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Pharmacy Director Department of Pharmacy Chi Mei Medical Center Tainan 704, Taiwan fax 886 6 2828101 cmh5500{at}mail.chimei.org.tw
Published Online, April 19, 2005. www.theannals.com, DOI 10.1345/aph.1E603
Case Report. A 52-year-old man with a history of gout who was treated on a chronic basis with indomethacin 25 mg 3 times daily and used a diet regimen to control disease symptoms developed an acute attack of gout. The patient did not have a family history of thrombosis or thromboembolic events. On April 21, 2003 (day 0), the patient had another acute gout attack and was prescribed celecoxib 200 mg/day instead of indomethacin at the primary care clinic. Five days later, he noticed discomfort in his left calf. He began to feel soreness at the posterior aspect of the left lower leg that extended to the anterior side of the lower leg and to the forefoot on day 6 (April 27). By the next day, the calf pain had increased to the extent that he had difficulty walking and his left forefoot had started to swell. He presented to a teaching hospital where physicians observed tenderness and slight swelling of the left leg and forefoot with slight blue mottling of color. Deep-venous thrombosis was diagnosed and other causes except celecoxib were ruled out. At that point, celecoxib was discontinued and the patient received further evaluation. Ultrasonography revealed that the vein within the head of the left gastrocnemius muscle was filled with a thrombus that extended into the left popliteal vein. The patient began treatment with subcutaneous enoxaparin sodium followed by oral warfarin for 4 months. In August, repeat ultrasonography showed that the venous thrombosis had improved. Low-dose aspirin therapy was prescribed and warfarin was discontinued. At that time, prothrombin time was 11.8 seconds (reference range 9.3-10.9) and activated partial thromboplastin time was 29 seconds (22-34); the international normalized ratio was 1.2 (<3.0).
Discussion. Recently, some investigators concluded that celecoxib tips the balance of prostacyclin/thromboxane in favor of thromboxane, leading to increased vascular and thrombotic events.2,3 The mechanism of venous thrombosis caused by COX-2 inhibitors is not completely known. The possible risk factor that we suspect in our patient may have been the mild immobility caused by the acute gout attack; however, it is not clear whether this event may have precipitated the thromboembolic event.
The question whether COX-2 inhibitors increase a patient's risk for thrombosis has been raised broadly, and rofecoxib has been withdrawn from the world market by its manufacturer because of increased risk for cardiovascular events. Other reports of celecoxib associated with ischemic complications and popliteal vein thrombosis1,4 showed a relative risk of COX-2 inhibitors for thrombotic events in individuals at risk. Unless or until this issue of risks associated with COX-2 inhibitors is resolved, physicians should assess the risks and benefits of using COX-2 inhibitors as antiinflammatory therapy. The adverse reaction was determined as probable according to the Naranjo probability scale.5
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