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Treatment Options for Gout by Jon Brady, Pharmd; Sarah Pupo, Pharmd; Eric Sidman, Pharmd; and Jennifer Malinowski Pharmd

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Treatment Options for Gout by Jon Brady, Pharmd; Sarah Pupo, Pharmd; Eric Sidman, Pharmd; and Jennifer Malinowski Pharmd CONTINUING EDUCATION Treatment Options for Gout by Jon Brady, PharmD; Sarah Pupo, PharmD; Eric Sidman, PharmD; and Jennifer Malinowski PharmD pon successful completion of this the body and dietary protein break down. Patients with activity, the pharmacist should be gout may produce more uric acid than can be solubi- able to: lized (overproduction) or they may not be able to excrete 1. Describe the pathophysiology enough uric acid (underexcretion). of gout. Gout was first characterized thousands of years U2. Recognize the clinical characteristics and ago. It was incorrectly thought to be a “disease of kings” various manifestations of gout. because of its predilection towards wealthier individuals 3. Explain symptom management strategies for who consume food and drink in excess. Interestingly, the acute gout attacks. treatment of gout preceded the actual understanding 4. Identify patients who are candidates for pro- of the pathophysiologic mechanisms. Herbal therapies phylactic therapy and select an appropriate such as active colchicum are still a part of therapeu- agent and dose based on patient and drug tic plans today. Standard treatment of gout has not characteristics. changed much in the past 50 years. However, recent 5. Establish monitoring plans for gout treat- drug approvals offer new approaches to therapy. The ments. purpose of this article is to highlight the pathophysiolo- 6. Provide appropriate patient education on gy, risk factors, non-pharmacologic, and pharmacologic non-pharmacologic strategies for gout, phar- treatments for gout, and to summarize the pros and macologic agents for acute gout and gout cons of each treatment. prophylaxis. PATHOPHYSIOLOGY Upon successful completion of this activity, the Gout is a type of arthritis associated with a disorder of pharmacy technician should be able to: purine metabolism characterized by the deposition of 1. Describe the pathophysiology of gout. monosodium urate (MSU) crystals in joints, bones, and 2. List the clinical characteristics and various soft tissues. These crystals result in a local immune manifestations of gout. response leading to pain, erythema, and inflammation 3. Recognize patients who may be experienc- at the affected site. Prolonged presence of crystals can ing an acute gout attack and recommend cause a sustained inflammatory response, often resulting pharmacist intervention. in tissue damage. 4. Explain non-pharmacologic symptom man- MSU crystals are derived from uric acid, a water-sol- agement strategies for acute gout attacks uble substance which has no physiological function and and prophylaxis. is an end product of purine metabolism. Purines ingested as dietary protein, as well as purines released from the More than six million adults in the United States DNA of degraded cells throughout the human body, are suffer from gout. Gout is an inflammatory joint metabolized in a stepwise process. The final steps in disease associated with abnormal uric acid the metabolic pathway involve the conversion of purine metabolism. Uric acid is formed when cells in nucleotides to hypoxanthine, which is then converted www.americaspharmacist.net March 2013 | america’s PHARMACIST 37 to xanthine via the enzyme xanthine oxidase. Xanthine follows the activation of these mediators and oxidase is also responsible for the conversion of xanthine neutrophils invade the affected area, removing to the uric acid end product. The majority of uric acid MSU crystals through the process of phagocy- excretion occurs renally and a small amount of uric acid tosis. The neutrophils are then lysed, releasing is broken down by bacteria in the colon and excreted via proteolytic enzymes into the joint or soft tissues the gastrointestinal tract. that further increase inflammation and contrib- Elevated serum concentration of uric acid and de- ute to the manifestation of gout symptoms. creased temperature of the local environment promote the precipitation of MSU crystals responsible for a gouty Patient Case attack. Increased uric acid concentrations are caused JG is a 45-year-old, obese, white male who by an imbalance between the metabolism and excretion comes to the pharmacy to purchase a bottle of of purines. aspirin for a swollen, painful toe. He appears The vast majority of gout patients (85–90 percent) to be very uncomfortable and is limping. He are underexcretors and do not eliminate uric acid effi- denies recent trauma to his foot and states he ciently. Primary causes of uric acid underexcretion include “never had pain this bad before and it’s been inherited disorders such as polycystic kidney disease, getting worse over the past hour.” His past familial juvenile hyperuricemic nephropathy, and medul- medical history is significant for hypertension, lary kidney disease. Secondary causes of decreased which is treated with losartan 50 mg daily, and renal excretion of uric acid include hypertension, chronic high cholesterol, which he manages with diet kidney disease, medications, and several metabolic and over-the-counter niacin. He quit smoking disorders. The resultant buildup of uric acid leads to the a couple years ago but does drink “a couple precipitation of MSU crystals in tissues, consequently 6-packs” on weekends. causing a gouty attack. Overproducers, the minority of patients, synthesize CLINICAL PRESENTATION OF GOUT excessive amounts of uric acid. Primary causes include The clinical presentation of gout is character- inherited enzymatic defects such as glucose-6-phos- ized by two clinical phases. The first phase phate dehydrogenase deficiency (G6PD), hypoxanthine- is associated with acute intermittent arthritis guanine phosphoribosyl transferase deficiency, and attacks that resolve on their own after seven to phosphoribosyl pyrophosphate synthetase deficiency. ten days. If high uric acid levels (defined as uric Secondary causes of uric acid overproduction include acid 6.8 mg/dL or more) are allowed to persist, excessive dietary purine intake, ethanol consumption, a second phase of chronic arthritis may occur. medications (such as chemotherapy agents), and Tophi, or crystal deposition, may be observed proliferative cancers. Increased uric acid production at this stage. Presence of tophi is considered may be compensated via increased renal elimination. a pathognomonic feature of gout. Chronic However, if renal elimination is not adequate to overcome tophaceous gout is seen more commonly in overproduction, serum uric acid levels rise. As with patients with gout for more than 20 years and is underexcretors, hyperuricemia from overproduction associated with multiple joint involvement and results in MSU crystal precipitation and gout symptoms. symptoms in between attacks. Deposition of MSU crystals results in the activation An acute gout attack is rapid, painful and of the innate immune system. MSU crystals are believed severely worsens within the first 24 hours. to interact with receptors of local dendritic cells and Table 1 summarizes the typical subjective and macrophages, which activate the immune response. The objective findings associated with an acute resultant production of interleukin 1 (IL-1) initiates a cas- gout attack. The most common site is the cade of pro-inflammatory mediators such as neutrophil metatarsophalangeal joint of the big toe and chemotactic factors, tumor necrosis factor (TNF ), knee joints. Gouty joint involvement is typically interleukin 6 (IL-6), and interleukin 8 (IL-8). Inflammation monoarticular (involves a single joint). Patients 38 america’s PHARMACIST | March 2013 www.americaspharmacist.net Table 1. Clinical Features of Gout Subjective Objective • Joint pain resulting in acute distress • Joint swelling • Unable to sleep due to pain • Erythematous joint • Severe pain on urination (gout kidney stones) • Joint is warm to touch • Elevated uric acid (can be normal) • Elevated erythrocyte sedimentation rate (ESR) • Mild fever • Uric acid calculi (kidney stones) • Joint damage and tophi of common sites such as the hand, wrist, elbow, and/or knee 65 years and older may present atypically with estrogen may increase uric acid secretion. There also ap- an insidious onset and involvement of multiple pears to be a link between family history of gout and risk joints and/or the hand or wrist. of developing symptoms. Drug-induced gout is an important therapeutic prob- RISK FACTORS lem for pharmacists to recognize. Thiazide diuretics and Table 2 summarizes common risk factors as- low-dose aspirin are two common medications associ- sociated with gout. Gout is strongly associated ated with hyperuricemia. Other medications associated with hyperuricemia, variably defined as serum with hyperuricemia are listed in Table 2. The majority of uric acid levels greater than 6.8–7mg/dL. One medications reduce renal elimination of uric acid, with study suggests levels of uric acid greater than the exception of chemotherapy which is associated with 10 mg/dL are associated with a 30 percent risk increased uric acid production due to cellular death. of developing gout over a five-year span. Men Substitution of therapeutic alternatives for these agents, are more likely to develop gout than women ini- when possible, may help to diminish attacks. Most clini- tially, although once women reach menopause cians opt to continue cardioprotective doses of aspirin as the difference is minimal. Declining amounts of the benefits outweigh the risks. Initiation of urate-lowering Table 2. Causes of Hyperuricemia Under-excretion Overproduction • Chronic kidney disease • Dyslipidemia • Renal failure/insufficiency
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