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Gout: the Basics

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Gout: the Basics Gout: The Basics Bernie R. Olin, Pharm.D., Associate Clinical Professor and Director, Drug Information, Auburn University, Harrison School of Pharmacy Universal Activity #: 0178-0000-12-104-H04-P | 1.5 credit hours (.15 CEUs) | Expires June 18, 2015 PROGRAM OBJECTIVES After completing this program, the participant will be able to: • Describe the etiology and pathophysiology of gout. quiz on page 58-59 • List the risk factors of gout. • Explain the clinical presentations and diagnosis of gout. • Review the treatment options for gout. INTRODUCTION ETIOLOGY AND PATHOPHYSIOLOGY Gout is an inflammatory arthritis caused by the deposition Gout is one of the most common forms of inflammatory of monosodium urate (MSU) crystals in synovial fluid and in arthritis in adults. The 2010 estimates for the United States are other tissues. It is also known as crystal arthritis and “the disease that 8.3 million people are affected (3.9%). This peaks for males of kings.”1-4 The “disease of kings” sprang from the observation in at 70-79 years (10%) and ≥80 years for females (6%). There are pre-modern times that gout was largely a disease of the affluent, due clearly ramifications for an aging population.8,9 to the association of consumption of rich foods (eg, meats, seafood) The underlying metabolic disruption necessary for the and alcohol with its symptoms.5 The word “Gout” is derived from development of gout is too much uric acid in the blood the Latin word gutta (or ‘drop’) and stems from the medieval belief (hyperuricemia). However, the presence of hyperuricemia does that the disease was caused by an imbalance of the bodies “humors,” not necessarily equate with gout symptoms as hyperuricemic some “dropping” into the afflicted joint, and conceptually not much patients may be asymptomatic. Physiologically, the serum reaches different from our modern understanding of the mechanism. In supersaturation with monosodium urate at approximately 7 mg/dL addition, podagra, or gout of the foot or great toe is derived via Latin (416 μmol/L) and the definition of hyperuricemia is a serum urate from Greek, from pous foot + agra a trap = foot trap or seizure.6 level of ≥6.8 mg/dL (404 μmol/L).1,8 Gout is among the earliest diseases to be described by Uric acid is a metabolic waste product from purines which are ancient physicians, first recorded by the Egyptians in 2640 BC. involved in the enzymatic processes of nucleic acid synthesis. In Descriptions are also given by Hippocrates (5th century BC) and normal humans, excess uric acid is excreted out through the kidneys. Galen (2nd century AD) that remain with us today. The word Other mammals’ metabolism is capable of going one step farther “gout” was first used as a disease description by Randolphus of and breaking down the uric acid to water soluble allantoin via an Bocking (1197-1258), a Dominican monk, who described podagra enzyme, uricase. A normal urate pool is approximately 1200 mg in as gutta quam podagram vel artiticam vocant, or the gout that is men and 600 mg in women. Increases of this urate pool occur due called podagra or arthritis.6 to excess production or under excretion of uric acid.8,10 If you have ever suffered from a gout attack, you are in Overproduction: Uric acid is produced from purines from good company as there have been, and are many prominent gout three sources: dietary purine, tissue nucleic acid to purine sufferers.7 They include Martin Luther, Francis Bacon, Michelangelo, nucleotide conversion and de novo synthesis of purine bases. The Benjamin Franklin, Charles Darwin and Isaac Newton. In addition, average human produces about 600 to 800 mg of uric acid daily. the course of history has been altered due to poorly timed gout Diet plays little role in the absence of metabolic disruption. There attacks in certain individuals. One supported legend is that William are two enzyme abnormalities that result in overproduction of uric Pitt (1759-1806), a member of the British Parliament and a acid. The first is an overactivity of phosphoribosyl pyrophosphate supporter of the colonies, was absent on several occasions due to (PRPP) synthetase in the nucleic acid synthesis process and severe gout. Had he been present for key debates and votes, the consequently causes an increased production of uric acid. The Boston Tea Party and perhaps the Battle of Bunker Hill may have second abnormality is an enzyme deficiency, hypoxanthine- been avoided. guanine phosphoribosyl-transferase (HGPRT) that causes a 46 ALABAMA PHARMACY ASSOCIATION SUMMER 2012 shift of production to guanine and hypoxanthine which is then metabolized to uric acid. Of note is that there is a relatively rare CLINICAL PRESENTATION AND DIAGNOSIS condition of a complete absence of HGPRT that results in the “The patient goes to bed and sleeps quietly until about two in Lesch-Nyhan syndrome, a childhood disease characterized by the morning when he is awakened by a pain which usually seizes the excessive production of uric acid in addition to choreoathetosis great toe, but sometimes the heel, the calf of the leg or the ankle. The and mental retardation.8,10 pain resembles that of a dislocated bone … and this is immediately The latter part of purine metabolism leads to the compounds succeeded by a chillness, shivering and a slight fever … the pain hypoxanthine and to xanthine which then is metabolized to increases, which is mild in the beginning but grows gradually more uric acid via xanthine oxidase. This is the first attack point for violent every hour … so exquisitely painful as not to endure the preventative therapy, inhibiting the xanthine oxidase and preventing weight of the clothes nor the shaking of the room from a person the formation of uric acid. The other two major areas are after uric walking briskly therein.” [Thomas Sydenham (1624-1689)]5,12 acid formation. The uricases breakdown uric acid to water-soluble allantoin and the uricosurics promote the excretion of uric acid. The DIAGNOSIS agents for acute gout attacks all work to alleviate the inflammatory The diagnosis of gout is divided into primary and secondary. response of the uric acid crystallization in the joint space.3,8,10 Primary gout is generally unrelated to an identifiable cause while Underexcretion: In the normal human uric acid is largely secondary gout is related to a stimulating factor, such as drugs, excreted through the kidney and a small amount through the concomitant disease or known genetic mutations. The most gastrointestinal tract (approximately 2/3 and 1/3, respectively). recent guidelines are from European League Against Rheumatism Excretion through the kidney is not completely defined and (EULAR) from 2006; their report is in two parts, addressing involves several mechanisms of passive and active transport in the diagnosis and management recommendations.13,14 There are 10 glomerulus. It is estimated that 80% to 90% of patients with gout diagnostic recommendations:13 have some disorder with the urinary excretion of uric acid.8 1. “In acute attacks the rapid development of severe pain, Therapeutic options for treatment of hyperuricemia/ swelling, and tenderness that reaches its maximum within just gout revolve around these two functions of overproduction or 6 to 12 hours, especially with overlying erythema, is highly underexcretion of uric acid. Determination can be made by suggestive of crystal inflammation though not specific for gout. measuring the amount of uric acid excretion over 24 hours. This 2. For typical presentations of gout (such as recurrent podagra can be done on a purine-free diet for 3-5 days (preferred but with hyperuricaemia) a clinical diagnosis alone is reasonably very difficult to accomplish), or on a regular diet. On the purine- accurate but not definitive without crystal confirmation. free diet, over-producers will excrete >600 mg uric acid, while 3. Demonstration of monosodium urate (MSU) crystals in underexcretors provide <600 mg. On a regular diet, excretion of synovial fluid or tophus aspirates permits a definitive diagnosis >1000 mg over 24 hours are over-producers.8 of gout. Risk factors:1,2,8 4. A routine search for MSU crystals is recommended in all Drugs: Thiazide diuretics, cyclosporine, ethambutol, synovial fluid samples obtained from undiagnosed inflamed joints. pyrazinamide, levodopa, cytotoxic drugs, tacrolimus, ribavirin and 5. Identification of MSU crystals from asymptomatic interferon, teriparatide and aspirin (low dose, <1 g/day). However, joints may allow definite diagnosis in intercritical periods. even with small, cardioprotective doses of aspirin (75mg daily), the 6. Gout and sepsis may coexist, so when septic arthritis is rate of uric acid excretion was decreased by 15% that resulted in suspected Gram staining and culture of synovial fluid should a small but significant rise in serum uric acid concentrations. This still be performed, even if MSU crystals are identified. decrease in uric acid clearance was observed within one week of 7. While being the most important risk factor for gout, initiating low-dose aspirin therapy. Although the increase was small serum uric acid levels do not confirm or exclude gout, as many a clinical risk/benefit assessment will be needed per patient.11 people with hyperuricaemia do not develop gout, and during Diet: A high purine diet includes meat and seafood, alcohol acute attacks serum levels may be normal. (beer and liquors), soft drinks (with sugar) and fructose-containing 8. Renal uric acid excretion should be determined in selected food/drinks. Foods with a decreased risk include coffee, dairy gout patients, especially those with a family history of young onset products and vitamin C. gout, onset of gout under age 25, or with renal calculi. Conditions: insulin resistance, metabolic syndrome, obesity, 9. Although radiographs may be useful for differential renal insufficiency, hypertension, congestive heart failure, organ diagnosis and may show typical features in chronic gout, they are transplantation, hospitalization and surgery.
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