Rheumatology Advance Access originally published online on December 6, 2005
Rheumatology 2006 45(2):234-235; doi:10.1093/rheumatology/kei022
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LETTER TO THE EDITOR |
Role of secondary hyperparathyroidism in spontaneous rupture of the quadriceps tendon complicating chronic renal failure
Orthopaedic Surgery Department, André Mignot Hospital, Versailles, 1 Nephrology Department, Necker Hospital and 2 INSERM U681, Institut Biomédical des Cordeliers, Paris, France
Correspondence to: O. Thaunat, INSERM U681, Institut Biomédical des Cordeliers, 15 rue de l’Ecole de Médecine, 75006 Paris, France. E-mail: olivier.thaunatpastu{at}free.fr
SIR, Ruptures of the extensor mechanism are relatively rare injuries. Unilateral rupture is more common, especially in older individuals. Thus, simultaneous and spontaneous rupture is a very rare condition and only a few cases have been reported in the literature to date. We would like to report a new case of spontaneous bilateral rupture of the quadriceps tendon in a patient with chronic renal disease, illustrating the deleterious role of secondary hyperparathyroidism.
A 31-yr-old man was admitted to our department for acute onset of knee pain and inability to extend the knee, which occurred without evidence of trauma while he was going downstairs. Physical examination showed a palpable defect in the quadriceps tendons, inferior displacement of the patella (patella baja), proximal ecchymosis, and swelling. Evaluation of range of motion revealed complete loss of active knee extension. The diagnosis of bilateral simultaneous rupture of the quadriceps tendons was suspected and further confirmed by knee radiographs, showing inferior patellar displacements without fracture. Additionally, marked radiological signs of osteitis fibrosa as well as dystrophic calcifications of the tendons were noted (Fig. 1). The patient never took glucocorticoids, aluminium compounds or fluoroquinolone. His past medical history was, however, significant for chronic renal failure (calculated creatinine clearance 12 ml/min) due to Berger's disease diagnosed 8.5 yr before. He was also known to have severe secondary hyperthyroidism [parathyroid hormone (PTH) 1099 pg/ml; normal range 10–46 pg/ml] with high calcium phosphate product (5.88 mmol2/l2; normal range: 1.8–3.7 mmol2/l2) and increased plasma alkaline phosphatase activity (368 UI/l; normal range: 40–130 UI/l) because he was non-compliant with the vitamin–calcium therapy.
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The tendons were repaired using a non-absorbable suture passed through the patella using three tunnels. After surgery, his knees were immobilized in extension for 6 weeks, followed by gradual weight-bearing and gait training with braces. He was weaned off the braces as he increased the range of motion and strength in his knees. The course was satisfactory, both knees recovering a full range of motion within a 4-month period.
Simultaneous bilateral rupture of the quadriceps tendon is a very rare condition, which generally occurs in association with underlying chronic metabolic disorders such as gout, obesity, diabetes mellitus or end-stage renal failure [1]. In this last situation, the frequency of this complication, although difficult to determine, is thought to be lower than 3.5% [2]. Previous reports have pointed out a relation between the duration of haemodialysis and the occurrence of spontaneous tendon ruptures, suggesting that tendinous weakness resulted in these patients, from malnutrition, ß2-amyloidosis [3] or accumulation of uraemic toxins [4], all classical complications of long-term chronic haemodialysis. Our observation, however, does not support such hypotheses. The spontaneous tendon rupture in our patient seems thus to have resulted rather from secondary hyperparathyroidism, as previously proposed by De Franco et al. [5]. Secondary hyperparathyroidism is indeed a classical complication of chronic kidney disease [6]. The pathophysiology of the disorder starts with retention of phosphorus resulting from the decrease in glomerular filtration rate, which leads to hypocalcaemia that stimulates PTH. The latter causes phosphaturia, with restoration of serum phosphorus and calcium towards normal. However, this occurs only at the expense of elevated serum PTH levels. High PTH levels result in high bone turnover, which in turn is responsible for subtendinous bone resorption at the sites of insertion. The occurrence of repeated minor avulsion fractures of the weakened bone cortex at the tendon insertion site precedes the final total tendon rupture, which then occurs after a minor trauma (spontaneous rupture) [2].
In addition to the previous mechanism, high calcium phosphate product in such patients leads to dystrophic calcifications of soft tissue, which further weaken the tendon and participate in the rupture [7, 8].
In conclusion, this case supports the role of secondary hyperparathyroidism in spontaneous rupture of the quadriceps tendon in chronic renal disease. Clinicians should be aware that careful management of vitamin–calcium therapy in such patients should efficiently prevent this severe complication, which is responsible for long hospitalization and prolonged morbidity.
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The authors have declared no conflicts of interest.
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