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Reactive arthritis and ruptured Achilles tendon
  1. L STAFFORD,
  2. J BERTOUCH
  1. Rheumatology Department, Prince Henry Hospital, Sydney, Australia
  1. Dr J V Bertouch, Suite 6D, The Wales Medical Centre, 66 High Street, Randwick NSW 2031, Australia.

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It is widely accepted that reactive arthritis is associated with enthesitis. We recently saw a patient with chronic Achilles tendonitis who suffered a rupture of this tendon at the tendocalcaneal insertion.

A 22 year old male locksmith presented in December 1994 with bilateral metatarsalgia and right fourth toe dactylitis. Naproxyn was introduced with partial resolution of symptoms. In April 1995 he developed synovitis in the left knee, both ankles, and enthesitis in the right Achilles tendon, right posterior tibialis tendon, and bilateral plantar fascitis. There was no history of rash, inflammatory eye disease, back pain, gastroenteritis or genitourinary symptoms. Investigations revealed an erythrocyte sedimentation rate (ESR) of 25 mm 1st h, HLA B27 positive, increased serum IgM antibodies toYersinia enterocolitica 05 (optical density 0.581) (Yersinia 03 and 09 negative) despite negative stool cultures and synovial fluid from the knee contained 10.9 × 109 white blood cells (80% neutrophils, Gram stain negative, culture negative and no crystals). A diagnosis of reactive arthritis presumably secondary to Yersinia enterocolitica was made. Indomethicin 50 mg thrice daily and sulphasalazine 1 g thrice daily were initially given. Because of continuing active disease with recurrent massive knee effusions prednisone 20 mg in the morning and methotrexate 7.5 mg weekly were added and most of his symptoms improved, although clinically his right Achilles tendon was still troublesome. Prednisone was tapered. In October 1995 he presented with a flare up of disease (especially his right Achilles tendon) after an episode of gastroenteritis. On this occasion the ESR was 8 mm 1st h and repeat Yersinia enterocolitica 05 IgM serology had fallen (optical density 0.191), but stool cultures grew Campylobacter jejuni. He continued taking prednisone, sulphasalazine, and methotrexate and his joint symptoms improved. However clinically and symptomatically a low grade enthesitis continued in the right Achilles but local corticosteroid injections were not used.

In January 1996 when stepping out of a parked vehicle onto the right foot, he heard a ‘snap’ and suffered intense pain in the back of the heel. A clinical diagnosis of Achilles tendon rupture was made and surgical exploration and repair was undertaken. At operation rupture had occurred at the calcaneal insertion.

Despite the commonly recognised association of Achilles tendonitis with inflammatory arthritis surprisingly few reports of rupture have been recorded. Associated conditions include rheumatoid arthritis,1 systemic lupus erythematosus,2 3and gout,4 but no cases with reactive arthritis were found. Most patients had received oral or peritendon corticosteroids. There are a number of case reports where ruptured Achilles tendons have occurred with oral corticosteroids in patients with respiratory disease.5 6 There were no case reports of ruptured Achilles tendons with sulphasalazine or methotrexate without concomittant oral or percutaneous corticosteroid therapy. The usual site of rupture of the Achilles tendon is 2–6 cm proximal to the calcaneal insertion. In this area there is a reduction in both the number and mean relative area of vessels.7 In this case although the patient was taking prednisone, the rupture was at an unusual site—the tendocalcaneal insertion—suggesting that enthesitis had led to weakening of the tendon in this position. None of the previous reports have shown rupture at the tendocalcaneal insertion. It is interesting to speculate, that in this case suppressing inflammation by local corticosteroid infiltration around the Achilles tendon may have prevented rupture.

In summary we have reported a young man with a short history of reactive arthritis in which both yersinia and campylobacter have been implicated as triggering organisms. He required aggressive treatment with non-steroidal anti-inflammatory drugs, oral corticosteroid, sulphasalazine, and methotrexate to control disease with the main symptomatic area being enthesitis of the Achilles tendon. He sustained a rupture of the Achilles tendon at the tendocalcaneal junction implicating enthesitis as the predisposing factor.

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