Gout: An Interview with Dr. Lawrence Edwards, Chairman and CEO of GUAES

Lawrence Edwards ARTICLE IMAGE

What is gout and who does it affect?

Gout is the most common form of inflammatory arthritis that affects adults. It's a disease caused by the presence of uric acid crystals in and around the joints. It's a disease that's becoming more and more common. It probably has doubled in its prevalence worldwide over the past twenty to thirty years.

Gout primarily affects adults. We think of it mostly as a disease of men, although post-menopausal women are just as likely to get it in the older age group as men are. Men frequently will start getting it in their forties and fifties; they then have this form of arthritis throughout their life if it’s not treated appropriately.

What is known about the causes of gout and why is the condition not well understood?

The causes of gout are actually very well understood. It's caused by the accumulation of uric acid within the body. This could be caused by several processes – the most common one is that the kidneys simply don't get rid of enough uric acid, given how much is in the blood system.

Once the uric acid gets above a certain level it starts forming crystals – it comes out of a solution around the joints, and that's the setup for the disease process.

The other mechanisms by which uric acid can be elevated include increased breakdown of cells around the body because of different medical conditions. Diseases like skin psoriasis, where there's a lot of turnover of cells, can lead to elevated uric acid levels. In any type of condition where there's a lot of cell turnover, usually in the bone marrow, it can lead to this kind of problem as well.

Plus there are a number of medications that can raise the uric acid level. Some of them are quite commonly used medications, like the diuretics for edema, or certain types of medications that are used for elevated blood lipids, triglycerides predominantly.

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The number of patients with gout is said to be rising in many industrial countries including the US. What do you think is responsible for this increase?

There are a lot of factors that are responsible for the epidemic of gout that's been taking place. It certainly parallels the obesity epidemic that is increasing worldwide. It also is partially caused by the fact that, like all chronic diseases where the people don't actually die from the disease and as the population ages, more and more people have the disease. We're living longer and therefore diseases that are lifelong diseases tend to accumulate.

The other problems, in addition to the obesity epidemic and increased longevity, would be some of the common medications that we use. For instance, low-dose salicylates, aspirin, blood pressure medications and diuretic medications that are used for elevated blood pressure can increase uric acid levels.

In some cases, food stuffs are at least partially responsible both for the obesity and for the uric acid problems. Here, high fructose corn syrup is usually mentioned due to its widespread use in plenty of sweetened beverages we may drink.

How is gout currently diagnosed? Why can diagnosis of gout often be difficult and what do you think can be done to improve the process?

The standard diagnosis involves putting a small needle into the painful joint and withdrawing some of the fluid, then looking at it under a specialized microscope that enables the health care provider to see these uric acid crystals in the joint. That's the definitive diagnosis of gout, and it's been the gold standard for more than fifty years.

The problem with this is that most gout patients see primary care physicians who have no interest in putting needles into joints. So, out of all the patients diagnosed with gout, probably less than ten percent will have had this definitive diagnostic test.

What physicians and health care providers rely on then is the clinical diagnosis: does it look like a textbook example of what gout would look like? Gout is a fairly dramatic form of arthritis. It has a very sudden onset. The joint will go from absolutely painless to the maximum amount of pain that the person could imagine being in that joint over a very short period of time – eight to twelve hours would be the time frame. It maintains that level of excruciating pain for several days, and then in the natural course of things, even without medication treatment, it will gradually subside over a period of a week. This is what a gout attack sounds like in its typical form.

If a patient comes in with a history like that, then the clinicians usually have to distinguish the very acute painful joint as either having gout or potentially an alternative diagnosis. This could be diagnosed as an infection in the joint. That's a very serious condition. If the patient has reason for infection – if they're immune-compromised, if they have had surgery, if there's some intervention that would have made them have an infection elsewhere in their body – then the concept of an infected joint would be higher on the list.

So, mostly the diagnosis of gout rests on a clinical prescription. The closer it gets to that very classic description of a gout attack, the more assured the physician could be that it is gout. But it's not an absolutely definitive diagnostic test as draining the fluid and looking for crystals would be.

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What treatments are available for gout? Why are only 10 percent of patients said to be receiving proper treatment for gout? What needs to be done to help the other 90 percent?

There are some very good treatments for gout. The problem is that there's confusion both from the patients’ viewpoint, as well as from the clinicians’ viewpoint, about how to use these medications. There have been some excellent guidelines that have come out over the past five or six years. The British Society for Rheumatology presented their guidelines almost seven years ago. Then EULAR, the European League Against Rheumatism, came out with their guidelines five years ago now. The American College of Rheumatology, just this past November, came out with their guidelines.

They all say essentially the same thing – that there are excellent medications for treating the acute symptoms of gout – the very painful part, but that's only the temporizing mode. That only gets patients through this painful process. The real substantive treatment for gout has to do with lowering the uric acid. Most societies that have put out guidelines agree that uric acid has to be at a level that's certainly less than 6 milligrams per decilitre (mg/dL). The conversion over in the UK would be about 360 micrograms per litre (μg/L).

The longest existing form of therapy is Allopurinol. It came out in the market in the mid-1960s. It's been available, but has been very poorly used by most clinicians, in that they weren't treating to these targeted uric acid levels.

Most patients have been treated with too low a dose of Allopurinol over the past 50 or 60 years to really make a substantial difference in their gout. Very standard doses of Allopurinol are between 100 and 300 milligrams. In fact, 97 percent of all doses of prescriptions for that drug are given out in that range.

However, we know that you don't even control half of the patients with gout until you're well above 300 milligrams a day. So, we need to use the entire range of Allopurinol’s dosing in order to get patients’ uric acid levels under control. People have been hesitant to do that because there's been some concern about the reactions to higher doses of Allopurinol.

The other drugs that have more recently come out on the market include Febuxostat, which is not available in all countries. It's functionally very similar to Allopurinol, but has enough differences that patients that were intolerant for any of a number of reasons to Allopurinol can take Febuxostat. That had been a problem in preceding decades where if somebody had an allergic reaction to Allopurinol, or they just weren't tolerant of it for gastrointestinal reasons or rashes, they had no other medication to turn to.

But now there are plenty of good options. New drugs for lowering uric acid are becoming available every couple of years. I think there is going to be less of a problem in finding a drug that a person can take to lower their uric acid level.

Is there any evidence to support a link between the consumption of fresh cherries and cherry juice and lower uric acid levels?

There is some evidence now. There's been a lot of “folklore” medicine surrounding this for decades. The actual ability of cherries and cherry juice to satisfactorily treat gout remains a major question. The question of lowering uric acid levels by having people on this concentrated cherry juice, or consuming very large quantities of fresh cherries or tart cherries, has been answered. Yes, you can lower uric acid. You can also do this with other fruits that contain high concentrations of vitamin C and other nutritious components of the cherries.

For instance, blueberries have a very similar type of effect, as does taking vitamin C tablets between 500 milligrams and 1000 milligrams a day. It's never going to be viewed as an adequate therapy in and of itself, but combined with other lifestyle and diet changes, it can be helpful.

Why do you think many people do not believe gout is a “serious” condition? How are the Gout & Uric Acid Education (GUAES) trying to change this?

I think many people that don't have the disease, don't believe it's a serious condition. Other people's pain is easy to ignore. Gout is a very serious problem. I think that for hundreds of years gout has been the butt of joke lines - somebody's kind of hobbled up with gout, and, for unknown reasons, people think this is funny. I think part of it, historically, was that gout was a disease that affected the upper class. It was a disease associated with excessive consumption. And so, if somebody in the upper class was hobbling around and in pain that probably was rather funny to the common people. We know that's not who gets gout now. Any member of any social strata can get gout, and it's not necessarily because of excessive consumption.

We know there's extensive genetic control of this disease. A family history of gout is a fairly good predictor that offspring will develop this as well.

People think of gout only as these painful episodes that come and go. So, it's something that people get over. Sure they're having a lot of pain now, but a week from now, they'll be OK. Some even think that when the pain goes away, they don't have gout. Well, they have gout all of the time. Gout that's in the joint, even when it's not symptomatic, is causing boney destruction. So, people don't view it as a serious disease. They don't see that the end result of this disease, after a patient has been having symptoms for a decade or more, this evolves into a chronic disabling form of arthritis very similar in appearance and very similar in its degree of disability and dysfunction as rheumatoid arthritis.

Nobody thinks rheumatoid arthritis isn't a serious disease. Nobody thinks that rheumatoid arthritis is funny. Yet those misperceptions are held about gout. That's part of what we do at the Gout & Uric Acid Education Society. We try and correct these misconceptions, putting a little different face on gout and having people take it more seriously.

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What disease myths and stereotypes about gout would you like to dispel?

The main one is that it's not a serious disease. Gout is a disease that not only can cause permanent joint destruction and disability, but high uric acid levels have now been shown to be associated with a number of other very serious medical conditions, including kidney disease, heart disease, stroke, hypertension, and diabetes. All of these are associated conditions with gout. Certainly controlling the uric acid has some benefit on all of these other diseases. So, it's a disease that should be taken seriously.

The other component is that it's a disease that's self-inflicted, kind of like tobacco smoking. The population in general doesn't have a great deal of sympathy for people that are suffering from chronic lung disease from smoking, or maybe even lung cancers. They think this has been brought on by their own choices.

That's not the case with gout. I take care of hundreds of gout patients, and most of them are fairly fit, very normal appearing men and women who are active, who are not over indulgent in any type of food or alcohol, yet they have a very painful form of arthritis. So, people just have to get away from those old cartoonish visions of what gout is and change their view into something with a little more compassion.

What are the key areas that require further research?

There's still a whole lot about gout that we don't know. For instance, patients come in and tell us what they think are the events that trigger these painful episodes. Sometimes they're correct. Sometimes overindulgence in a particular type of food, such as shellfish or red meat, or even beer, will set off these attacks.

But more often than not there's no obvious trigger for the gout attack. So, if we understood that aspect of the disease a bit better, we would certainly be able to control the painful symptoms of it.

One aspect that is being looked at more is new, exciting imaging techniques that can do a scan of the body and give us a fairly good quantitation of how much uric acid there is in the body. We don't have a test at this time that tells us that. But it would be the ultimate standard in how we would lower people's uric acid and how long we would persist with very potent forms of uric acid lowering therapy.

Do you think it will ever be possible to prevent gout?

I think the more we learn about genetics, we certainly will be able to predict who is likely to get gout from a genetic standpoint. In those patients, we could address the potential risk factors and dietary and lifestyle factors that might lead to earlier gout or worsening of gout. If patients avoided certain types of foods, if they remained active, if they avoided certain types of medications for other conditions, then they might in fact not get gout even though they're genetically predisposed to it.

Where can readers find more information?

They can visit our website and social media pages:

About Dr Edwards

Lawrence Edwards BIG IMAGEN. Lawrence Edwards, M.D. is a specialist in internal medicine and rheumatology, and serves as professor of medicine in the Division of Clinical Immunology at the University of Florida in Gainesville, Florida. He is also program director of the Medicine Residency Training Program and vice chairman for the Department of Medicine at the University. In addition, he is the chairman and chief executive officer for the Gout & Uric Acid Education Society.

Dr. Edwards is an active member of multiple organizations and societies within the medical community including 25 committees, both regional and national.

He currently serves on the executive council of the American College of Physicians and for the past 18 years sat on the University of Florida Medical Center’s General Clinical Research Center Advisory Committee. He also is an executive committee member of Medical Service, Veterans Administration Medical Center in Gainesville, Florida.

He has authored more than 100 scientific publications and more than 15 books and/or book chapters. His book credit includes “Rheumatology for the House Officer,” and textbook chapters for Arthritis and Allied Conditions (15th Edition) and Clinical Primer of Rheumatology.

Dr. Edwards is an authoritative lecturer who has been the recipient of many academic honors and awards. He received the American College of Physicians, Florida Chapter, Teacher of the Year recognition and has been an invited speaker at the American College of Rheumatology’s symposium on Hyperuricemia and Gout ― the first symposium on this disease in nearly 20 years.

Dr. Edwards received a bachelor’s degree from the University of Notre Dame in Notre Dame, Indiana, and his medical degree from the University of Miami School of Medicine in Miami, Florida. Dr. Edwards performed his medicine internship and residency at Creighton University Affiliated Hospitals in Omaha, Nebraska, and served as a research fellow in the Rackham Arthritis Research Unit at the University of Michigan Medical Center in Ann Arbor, Michigan.

April Cashin-Garbutt

Written by

April Cashin-Garbutt

April graduated with a first-class honours degree in Natural Sciences from Pembroke College, University of Cambridge. During her time as Editor-in-Chief, News-Medical (2012-2017), she kickstarted the content production process and helped to grow the website readership to over 60 million visitors per year. Through interviewing global thought leaders in medicine and life sciences, including Nobel laureates, April developed a passion for neuroscience and now works at the Sainsbury Wellcome Centre for Neural Circuits and Behaviour, located within UCL.


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  1. Steve Fellows Steve Fellows Australia says:

    Such an exact and true representation of how gout effects me personally. I have been taking Allopurinol since my initial diagnosis some years ago - although only 100mg a day. I still have the occasional flare up but with the help of Indocid I can catch it early enough to prevent an extreme pain episode.

The opinions expressed here are the views of the writer and do not necessarily reflect the views and opinions of News Medical.
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