Medications that cause gout

Avoid Gout Flare-Ups

Once you’ve had a painful gout flare-up, you’ll never want to experience another one.

“We really think of it as an explosive arthritis, where you go from zero to 60 in 24 hours,” says rheumatologist Rebecca Manno, MD, MHS, assistant professor of medicine at Johns Hopkins University School of Medicine. “People say gout can be some of the most severe and worst pain they’ve ever experienced.”

But there are other reasons for gout prevention than just pain, says Manno.

“Gout can be more than just a nuisance. It can cause destruction in the joint itself,” she says. “Once there’s been damage done to the joint from gout — that we cannot reverse.”

You don’t have to sit around and wait for a gout attack in order to treat it. You can help avoid gout flare-ups by lifestyle changes and medication. Here are some tips for gout prevention.

  • Avoid gout triggers. Although it’s impossible to completely avoid all purines in your diet, if you know which foods tend to set off your gout attacks, try to avoid them. You may still be able to enjoy foods with fewer purines such as beans, lentils, and asparagus.
  • Preventive medication. If you have two or three gout flares in one year, many doctors will suggest daily medicine — such as feboxostat (Uloric), allopurinol (Lopurin, Zyloprim), and probenecid (Benemid) to lower uric acid level in the blood, and colchicine (Colcrys), to help prevent future attacks. In the first few months that you take the medicine, be aware that the gout prevention drugs may actually cause an attack. Your doctor will prepare you for this possibility by giving you medicine to take in the event you have a flare.
  • Healthy lifestyle. Eating a healthy diet, reducing or eliminating alcohol, and exercising regularly can help prevent gouty arthritis attacks and keep your uric acid level stable. Remember to drink water when exercising to avoid flare-ups due to dehydration.
  • Lose weight. If you are overweight, work with your doctor to develop a weight loss plan. Being overweight can contribute to elevated levels of uric acid and lead to gout attacks. “When we talk to patients about foods they should avoid, we also talk about weight,” says Manno. “There’s definitely a risk factor with being overweight.”

What Are Gout Treatments and Medications?

While some medications are used to treat the hot, swollen joint, other medications are used to prevent further attacks of gout. With any of these medications, call a doctor if you think they are not working or if you are having other problems with the medication.

Medicines used to treat acute gout and/or prevent further attacks are as follows:

  • Nonsteroidal anti-inflammatory drugs (NSAIDs)
    • Examples include indomethacin (Indocin), ibuprofen (Advil), and naproxen (Aleve). Newer drugs such as celecoxib (Celebrex) can also be used. Aspirin should not be used for this condition.
    • High doses of anti-inflammatory medications are used to control the inflammation and can be tapered off within a couple of weeks.
    • Tell a doctor about other health problems, particularly if you have a history of peptic ulcer disease or intestinal bleeding, if you are taking warfarin (Coumadin), or if you have problems with kidney function.
    • The primary complications of these medications include upset stomach, bleeding ulcers, and decreased kidney function.
  • Colchicine (Colcrys)
    • This medication is given in two different ways, either to treat the acute attack of arthritis or to prevent recurring attacks.
    • To treat the hot, swollen joint, colchicine is given rapidly (generally, two tablets at once followed by another tablet an hour later).
    • To help prevent an attack from coming back, colchicine can be given once or twice a day. While the chronic use of colchicine can reduce the attacks of gout, it does not prevent the accumulation of uric acid that can lead to joint damage even without attacks of hot, swollen joints.
    • Tell a doctor if you are experiencing any problems with kidney or liver function.
  • Corticosteroids
    • Corticosteroids such as prednisone (Meticorten, Sterapred, Sterapred DS) are generally given when a doctor feels this is a safer approach than using NSAIDs.
    • When given by mouth, high-dose corticosteroids are used initially and tapered off within a couple of weeks. It is important to take these medications as prescribed to avoid problems.
    • Some complications with the short-term use of corticosteroids include altered mood, elevated blood pressure, and problems with glucose control in patients with diabetes.
    • Corticosteroids can also be injected into the swollen joint. Resting the joint temporarily, after it is injected with steroids, can be helpful.
    • Occasionally, corticosteroids or a related compound, corticotropin (ACTH), can also be injected into the muscle or given intravenously.

In addition to low-dose colchicine, other medicines used to prevent further attacks of gout and lower the level of uric acid in the blood include the following:

  • Probenecid (Benemid)
    • This medication helps the body eliminate excess uric acid through the kidneys and into the urine.
    • Drink at least 2 liters of fluid a day while taking this medication (to help prevent uric acid kidney stones from forming).
    • Advise a doctor if you have kidney problems or a history of kidney stones or if you are taking aspirin. You may need to take allopurinol (see below) instead.
    • There are a number of drug interactions with probenecid, so advise a doctor of other medications. If prescribed a new medication, let a doctor know that you are taking probenecid.
  • Allopurinol
    • This medication decreases the formation of uric acid by the body and is a very reliable way to lower the blood uric acid level. Allopurinol is currently the gold standard of maintenance therapy.
    • Advise your doctor if you have kidney problems. Allopurinol can be still used, but the dose may need to be adjusted.
    • Common side effects include stomach pain, headache, diarrhea, and rash.
    • Discontinue allopurinol if you develop a rash or a fever, and call your doctor.
    • A very rare risk of allopurinol hypersensitivity exists. This problem can cause a severe skin rash, fever, kidney failure, liver failure, bone marrow failure, and can be fatal.
    • Advise your doctor if you are taking azathioprine (Azasan, Imuran), 6-mercaptopurine, or cyclophosphamide (Cytoxan, Cytoxan Lyophilized, Neosar); dose adjustments of allopurinol may be needed.
    • Ampicillin (Principen) is more likely to cause a rash if you are taking allopurinol.
  • Febuxostat (Uloric)
    • Febuxostat is the first new medication developed specifically for the control of gout in over 40 years.
    • Febuxostat decreases the formation of uric acid by the body and is a very reliable way to lower the blood uric acid level.
    • Febuxostat can be used in patients with mild to moderate kidney impairment.
    • Febuxostat should not be taken with 6-mercaptopurine (6-MP), or azathioprine.
  • Pegloticase (Krystexxa)
    • Pegloticase is a PEGylated uric acid-specific enzyme given intravenously that is indicated for the treatment of chronic gout in adult patients refractory to conventional therapies described above.
    • Pegloticase should be avoided if you have G6PD enzyme deficiency.
    • Serious allergic reactions can occur with pegloticase, including life-threatening anaphylaxis.

It is important to understand that these maintenance medications are used to lower the uric acid well below normal to prevent recurrent gouty arthritis attacks. Generally, doctors want the blood uric acid level to be below 6.0 mg/dL. This level of uric acid is referred to as the “target level” or “goal” of therapy.

FDA Approval: New Gout Medication for High Uric Acid Levels

The latest US Food and Drug Administration (FDA) approval goes to a Zurampic (lesinurad), a drug to help treat gout, a type of arthritis classified by severely painful joints.

Gout occurs when there is too much uric acid builds up in the body. When this happens, patients experience redness and soreness. Zurampic was approved to treat high levels of uric acid in blood, called hyperuricemia, when used with a xanthine oxidase inhibitor (XOI), which is a drug used to reduce uric acid production in the body.
“Controlling hyperuricemia is critical to the long-term treatment of gout,” Badrul Chowdhury, MD, director of the Division of Pulmonary, Allergy and Rheumatology Products in the FDA’s Center for Drug Evaluation and Research, said in a news release.

  • The MD Magazine Gout condition center

Zurampic helps the kidneys excrete uric acid by inhibiting the transporter proteins involved in uric acid reabsorption, according to the statement. Three studies consisting of 1,537 patients for up to one year supported the safety and efficacy of the drug. The Zurampic-XOI combination reduced serum uric acid levels in comparison to placebos.
Headache, influenza, increased blood creatinine, and gastroesophageal reflux disease were the most common side effects associated with Zurampic. However, the FDA is requiring a study to further analyze safety for renal and cardiovascular health.
“Zurampic provides a new treatment option for the millions of people who may develop gout over their lifetimes,” Chowdhury said.
What to Read Next >>> Gout Means Increased Risk of Atrial Fibrillation

Certain Medications Can Cause Gout

By

Paige Greenfield

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You already know that eating foods rich in purines like dried beans and liver can lead to a buildup of uric acid in the blood. But those aren’t the only culprits that contribute to gout. Certain medications used to treat other conditions may increase uric acid levels, too.

If you take one of the medications listed below and experience gout, it’s worth asking your doctor if there could be a connection.

Diuretics (Diuril, Saluron, Thalitone). These are commonly taken to help conditions such as high blood pressure and heart failure. Diuretics are the biggest troublemaker, boosting the risk of gout attacks by 20%. Diuretics are also called “water pills” because they help your body get rid of excess fluid. However, diuretics can decrease the kidneys’ ability to remove uric acid. As a result, uric acid levels in the blood may rise and lead to a gout attack.

Gout: From Famous Kings to Average Americans

The effects of gout remain the same—but the causes and treatments have evolved with time.

Aspirin. The pain reliever may seem like a good idea for treating gout symptoms, but it can have the opposite effect. That’s because aspirin may prevent the kidneys from removing uric acid. Your doctor will prescribe other types of pain medications for treating gout.

Niacin. In prescription form, niacin, a form of vitamin B3, may help lower cholesterol levels. Lower doses of niacin are also found in dietary supplements. However, in very large quantities—3 grams or more per day—it can contribute to serious problems, including gout.

Levodopa (Sinemet and Stalevo). This medication helps control symptoms in people with Parkinson’s disease, but it also increases the level of uric acid in your body.

Cyclosporine (Gengraf, Neoral, Sandimmune). This drug is often given to people who have received an organ transplant to prevent rejection. It suppresses the immune system, but it can increase uric acid levels as well.

All about gout

Updated: July 3, 2019Published: April, 2010

This old disease is becoming more common, but gout can be easily treated and then prevented — with the right care.

Unless you’ve experienced it firsthand or know someone who has, gout may seem like a museum piece of a disease — a condition that once afflicted corpulent men of means but doesn’t get mentioned much these days. Even the name seems archaic and unscientific. Gout comes from gutta, Latin for drop, a reference to the belief that it was caused by a drop-by-drop accumulation of humors in the joints.

But gout is still very much with us, and the number of Americans affected seems to be increasing, at least partly because of the obesity epidemic. Gout remains a disease that mainly affects middle-aged and older men, although postmenopausal women are vulnerable too, perhaps because they lack the protective effect of estrogen. The diuretics (“water pills”) that many people take to control high blood pressure are another contributing factor. Gout can also be a problem for transplant recipients. There are several reasons for this but medications, such as cyclosporine, taken to reduce the chances of organ rejection and reduced kidney function are major contributors.

The encouraging news is that almost all gout cases are treatable. In fact, gout is one of the few treatable and preventable forms of arthritis, an umbrella term for dozens of conditions that cause inflammation in the joints. The challenge is making sure people get the gout care they need and follow through on taking medications.

What causes gout?

Purines are a group of chemicals present in all body tissues and in many foods. Our bodies are continually processing purines, breaking them down and recycling or removing the byproducts. Uric acid is one of the byproducts and, normally, any excess leaves in the urine. But in some people, the system for keeping levels in check falls out of kilter. Usually it’s because the kidneys aren’t keeping up and excreting enough uric acid, but sometimes it’s a matter of too much uric acid being produced or it’s a combination of both.

Gout occurs when surplus uric acid coalesces into crystals, which causes inflammation in the joints. Pain, swelling and loss of joint motion are typical. (Technically, the crystals consist of sodium urate, although for simplicity’s sake they’re often referred to as uric acid crystals.) The crystals appear most often in the joints, but they may also collect elsewhere, including the outer ear, in the skin near the joints, and the kidney.

High concentrations of uric acid levels in the blood — the medical term is hyperuricemia — are necessary for the crystals to form. Yet many people with hyperuricemia never develop gout, and even when they do, they often have had high levels of uric acid in their blood for years without any symptoms. People with hyperuricemia with no symptoms might be coached to make lifestyle changes — losing weight would often top the list — but hyperuricemia by itself is usually not treated.

Gout predisposing factors

Dr. Hyon K. Choi, now at the Massachusetts General Hospital in Boston, and epidemiologists at Harvard have used data from the Harvard-based, all-male Health Professionals Follow-up Study to make a series of comparisons between the 730 men in this study who developed gout during a 12-year period and the vast majority of those in the study who did not. The result is an impressive dossier on the risk factors for gout, at least as they pertain to men.

Dr. Choi’s findings on weight weren’t surprising and fit the stereotype: gout is, in fact, a heavy man’s disease. Eating lots of meat and seafood and drinking lots of alcohol spells gouty trouble. And the Homer Simpsons of the world are gout candidates: two-or-more-a-day beer drinkers are more than twice as likely to get gout as nonbeer drinkers, which makes sense, because beer contains a lot of purines.

Soft drink fanciers might be in the same gouty boat. High fructose intake was linked to gout in a Choi-led study published in 2008. Uric acid is one of the products of fructose metabolism, and there’s good evidence from controlled feeding studies that fructose increases uric acid levels in the blood. Much of the fructose in today’s American diet comes from the high-fructose corn syrup (which is about half fructose and half glucose) that’s used to sweeten soft drinks and many other foods and drinks.

High blood pressure is another major risk factor for gout. It gets complicated, though, because the diuretics taken to lower high blood pressure increase uric acid levels, so the treatment as well as the disease is associated with gout.

Finally, gout does run in some families and we know that certain genes increase the risk of gout.

Gout symptoms and complications

Gout is not gout until symptoms occur. When they do, they usually come on suddenly and, at least initially, affect a single joint. Within hours, that joint becomes red, swollen, hot, and painful — they’re called gout attacks for a reason. It’s easy to mistake a gout attack for a localized infection of a joint. The metatarsophalangeal joint at the base of the big toe (where the toe meets the foot) is often the site of the first attack, but the knees, ankles, and joints between the many small bones that form the foot are also common sites. People who already have osteoarthritis — the most common form of arthritis — often experience their gout attacks in the joints of the finger

As is true for many painful conditions, the first-line treatment for a gout attack is taking one of the nonsteroidal anti-inflammatory drugs (NSAIDs), such as diclofenac, ibuprofen, or indomethacin. For people who can’t take NSAIDs, a drug called colchicine is an alternative. It’s been used for centuries — maybe even longer — specifically for gout. The trouble with colchicine is its side effects, especially the copious diarrhea. If neither an NSAID nor colchicine is an option, then gout attacks can be treated with an oral corticosteroid, such as prednisone, or with corticosteroid injections into the joints.

Preventing gout attacks

For years, gout patients were told they had to follow a purine-restricted diet to stave off attacks, but those diets weren’t very effective and people had a difficult time sticking to them. Now the easier-said-than-done advice is to lose weight, and also to cut back on alcohol, especially beer. Big meat and seafood eaters may be told to curb their appetites and instead eat more low-fat dairy foods. Diuretics tend to increase uric acid levels. If someone with gout is taking one, a doctor might explore lowering the dose or switching to a different medication.

But the most important fork in the road for gout sufferers is whether to start taking a drug that will lower their uric acid levels. Once people start taking these drugs, they usually must take them for the rest of their lives. Going on and off a uric acid–lowering medication can provoke gout attacks. Experts have differing opinions, but many agree that the criteria for starting therapy include frequent (say, two or three times a year) attacks, severe attacks that are difficult to control, gout with a history of kidney stones, or attacks that affect several joints at a time. Guidelines also recommend uric acid-lowering treatment if a person with gout also has kidney disease.

Allopurinol is the first-line uric acid–lowering drug. It needs to be taken only once a day and reduces uric acid levels regardless of whether the root problem is overproduction of uric acid or inadequate clearance by the kidneys. Sometimes people develop a mild rash when they start allopurinol, although rarely there’s a dangerous allergic reaction. Old guidelines warned against prescribing allopurinol for people with kidney disease, but with proper dosing, the drug is usually well tolerated and effective even for people with kidney disease. Underdosing has long been a problem. The standard starting dose is 100 mg per day (or less if a person has kidney disease); many doctors do not increase it above 300 milligrams (mg), but that might not be enough to reach the commonly accepted target level for uric acid of 6 milligrams per deciliter (mg/dL). Most people can take doses of 400 mg or more (if needed) without any problems, although higher doses do mean taking extra pills.

A newer drug, febuxostat (Uloric), is similar to allopurinol in the way it works. In head-to-head trials, febuxostat looked to be more effective than allopurinol at controlling uric acid levels, although that was likely because the allopurinol dose in the study was too low. As a new, brand-name drug, febuxostat is far more expensive than allopurinol.

Probenecid is a third choice. Like allopurinol, it’s been on the market for decades, so it has a long track record. Probenecid works by increasing uric acid excretion by the kidneys so it can trigger the development of kidney stones and is not a good option for people with kidney problems. Another drawback to probenecid is that it has to be taken twice a day.

Perhaps the biggest problem with the uric acid–lowering therapy is sticking with it. A number of studies have demonstrated that up to 80% of people prescribed allopurinol were taking it incorrectly or not at all. Poor adherence is understandable. Once people are taking an effective gout prevention medicine, there are usually no immediate symptoms to remind them to take the pills daily. And the memory of the last attack is bound to fade, no matter how excruciating it might have been.

Many types of arthritis cannot be prevented and lack medical treatments that reliably work. Gout is different – the treatment is usually straightforward and highly effective. So, if you have gout, ask your doctor about treatment options. Although gout is on the rise, there are now good treatment options for this ancient disease.

The Health Letter thanks Dr. Robert Shmerling for his help with this article. Dr. Shmerling is the clinical chief of the Division of Rheumatology at Beth Israel Deaconess Medical Center in Boston.

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Gout is a prevalent and debilitating disease. It is progressive in nature and it can be precipitated by many things. It is similar to other arthritis diseases in that it involves inflammation, effects the joints, and causes severe pain. Unlike osteoarthritis and some other forms of arthritis that are strictly localized to the joint, gout can affect the entire body, leaving the patient completely incapacitated and even hospitalized if not treated properly. This paper will discuss Gout and is meant to be a guide for Nurse Practitioners to use in practice.

Definition, Pathophysiology, and Epidemiology

Gout is defined as a type of arthritis because it involves an inflammation of the joints. A definition by Vannucchi, 2012, is that it is “characterized by elevated serum uric acid (SUA) levels, inflammation, and urate crystal deposition in and around joints causing acute, intense pain” (p 191). Gout has been around since the 18th century. It was known to affect the rich man and was depicted in many cartoons as a demon gnawing relentlessly at ones joint (Harvard Health Letter, 2010). Even the name is ancient. Gout comes from the Latin word for drop, which came from the belief that “gout happened from drop by drop humors accumulating in the joints” (Harvard Health Letter, 2010, p3). Rich men were often overweight and indulged in meat, alcohol, and seafood; even now this can be considered a disease of an overweight individual due to its pathophysiology. The etiology is too much uric acid in the blood, but it is also linked to genetic factors.

As stated in the introduction, gout is a prevalent disease. According to Hilaire and Wozniak, 2010, “an estimated 3 to 5 million suffer and its prevalence appears to be increasing. Gout affects about 2% of men (>30 years) and women (>50 years)” (p 84). Gout affects 2% of people, which is more than rheumatoid arthritis. This disease does affect black men more often than other groups and this is most likely due to the large incidence of hypertension in this group (Dunphy, Winland-Brown, Porter, Thomas, 2011). The risk factors include, hypertension, advanced age, male gender, postmenopausal women, high BMI, high alcohol intake, diet high in meat and seafood, and genetic influences (Hilaire & Wozniak, 2010). Certain drugs such as low dose aspirin and diuretics can also contribute to an acute attack of gout. The associated co-morbidities with hyperuricemia and gout are diabetes mellitus, hypertension, metabolic syndrome, obesity, cardiovascular disease, hyperlipidemia, and renal manifestations (Hilaire and Wozniak, 2010).

In 90% of cases of gout the cause is under excretion of uric acid not overproduction of it (10%). Uric acid is the end product of catabolism of purines (Vannucchi, 2012). Xanthine and hypoxanthine, a byproduct of purines catabolism, is broken down by xanthine oxidase to produce uric acid. Uric acid is then excreted by the alimentary or urinary systems. If there is excess uric acid, from eating a lot of meat, drinking a lot of alcohol, or poor kidney function, then uric acid in the form of monosodium urate crystals, gets deposited around the joints (Hilaire and Wozniak, 2010). A bump or injury to the area can release the crystals into the joint space causing an acute exacerbation of gout. Other things that can cause the crystals to be released is acute stress caused by surgery or infection. There are four critical stages of gout. The first stage is called the asymptomatic stage. This stage is characterized by no symptoms or gout, but the uric acid level is usually greater than 6.5 mg/dL (Vannucchi, 2012). No history of gout attacks has been recorded, but the deposition of urate has begun at this stage and these deposits can directly contribute to organ damage. The next stage is an acute attack. A traumatic event, such as an infection or trauma (even just stubbing a toe), will cause the crystals to dislodge and enter the joint space. This involves acute inflammation and intense pain. This is the phase where management needs to be optimized. The intercritical stage is the time between gouty flare ups. “When the crystal deposits continue to accumulate, patients develop stiff and swollen joints leading to the final phase, chronic advanced gout. This includes long-term complications of uncontrolled hyperuricemia such as chronic arthritis and tophi” (Hilaire and Wozniak, 2010). Tophi are large nodules of crystals that have deposited in soft tissue. This phase is uncommon because it can be avoided with proper management. Refer to the management section for ways to properly prescribe medications for this disease.

Social Determinants

The social determinants of this disease are age, race, and gender. Black males between the ages of 40 and 50 will be the group that is most affected potentially because this group is largely affected by severe hypertension and kidney diseases (Dunphy, Windland-Brown, Porter, Thomas, 2011). The prevalence of this disease is increasing and this is thought to be because of an increase in the use of diuretics and low dose aspirin, but also because there is a large group of people getting older, namely the baby boomers. Another reason this disease may be becoming more prevalent is the greater amount of kidney disease and overweight individuals, which are both associated with gout.

Case Study

Michael is a 53 year old African American male that presents with an excruciatingly painful, and hot index finger on his right hand. He is in so much distress because he is right handed and works construction; He states, “I haven’t been able to work the past week because the pain has been so bad and it has only gotten worse.” He states he tried taking ibuprofen and Tylenol, but they only relieve the pain for a short while. He does not remember bumping his finger on anything or having any recent trauma but states that it is possible since he works construction. He has also used ice on it and this has helped some. “I have also felt feverish the past two days, I think I might be getting sick.” When asked about drinking he admitted to drink a beer every night and does not have the “best diet.”

Family history includes gout, diabetes mellitus type II, hypertension, coronary artery disease, and hyperlipidemia on his paternal side. Hypertension on his maternal side.

Medical diagnoses include: hypertension, hyperlipidemia, and diabetes mellitus type II. Medications include Hydrochlorothiazide/Lisinopril 25mg/40mg PO Daily, Metformin 500mg PO BID, aspirin 81mg Daily, and atorvastatin 40mg PO daily.

Weight: 250lbs, Height: 5 foot 9 inches, BMI: 36.9, BP: 165/88, HR: 67, Temp: 99.2

On physical exam, a swollen and red middle interphalangeal joint of the index finger is noted. Tenderness and heat upon palpation of this joint. Limited range of motion in right hand, especially at the index finger. Left hand has full range of motion with no redness, swelling, or tenderness. Diagnostic tests include: a serum uric acid level, BUN, creatinine, ESR, CBC (focusing on the WBC level), and an x-ray of the finger. Serum uric acid level: 9.0 mg/dL; WBCs 12,000 10^6/L; Creatinine: 1.34 mg/dL, BUN: 38, and ESR is elevated. The x-ray of the joint revealed “punched out” erosions of bone (Dunphy, Windland-Brown, Porter, Thomas, 2011). Differential diagnoses include gout, Rheumatoid arthritis, osteoarthritis, fracture, or trauma (Mead, Arabindoo, & Smith, 2014). Fracture, osteoarthritis and trauma was ruled out with x-ray. Rheumatoid arthritis can be ruled out with history and presentation.

Management and Patient Education

Due to the prevalence of gout, understanding how to manage it is a very important part of being a primary care provider. Part of managing gout is understanding when and why flare-ups occur therefore keeping a complete record of flare-ups will be important (Mead, Arabindoo, & Smith, 2014). In the asymptomatic phase there is no gout attack and the patient does not present with symptoms therefore there is no management. The acute phase requires quick, usually within the first 24 hours of onset, and effective treatment at the first sign of the attack. Most of the time the acute attack will occur in the joint of the big toe, often referred to as podgara (Dunphy, Windland-Brown, Porter, Thomas, 2011). “For moderate pain involving a few small joints or one or 2 large joints, monotherapy with a nonsteroidal anti-inflammatory drug (NSAID), a corticosteroid, or colchicine is recommended. For severe pain and/or polyarticular involvement (≥4 joints in more than one region of the body), combination therapy is recommended (eg, colchicine and either an NSAID or a corticosteroid).” (Mead, Arabindoo, & Smith, 2014). Colchicine is a first line anti-gout medication that is given when the first symptom of a gout attack occurs and should not be given 36 hours after an attack starts. Dosing is 1.2 mg loading dose, followed by 0.6mg every hour until resolution (do not exceed 1.8mg/day and do not repeat dosing for more than 3 days) (Mead, Arabindoo, & Smith, 2014). Naproxen (250mg PO TID) or Indomethacin (50mg PO TID) can be used for NSAID therapy and should be given every eight hours for pain relief (Mead, Arabindoo, & Smith, 2014).

Chronic gout has a very different treatment. The goal of therapy for chronic gout is to keep the uric acid level below 6.0 mg/dL (Mead, Arabindoo, & Smith, 2014). There are several qualifying factors for chronic gout therapy. “Patients who meet one or more of the following criteria qualify for ULT: the presence of tophi, ≥2 acute attacks per year, chronic kidney disease (CKD) stages 2 through 5, and a history of urolithiasis” (Mead, Arabindoo, & Smith, 2014, p 710). If a patient has evidence of tophi, they should continue NSAID therapy for six months after serum urate levels reach target and until tophi resolve or if no tophi, three months after urate levels reach target and no evidence of tophi.

The first line therapy for chronic gout is Allopurinol taken daily. Allopurinol is a type of xanthine oxidase inhibitor. Febuoxstat is in the same category, but is more expensive and the Food and Drug Administration (FDA) warns against hepatic failure while on this medication (Mead, Arabindoo, & Smith, 2014). Allopurinol should be initiated at 100 mg daily and titrated up by 100 mg every 2-5 weeks until target uric acid levels are reached. This should be continued indefinitely. In the case of xanthine oxidase inhibitor allergy, Probenecid can be used instead. Probenecid is an uricosuria agent and should be dosed at 250mg twice a day and titrated until target serum uric acid levels are reached (Mead, Arabindoo, & Smith, 2014).

Patient who fail this therapy should be placed on Pegloticase, which is a new medication that is administered intravenously every two weeks. This medication is a urate oxidase enzyme that converts uric acid to allatonin, which is then water soluble (Mead, Arabindoo, & Smith, 2014). This is a VERY expensive medication and should only be used as a last resort to decrease urate levels. Consider medication noncompliance and re-education before putting a patient on this medication.

Other considerations for managing gout is lifestyle changes with diet. “A diet extremely high in protein and fat with very little carbohydrate intake may induce ketogenesis, which is known to be an inhibitor of uric acid excretion. Another inhibitor of uric acid excretion is elevated lactate levels, which can be induced by alcohol ingestion. Refined sugar also exacerbates the issue through the increase in dietary fructose” (Connery, 2013, p 24). Patients with gout should stay away from alcohol, but, if unable to avoid, the safest type is dry wines due to the low alcohol, sugar, and purine content. Beer is the most unsafe type due to the guanosine (a type of purine) content. Manufacturers today are adding high fructose corn syrup to everything, but the biggest perpetrator is drinks. Sugary drinks, including, soda and juice, should be avoided to keep the uric acid levels low (Harvard Health Letter, 2010). High protein diets that can exacerbate gout attacks include meat and seafood, which should be limited to 0.8g/kg/day (Connery, 2013).

Another factor that should be considered is diuretics. Hypertension is a significant problem in the adult population and many people are well controlled on diuretics such as hydrochlorothiazide. But multiple studies have been done that show an increase in gouty attacks while on a diuretic. A study of almost 25,000 people with gout showed a significantly increased risk of a gout flare-up when a diuretic was used. “Diuretics increase the net reabsorption of uric acid in the proximal tubule of the nephron and thereby reduce urinary excretion and increase the risk of hyperuricaemia and gout. The increase in serum uric acid concentration and the risk of gout caused by diuretics may be noted within a few days of the start of treatment” (Choi, Soriano, Zhang, & Rodríguez, 2012, p 4). This study also noted that the use of losartan greatly reduced the amount of serum uric acid by 20-25% by producing a uricosuria effect similar to that of probenecid (Choi, Soriano, Zhang, & Rodríguez, 2012). Notably, the effect was not found when other angiotensin II antagonists were used (e.g valsartan).

Role of Nurse Practitioner and Referral

Nurse Practitioners managing patients with gout should be highly aware and sensitive to an oncoming acute gout attack in their patients. A good health history during a flare-up is the best way to effectively manage gout. Patients with chronic kidney disease, obesity, family history of gout, hypertension, and metabolic syndrome should all be considered at high risk for crystalline deposition of uric acid in the joints. Patients that drink alcohol, especially beer, in addition to these risk factors are at an even greater risk. Educating patient about their risk will be an essential component of managing this disease. Diet recommendation is another component. Low fat, less alcohol, low protein (including seafood), and low fructose should all be considered when educating. It is important to be specific about what foods to avoid because some people do not understand the crawfish or soda they are consuming is contributing to their gout attacks. Managing hypertension is another component and this includes ensuring that patients with gout are not taking diuretics that are proven to contribute to this problem. Using Losartan instead can reduce uric acid levels and keep blood pressure under control. A referral to an rheumatologist should be made for patients with frequent acute attacks, persons younger than 35, renal insufficiency, and premenopausal women (Dunphy, Windland-Brown, Porter, Thomas, 2011). Creating a trusting relationship with patients if the best way to ensure that their gout is managed properly.

Conclusion

Gout presentation is distinct from other arthritis issues. It should be managed aggressively and effectively. Nurse Practitioners are great resources for gout patients because of the preventable nature of the disease. Education on what foods to avoid and risk factors associated with gout are essential. Chronic gout is preventable if patients have the right resources and knowledge to manage it.

All about gout. (2010). Harvard Health Letter, 35(6), 1-3 3p.

Clark Connery, G. (2013). Renal Nutrition Update. Renal & Urology News, 12(3), 24.

Hilaire, M., & Wozniak, J. (2010). Gout: overview and newer therapeutic developments. Formulary, 45(3), 84-90 7p.

Mead, T., Arabindoo, K., & Smith, B. (2014). Managing gout: There’s more we can do. Journal Of Family Practice, 63(12), 707-713 7p.

Vannucchi, P. (2012). Understanding, Diagnosing, and Treating Gout. Podiatry Management, 31(4), 191-200 10p.

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