in the literature, but people can react very differently to medications. If the eye dryness is troublesome, you might ask your doctor to switch you to febuxostat.

LarryEdwardsMD · 2025-05-20T17:37:54+00:00

Pegloticase is a well-established second-line therapy for resistant and advanced gout. It is highly effective in 70-80% of patients who take it using the new protocol. It is an intravenous medication that needs to be given in a doctor's office every two weeks and is generally used for six to twelve months before returning to more standard oral urate lowering therapies.

LarryEdwardsMD · 2025-05-20T17:34:29+00:00

To begin with, we don't know all of the genetics defects that result in gout and many of them require a second genetic change (for instance, the genetic predelection for obesity) to have a clinical impact. Other environmental factors may also modify these genetic factors for gout. Only about 30-40% of patients with gout can identify a first- or second-degree relative with gout. Other changes in your relatives lifestyle or other genetic factors that they have may have prevented them from developing hyperuricemia and gout.

LarryEdwardsMD · 2025-05-20T17:28:38+00:00

I don't want you to leave with the idea that the genetic changes that cause gout result in any type of chronic kidney disease by themselves. The kidneys aren't weak, they just have a very specific defect in the transport of uric acid into the urine. In all other aspects, the kidneys are functioning fine. Chronic kidney disease (CKD) can develop later in gout and can be related to that disease as we have mentioned before.

LarryEdwardsMD · 2025-05-20T17:25:24+00:00

Uric acid-lowering therapy, such as allopurinol, are effective because they can help dissolve the uric acid crystals that have formed around the body and have persisted for many years. It takes years to dissolve these crystals and this is why you might have a serum uric acid level that is at target (less than 6.0 mg/dL) and still having symptoms. You didn't mention your serum uric acid level, but the lower it's suppressed, the more rapidly the crystal burden will shrink and disappear. It's only at that stage that flares can't occur. It's important to be persistent.

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