Renal Unit and
1 Department Of Orthopaedics and Rheumatology, Royal Adelaide Hospital, Adelaide, Australia
SIR, A 27-yr-old woman presented to the emergency department unable to walk following a fall. She had been diagnosed with systemic lupus erythematosus (SLE) in 1987, with rash, alopecia, arthritis, thrombocytopenia and positive anticardiolipin antibodies. There was renal involvement, with diffuse proliferative glomerulonephritis on biopsy, but no impairment of renal function. Drug therapy had included hydroxychloroquine, azathioprine, non-steroidal anti-inflammatory agents and two 6-month courses of monthly i.v. cyclophosphamide. There was an extensive history of exposure to corticosteroids over many years, with multiple intravenous boluses of methylprednisolone for acute flares of arthritis, and high maintenance doses of oral steroids. For several years the dose of prednisolone could not be lowered below 10 mg daily, owing to relapse of symptoms. She also received intra-articular corticosteroid injections, but not to the knees. Complications of long-term corticosteroid use included morbid obesity, a Cushingoid appearance, cataracts and osteoporosis. She had a five pack-year smoking history. Other regular medications included calcitriol, atorvastatin, omeprazole and celecoxib.
Sixteen months prior to the current presentation she sustained a spontaneous rupture of the right Achilles tendon. This was treated conservatively with a plaster cast for 2 months. She regained complete function and mobility.
Four weeks prior to admission, she presented with worsening arthralgias, fatigue, malar rash and proteinuria, with normal renal function. She was on prednisolone at 11 mg daily, which was temporarily increased to 50 mg daily. Mycophenolate mofetil at 500 mg twice daily was commenced. Improvement in all symptoms was noted after 2 weeks.
On the day of admission she stumbled whilst walking on a level surface, falling onto her knees and then her right hip. Following this she had severe bilateral knee pain and was unable to move her legs or bear weight. On examination both knees were exquisitely tender to palpation, particularly over the patellae. Active and passive movements at the knee joints were severely limited owing to pain. There was no joint effusion, swelling or erythema, nor active synovitis in any other joint. She did not have a fever. Blood tests revealed a normal full blood count, erythrocyte sedimentation rate 51 mm/h (NR: 012 mm/h), C-reactive protein 23 mg/l (010 mg/l), anti-double-stranded DNA antibody >50 IU/ml (<8 IU/ml) and antinuclear antibody titre 1/160.
A lateral radiograph of the right knee is shown in Fig. 1, demonstrating patella alta. The disruption of the patellar tendons can be seen by careful inspection of the soft tissue planes on the lateral radiograph. The appearances were similar for the left knee. Magnetic resonance imaging of the knees confirmed the diagnosis. She underwent surgery the following day, with repair of the tendons and placement of defunctioning wires from the patella to the tibial tubercle. The dose of mycophenolate was increased and this allowed reduction of the prednisolone dose to 9 mg daily. The wires were removed 3 months later.
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Single patellar tendon rupture in patients with SLE has been well described, though it is uncommon, occurring in less than 3% of patients in one series that reviewed 180 patients with long-standing SLE [1]. All of the affected patients in this series had chronic prednisolone exposure, duration of disease greater than 7 yr and deforming arthritis of the hands. Our patient did not have the latter clinical association.
Bilateral, concurrent and spontaneous rupture of the patellar tendons is very uncommon. It can occur in patients without any systemic disease or corticosteroid usage, usually during sporting activities or following traumatic injury [2], but also spontaneously [3]. Bilateral rupture has also been associated with chronic renal failure [4, 5], rheumatoid arthritis [6], hyperparathyroidism [5, 7] and local corticosteroid injections [8]. Bilateral patellar tendon ruptures associated with SLE are extremely rare, with very few cases described previously [9, 10].
The diagnosis of patellar tendon rupture is made on clinical features such as inability to extend the knee or straight leg raise, pain and swelling over the patellar tendon and palpable defects in the tendon, as well as radiological investigation including ultrasonography.
The mechanism of tendon rupture in this case appeared to be related to sudden hyperflexion of the knee joints during the fall. Inflammatory arthritis and tenosynovitis can affect tendon integrity and predispose patients to tendon rupture [10]. The patient's weight, long duration of inflammatory disease, chronic corticosteroid use and previous evidence of tendon weakness placed her at risk of this particularly rare and unusual complication.
Notes
Correspondence to: R. Faull, Renal Unit, Royal Adelaide Hospital, North Terrace, Adelaide, SA 5000, Australia. E-mail: rfaull{at}mail.rah.sa.gov.au
References