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Acute Gouty Arthritis


A 49-year-old man complains of sharp pain in the medial left ankle that begansuddenly 3 nights earlier, waking him up. That night he also felt feverish anddiaphoretic, but those symptoms have subsided. The pain is present whenhe moves the ankle or when a shoe compresses the area. No other joints areinvolved. He denies trauma to the ankle or foot.

Case :1

Middle-aged Man With Acute Ankle Pain

A 49-year-old man complains of sharp pain in the medial left ankle that begansuddenly 3 nights earlier, waking him up. That night he also felt feverish anddiaphoretic, but those symptoms have subsided. The pain is present whenhe moves the ankle or when a shoe compresses the area. No other joints areinvolved. He denies trauma to the ankle or foot.


Except for his ankle pain, the patient feels well. Two months ago, mildessential hypertension was diagnosed and for the last 4 weeks he has taken athiazide diuretic. He has a history of significant allergy to sulfa drugs and penicillin.He consumes 1 to 2 alcoholic drinks per day and likely more on weekends-especially during the current football season.


This man is approximately 30 lb overweight. His blood pressure is115/78 mm Hg and he is afebrile. No tophi are evident. On the left ankle, themedial area below the malleolus is red, warm, and exquisitely tender to palpation.The range of motion in the ankle is decreased because of pain.


Hemogram and electrolyte levels are normal. Blood urea nitrogen level is28 mg/dL, creatinine is 1.3 mg/dL, and uric acid is 7.2 mg/dL.

Which of the following is the most appropriate therapy at this time?


Oral sulindac, 150 mg bid for 1 week.


Oral allopurinol, 300 mg/d for 1 week.


Intravenous colchicine, 2 mg.


Three oral 0.6-mg doses of colchicine.

Case 1:


This patient has

acute gouty arthritis.

His age, sex, andmonoarticular presentation are very typical of this entity.His obesity, high alcohol intake, recent initiation of a thiazidediuretic, and lack of systemic toxicity (which wouldsuggest infection) are also strong clinical clues.Definitive diagnosis requires direct identification ofuric acid crystals and the exclusion of infection, both ofwhich can usually be done in a hospital or a rheumatologist'soffice by aspiration of joint fluid. In a primary careoffice, this is not always practical. Most clinicians wouldstart treatment based on the presumptive diagnosis.Two issues must be addressed when therapy forgout is selected:

  • Alleviation of the acute attack.
  • Determination of whether long-term suppressive and/orhypouricemic maneuvers will be required.

The optimal immediate treatment is aspiration of jointfluid and intra-articular corticosteroid injection. However,this is not always available in the primary care setting.Thus, other therapies must be considered.Oral colchicine (choice D) is not unreasonable.However, in most trials, the incidence of adverse effectshas been higher with this agent than with other treatments.


Moreover, this patient's symptoms began 3nights ago, and colchicine is most effective when administeredat the first sign of arthritis-or at least within 24hours of onset.Intravenous colchicine (choice C) is rarely, if ever,indicated. When this drug is delivered intravenously, theGI side effects (especially diarrhea) that signal incipienttoxicity are bypassed, and life-threatening bone marrowsuppression can occur without warning. The only mortalityassociated with colchicine has occurred with intravenousadministration and/or in the presence of renal failure;most authorities strongly discourage the use of intravenouscolchicine.


Allopurinol is more useful in the long-term managementof gout. It inhibits xanthine oxidase, thereby both reducinguric acid synthesis and lowering uric acid levels.Thus, it is effective whether gout results from overproductionor underexcretion of uric acid. However, several featuresof the presentation preclude the use of allopurinolfor now:

  • First, none of the principal indications for long-term uricacid-lowering therapy are present. These include presenceof tophi, frequent attacks (more than 3 per year),and documented overproduction of uric acid.4
  • Second, the patient is having an acute attack, and maneuversto lower uric acid levels may worsen an acuteflare-although the risk of this remains uncertain.4
  • Finally, several reversible conditions that predispose toelevated uric acid levels and acute arthritis are present(obesity, alcohol use, and thiazide diuretic therapy). Eliminationof these conditions may obviate the need for longtermtherapy.

Thus, allopurinol therapy (choice B) is premature atbest and perhaps will not be needed at all.Although all might not agree, administration of anNSAID for 7 to 10 days (choice A) is an efficient therapyin patients such as this man. NSAIDs usually relievesymptoms in 24 hours, are reasonably inexpensive, andhave an acceptable toxicity profile in most patients. A varietyof NSAIDs have demonstrated efficacy and are interchangeable.

Outcome of this case.

A 1-week regimen of sulindacwas prescribed. The patient experienced significant reliefwithin 24 hours and was pain-free by day 4. His antihypertensiveagent was changed to an angiotensin-convertingenzyme inhibitor, which was effective and produced nochange in creatinine level. He was told to limit his alcoholintake and lose weight. At 6 months, he has not had arecurrence of acute gouty arthritis.




Bonnel RA, Villalba ML, Karwoski CB, Beitz J. Deaths associated with inappropriateintravenous colchicine administration.

J Emerg Med.



Becker MA. Clinical aspects of monosodium urate monohydrate crystal depositiondisease (gout).

Rheum Dis Clin North Am.



Baud FJ, Sabouraud A, Vicaut E, et al. Brief report: treatment of severecolchicine overdose with colchicine-specific Fab fragments.

N Engl J Med.



Terkeltaub RA. Clinical practice. Gout.

N Engl J Med.


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