New York Medical Journal

sponsored by St. Barnabas Hospital, Bronx, NY


KEYWORDS: Tendon rupture in Lupus, Bilateral tendon rupture


Tendon rupture is an uncommon complication in patients with systemic lupus erythematosus (SLE) who are treated with corticosteroids (1). The rupture usually occurs in great weight bearing tendons. The patellar, Achilles, and quadriceps tendons have been, in this order, the most frequently affected (2). A case is presented with re- rupture of patellar tendon and rupture of contralateral quadriceps tendon in the setting of SLE.


A 29 year old man was admitted to St. Barnabas hospital due to bilateral knee pain after he sustained a fall 3 weeks ago and another one 3 days ago onto both knees. Patient stumbled and fell while he was coming out of a grocery store. He developed immediate pain and limited range of motion of both legs. He was diagnosed with Stage III lupus nephritis approximately 7 years ago and was treated by his medical doctor in the community with corticosteroids and mycophenolic acid. He also has a history of traumatic right patellar tendon rupture 4 years ago which was repaired. On examination, patient was obese and had cushingoid facies. Bilateral Jaccouds-like arthropathy was present in interphalangeal and meta-carpal joints. A palpable defect was present in the right patellar tendon with the patella displaced and there was limited extension. A defect was also noted in the left quadriceps tendon with no active extension on that side. Plain film of the Right knee revealed extensive soft tissue swelling in infrapatellar region with large suprapatellar joint effusion and patella superior in position. Patient was diagnosed with sub acute re-rupture of right infrapatellar tendon and acute rupture of left quadriceps tendon that was confirmed by MRI. Intraoperatively, the quadriceps tendon was found to be avulsed from its bony insertion which was repaired. The patellar tendon which was previously avulsed from the patella was found to be avulsed from the tibial insertion. This was repaired with a reinforcing wire loop placed around the top of patella. Patient was discharged with bilateral posterior leg splints to short term rehabilitation.

Leg splints were removed one month later. Six months post injury he continues to follow up in orthopedic clinic and ambulates with a cane.



  Figure 1: MRI Right knee showing rupture of patellar tendon with superior displacement of patella.



  Figure 2: MRI Left knee showing rupture of quadriceps tendon with inferior displacement of patella.



  Figure 3 & 4: X-ray of Right knee prior and post surgery.



Corticosteroids have been implicated in tendon rupture, whether they be given orally, topically, or by local injection.(1) Glucocorticoids may inhibit the collagen synthesis either by an antimitotic action on fibroblasts(3) or by stimulating collagenase production (4). They may also affect the blood supply thereby weakening the tendons (5). Both impaired blood flow and diminished capacity for collagen synthesis interferes with the normal reparative process of a damaged tendon. This is most frequently the case with weight bearing tendons that are subjected to frequent trauma. (6, 7).

Corticosteroid use alone is unlikely to be the primary causative factor for tendon rupture in SLE. With this in mind it is useful to compare the incidence of tendon rupture occurring in patients with autoimmune disorders as well as non-immune disorders in which steroids are used. In the first instance, the two most common autoimmune disorders in which corticosteroids are used with great frequency are rheumatoid arthritis (RA) and SLE. Despite the fact that the prevalence in the United States of RA is about 10 times that of lupus( SLE prevalence rate: 21-100/100,000; RA prevalence rate: 800-1000/100,000), the reported incidence of tendon rupture involving tendons other than those of the fingers is much higher in patients with SLE. Corticosteroids are an important cornerstone of treatment in both of these disorders. Not surprisingly, though, glucocorticoids are often used at higher doses and for more prolonged periods of time in patients with SLE compared to those with RA because of the greater frequency of serious involvement of organ systems that occur in this disease. However, additional factors likely contribute to the increased prevalence of tendon ruptures in this group of patients. Vasculitic and thrombotic events certainly occur with greater frequency in patients with lupus than occur in patients with rheumatoid arthritis, which are potential mechanisms for the causation of ischemia in involved tendons of lupus patients. Also of interest is that patients with active SLE often have hyperlipidemia whereas patients with RA often have low cholesterol levels. (8, 9, 10). In one study of 67 SLE patients, 40 % of the patients had type 2a hyperlipoproteinemia and an equal percentage had type 4 hyperlipoproteinemia. (11) It is well known that some types of hyperlipidemia, such as type 2a hyperlipoproteinemia and type 4 hyperlipoproteinemia, can be associated with tendonitis, and at times, tendon rupture. (12, 13, 14) In patients with SLE who have chronic renal failure, secondary hyperparathyroidism may occur. This, too, can be associated with tendonitis and tendon rupture. In one such case report, hydroxyapatite and urate crystals were identified on histologic evaluation of the involved tendons.(2) In addition, myositis occurs more frequently in patients with SLE than in RA patients. When inflammation involves muscles, their respective tendons are also likely to be involved.

Asthma and Chronic obstructive pulmonary disease are two of the most common non immune disorders which are often treated with corticosteroids. Despite the great worldwide prevalence of these diseases, there are few case reports of atraumatic tendon ruptures in these populations of people. (15, 16, 17)

It is therefore evident that patients afflicted with SLE treated with steroids seem to be at a greater risk of spontaneous tendon ruptures than are patients with other autoimmune or non immune diseases in which corticosteroids are a common treatment modality. Disease modifying drugs, such as azathioprine, methotrexate, mycophenolic acid, and cyclophosphamide, should be considered as steroid sparing agents in those patients who require large steroid doses to control life threatening organ-system involvement. Lupus patients who must be on long term corticosteroids should be educated and monitored for symptoms and signs of tendon rupture. Early surgical repair with rehabilitation techniques leads to significant reduction in morbidity from tendon rupture (18).



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