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 The leading web portal for pharmacy resources, news, education and careers April 23, 2017
Pharmacy Choice - Gout Disease State Management - April 23, 2017

Gout Disease State Management

Gout
by Tara Muzyk, PharmD

Gout, a rheumatic disease which results from the deposition of uric acid crystals in tissues and fluids, manifests as sudden severe attacks of pain. The typical presentation of gout is tenderness and pain in the big toe but the patient may experience an atypical presentation where any joint can be affected. Gout occurs as a result of urate production (either normal or excessive) and the kidneys lack of ability to process the urate and eliminate it from the body fast enough. What the body cannot excrete it will store. In the case of excess urate the body will attempt to store it in the joint spaces. This will result in recurrent attacks of inflammation, chronic arthropathy, topaceous deposits and potentially uric acid nephrolithiasis.

The cause of gout can be due to high uric acid levels (primary) or due to the result of another disease state, medication or various other reasons such as dietary indiscretion (secondary). The majority of patients who experience gout will match the typical profile: older obese male, frequent alcohol intake, hypertensive, hyperlipidemic. Patients who do not meet this profile may be misdiagnosed therefore be on the lookout for patients who may experience gouty arthritis related to medications or poor lifestyle choices. Predisposing factors may include high consumption of meat, seafood, fatty or processed foods or alcohol. Trauma, surgery, dehydration and some medications (diuretics, aspirin) may also precipitate a gout attack.

There are three clinical syndromes associated with gouty arthritis: acute gouty arthritis, intercritical gout (or interval gout), and chronic recurrent and tophaceous gout. Acute gouty arthritis is characterized by severe pain, redness and swelling which reach the maximum in 24 hours and dissipate after that usually completely resolving in a few days or a week. As mentioned before, the big toe is the typical site of involvement but any joint can be involved. Lab tests performed during this period may be nonspecific for gout and uric acid levels maybe either high or low during an attack making the diagnosis difficult. Aspiration of the joint space may produce urate crystals. Once the acute period has subsided, the patient is said to have entered the intercritical period which is the symptom free period between flares. This is the time to draw uric acid levels and determine if the patient is an over producer or undereliminator of uric acid and to aspirate previously effected joints in the search for urate crystals. Once the diagnosis of gouty arthritis has been made, it is time to manage comorbid conditions, eliminate the cause of hyperuricemia and initiate urate lowering medications. Tophaceous deposits are the result of longer term untreated or undertreated gout, high levels of serum urate, diuretic use or treatment with cyclosporine. Larger deposits of uric acid may be apparent by visual or tactile inspection or may be determined by radiography or MRI.

Treatment for acute gout should be initiated as soon as gout flare symptoms are perceived by the patient. Gout flares will resolve faster if treatment is initiated right away. Because of this, the patient and provider should discuss abortive therapies at the initial appointment and the patient should receive counseling on which therapies are appropriate to take immediately upon initiation of a flare. Anti-inflammatory medications are the mainstay for treatment of an acute flare but may not be appropriate for all patients due to their renal and cardiovascular side effects. Since time is of the essence when treating a gout flare over the counter nonsteroidal anti-inflammatory medications may be the medication of choice due to easy access. Prescriptions for other medications should be filled as soon as received and kept on hand so therapy can be initiate as quickly as possible. Colchicine, glucocorticoids, and interleukin inhibitors are other medications which may be appropriate to treat an acute gout flare.

Once the initial flare has subsided and the diagnosis of gout has been made, prevention strategies should be initiated. These strategies include lifestyle modification, management of comorbid disease states, initiation of urate lowering therapies, and prophylactic therapy. Since weight loss and a healthy diet has been shown to decrease the risk for gout patients should be encouraged to choose a diet moderate in meat consumption and low in processed or fatty foods and alcohol. If a medication is deemed to be the reason for gout, every effort to choose an alternative medication should be made. Urate lowering medications should be initiated to reduce recurrent attacks and bony formations as well as dissolve any tophi which may have formed. Counsel the patient so that he or she understands that treatment for recurrent gout is continuous and lifelong. Treatment options may include uricosuric agents which enhance uric acid excretion, xanthine oxidase inhibitors which decrease urate formation, and uricase enzymes which catalyze the conversion to allantoin a more soluble purine product. The goal of therapy is to obtain and maintain a serum urate level of <6 mg/dL by slowly reducing the circulating urate by 1-2 mg/dL per month. If the patient fails to meet these goals, check for adherence to the treatment and life style changes, reevaluate the diagnosis, or consider an alternative therapy.

The keys to successful treatment of gout are proper hydration, therapeutic life style changes, adherence to treatment and the use of NSAIDS (colchicine or glucocorticoids) for quick resolution of an acute attack. Treatment is lifelong but maintaining urate levels <6 mg/dL will result in tophi resolution over time and a reduction in acute attacks of gout. As a result of following the treatment and lifestyle changes indicated above the patient may experience less frequent gout flares or may become free of flares all together leading to an improved quality of life.


References
  1. Center for Disease Control and Prevention. Gout. 2014. http://www.cdc.gov/arthritis/basics/gout.htm (accessed on 8/4/14)
  2. Emmerson B. Hyperlipidaemia in hyperuricaemia and gout. Ann Rheum Dis 1998; 57:509.
  3. O'Duffy JD, Hunder GG, Kelly PJ. Decreasing prevalence of tophaceous gout. Mayo Clin Proc 1975; 50:227.
  4. Becker MA, Jolly M. Hyperuricemia and associated diseases. Rheum Dis Clin North Am 2006; 32:275.
  5. Sutaria S, Katbamna R, Underwood M. Effectiveness of interventions for the treatment of acute and prevention of recurrent gout--a systematic review. Rheumatology (Oxford) 2006; 45:1422.
  6. Schumacher HR Jr, Boice JA, Daikh DI, et al. Randomised double blind trial of etoricoxib and indometacin in treatment of acute gouty arthritis. BMJ 2002; 324:1488.
  7. Rubin BR, Burton R, Navarra S, et al. Efficacy and safety profile of treatment with etoricoxib 120 mg once daily compared with indomethacin 50 mg three times daily in acute gout: a randomized controlled trial. Arthritis Rheum 2004; 50:598.
  8. Sivera F1, Wechalekar MD, Andrés M, Buchbinder R, Carmona L. Interleukin-1 inhibitors for acute gout. Cochrane Database Syst Rev. 2014 Sep 1;9:CD009993.
  9. Tran TH1, Pham JT, Shafeeq H, Manigault KR, Arya V. Role of interleukin-1 inhibitors in the management of gout. Pharmacotherapy. 2013 Jul;33(7):744-53.



Links - Gout
Arthritis Insight Gout Information

About.com Gout Page Information on the diagnosis, symptoms, treatments, and prognosis for gout.

MEDLINEplus Fact sheets and resources concerning gout and pseudogout compiled by the National Library of Medicine.

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