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Case Report |
Address correspondence to V. Santhi Swaroop, M.D., Dept. of Internal Medicine, Mayo Clinic, 200 First St., SW, Rochester, MN 55905, USA; tel 507 284 1551; fax 507 284 5370; e-mail vege.santhi{at}mayo.edu.
Abstract
We report a case of a 69-yr-old previously healthy man with acute spontaneous Achilles tendon rupture and severe tendonitis, which occurred after 2 weeks of steroid therapy for newly diagnosed giant cell arteritis. The Achilles tendon rupture was treated conservatively and the tendonitis resolved incrementally with steroid dose reduction. The patient made a complete recovery. In view of the widespread use of steroids in practice, this novel case presentation has important clinical implications. The tendon rupture early in the course of high-dose steroid therapy expands the understanding of this adverse reaction, which was previously reported only with long-term steroid therapy. The severe tendonitis responded to steroid therapy reduction suggesting a dose correlation. This report adds to a sole previous report of a spontaneous Achilles tendon rupture associated with giant cell arteritis.
(received 10 April 2003; accepted 15 May 2003)
Keywords: temporal arteritis, Achilles tendon, ruptured tendon, tendonitis, prednisone
Introduction
Traumatic rupture of the Achilles tendon is well established, particularly in recreational sports with dorsiflexion against a contracting calf and extending knee [1]. Although this tendon is the strongest in the body, it stiffens with age, and the usual site of rupture (ie, 3–5 cm above the insertion into the calcaneum) corresponds to a watershed in the blood supply [1]. Spontaneous rupture of the Achilles tendon is uncommon but has been reported in patients on quinolone therapy and in patients receiving long-term steroid therapy for rheumatoid arteritis, systemic lupus erythematous, and chronic obstructive pulmonary disease [2–6]. Herein, we report a novel case of an acute spontaneous Achilles tendon rupture in a patient with newly diagnosed giant cell arteritis receiving steroids.
Case Report
A 69-yr-old previously healthy active man presented with a 3-mo history of cough, fevers, night sweats, generalized large joint arthralgias, and progressive weakness. His medical history included diet-controlled hyperlipidemia and chronic low back pain. He did not drink alcohol, use tobacco, or use drugs recreationally. There was no history of abdominal pain, dysphagia, odynophagia, early satiety, nausea, vomiting, diarrhea, temporal artery tenderness, visual difficulties, jaw claudication, rash, synovitis, urinary problems, hematochezia, or melena. There was no history of recent travel.
On examination, the patient’s temperature was 36.3°C, the pulse was 74/min, the respiratory rate was 15/min, and the blood pressure was 120/60 mm Hg. The patient was pale and lethargic. No rash or lymphadenopathy were found. The temporal artery was not tender. The lungs and heart were normal, and abdominal examination showed no abnormalities. There was no peripheral edema. There was no synovitis with general joint stiffness on range-of-motion testing. The findings on neurologic and skin examination were normal. A stool specimen was negative for occult blood. Results of the patient’s baseline hematologic and clinical chemical tests are listed in Table 1
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). Prednisone therapy was instituted at a dose of 30 mg twice daily. The patient’s presenting symptoms completely resolved.
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X-ray of the left foot and ankle revealed only soft tissue swelling. The patient elected to pursue conservative therapy with immobilization in a gravity equinus cast. Despite immobilization, the patient continued to have severe bilateral Achilles tendon pain that progressed over a 2 week period to involve the extensor tendons of the elbows and knees. At this period, his sedimentation rate had become normal (1 mm/hr). The prednisone therapy was gradually tapered, decreasing the dose by 5 mg down to 20 mg daily every 4 weeks, depending on his symptoms and continued normalization of his laboratory and inflammatory markers. Below 20 mg prednisone daily, his taper goal was 2.5 mg every 4 weeks until 10 mg daily, and thereafter by 1 mg every 4 weeks until he was free of prednisone therapy. His symptoms decreased incrementally as the steroid therapy was reduced. He responded well to initiation of physical therapy and has made a complete recovery.
Discussion
In view of the widespread use of steroids in clinical practice, this novel case presentation has important implications. The occurrence of spontaneous tendon rupture early in the course of high-dose steroid therapy expands the understanding of this adverse reaction, which was previously reported only with long-term therapy. In addition, the symptoms in this patient were directly proportional to the amount of steroids used, and decreased with their reduction, suggesting a dose correlation. Finally, this report adds to the sole case previously reported in the literature of an Achilles tendon rupture associated with underlying giant cell arteritis [7].
Spontaneous Achilles tendon rupture is well established in patients taking long-term corticosteroids. Previous reports included patients taking oral corticosteroids from 4 mo to several yr [2–6]. Furthermore, multiple direct corticosteroid injections into a tendon are also associated with rupture [4,6]. The mechanism of the adverse reaction is unknown, but previous studies demonstrated that steroids affect the collagen tissue through antimitotic effects and activation of collagenase [4,6]. In addition, when topical corticosteroids penetrate the skin barrier, they inhibit the growth, regeneration, and repair of dermal connective tissues, with resultant atrophy [7]. In this case, the correlation of the onset of tendonitis symptoms after resolution of the presenting symptoms, with the induction of steroids, and subsequent response to reduction in dose suggest that the treatment probably caused this complication either by itself or in combination with the underlying vasculitis.
Vasculitis has been implicated in spontaneous Achilles tendon rupture in a case report [5]. Biopsies of the tendon in the patient revealed focal lesions of systemic angiitis. However, the patient was also taking concurrent corticosteroids, although the dose and temporal relation of the treatment to the complication were not included in the report. Histologic studies in patients with collagen-vascular disease, who have perivascular involvement, have shown derangements in the microarchitecture of the tendons and collagen tissue. These derangements lead to loss of structural integrity of the tendon and predisposition towards spontaneous rupture [5].
In conclusion, the tendon rupture early in the course of high-dose steroid therapy expands the understanding of this adverse reaction, previously reported only with long-term therapy. Furthermore, the severe tendonitis responded to steroid therapy reduction suggesting a dose correlation. Finally, this report adds to a previous report of a spontaneous Achilles tendon rupture associated with giant cell arteritis.
References
This article has been cited by other articles:
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  S. Aydin, P Atagunduz, E Filippucci, S Yavuz, and H Direskeneli A rare case of spontaneous, bilateral Achilles tendon rupture in systemic lupus erythematosus and a review of the literature Lupus, November 1, 2008; 17(11): 1051 - 1052. [PDF]
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 R. McQuillan and P. Gregan Tendon rupture as a complication of corticosteroid therapy Palliative Medicine, June 1, 2005; 19(4): 352 - 353. [PDF]
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