Tendon Ruptures in Patients with Systemic Lupus Erythematosus Treated with Corticosteroids

James Morgan and Daniel J. McCarty

There have been only 5 case reports in English of tendon rupture in SLE since 1958 (Table 1). Two additional cases involving three patellar tendons and four extensor digitorum tendons are reported here.

CASE REPORTS CP is a 33-year-old white woman who developed

a telangiectactic skin rash and a positive lupus ery- thematous (LE) cell preparation in 1965. Forty mil- ligrams of prednisone were taken daily through 1973. In 1970 a repeat LE cell preparation was posi- tive and antinuclear antibody by immunofluores- cence (ANIF) was reactive at 1 to 32 with a mixed pattern. Twenty-four-hour urine collections revealed 400 mg of protein and a normal creatinine clear- ance. A renal biopsy showed a focal proliferative glomerulonephritis with 3+ diffuse granular stain- ing for IgG and complement. Hemoglobin was 13.1 g, with a white blood count of 3200 and a normal differential. A skin biopsy revealed positive IgM and IgC at the dermal-epidermal junction and peri- vascularly in the papillary dermis. From 1971 to the summer of 1973, the patient developed bouton- niere deformities of both hands and generalized erythematous telangiectactic scaly dermatitis due to

From the Section of Arthritis and Metabolism, Department of Medicine, University of Chicago, 950 East 59th Street, Chicago, Illinois 60637.

Work supported by a Clinical Research Center Grant from T h e Arthritis Foundation.

JAMES MORGAN, MD: Medical Resident, University of Chicago; DANIEL J MC CARTY, MD: Formerly Pro- fessor of Medicine and Head, Section of Arthritis and Metabolic Diseases. Presently Professor and Chairman, Department of Medicine, The Medical College of Wisconsin, 8700 West Wisconsin Avenue, Milwaukee, Wisconsin 53226.

Address reprint requests to Dr McCarty. Submitted for publication March 26, 1974; ac-

cepted May 13, 1974.

SLE, a persistent dermatophytosis and a toxic reac- tion to INH.

On July 4, 1973, while leaving a bus, she felt a sudden severe pain in her right knee, and fell from the bus on her outstretched hands. A right infra- patellar tendon rupture was diagnosed a t a local hospital atid her right leg was casted for 3 weeks at which time she was transferred to the University of Chicago Hospitals.

Examination on admission revealed an anxious woman with marked alopecia and a generalized erythematous scaly dermatitis, most prominent over the back and malar areas. Her blood pressure was 120/80 mmHg, pulse 95, respiration 16, temperature 37.2 Celsius. Examination also revealed: a) acromio- clavicular separation of the right shoulder; b) marked \casting of the right quadriceps muscles with a defect in the right infrapatellar tendon and inability to extend the knee; c) rupture of the extensor digitorum communis of the right hand; and d) generalized proximal muscle weakness.

Electrolytes, urea nitrogen, creatinine, liver func- tion studies, uric acid, urinalysis, hemoglobin and platelet count were normal. The white blood cell count was 1900 with 557, polys, 57, bands, 30/, metamyelocytes, 307, lymphocytes, 67, monocytes, and 1% eosinophils. A chest film showed increased basillar interstitial markings. Hand films revealed diffuse osteoporosis with no juxta-articular erosions. A Westergren erythrocyte sedimentation rate was 34 mm/hr; hemolytic complement 125 units (nor- mal 180-330 p); and creatiniiie clearance 115 ml/ min. ANIF was positive at 1 to 40 in a rim pattern and DNA antibodies (Farr test) was 4O0& (normal < 251z). Bone marrow aspirate revealed an increase in the myeloid/erythroid in an otherwise hypo- cellular marrow.

6-Mercaptopurine, 75 mg daily was given, and over a 4-week period, the steroid dose was decreased from 40 to 5 mg daily. Initially a hinged knee brace was applied and she was able to walk using plat- form crutches.

A repair of the right infrapatellar tendon was performed 2 months later, but specimens of tendon

Arthritis and Rheumatism, Vol. 17, No. 6 (November-December 1974) 1033

MORGAN AND McCARTY

Table 1. Tendon Ruptures in SLE

Authors Year Rupture of Tendon(s)

Martin et a/ (13) 1958 Bilateral, patellar Cowan and Alexander (10) 1961 Bilateral, Achilles Lee (11) 1961 Bilateral, Achilles Twining et a/ (14) 1964 Bilateral, quadriceps Loten et a l (12) 1973 Extensor tendons of one hand Morgan and McCarty Present Paper Bilateral, patellar; extensor tendons of one hand

were not removed. She had an extension lag of 10” 3 months after surgery. Her right hand was placed in a spring activated splint and a repair of these tendons is planned.

AS is a 48-year-old white woman who had a splenectomy at the University of Chicago Hospitals in 1949 for idiopathic thrombocytopenic purpura. From 1949 to 1953 she was seen frequently for complaints of arthralgias, pleuritic chest pain, and a telangiectactic malar rash. In 1952 she was diag- nosed as having SLE on the basis of her previous history, a false-positive test for syphilis and a posi- tive lupus erythematosus (LE) cell preparation. A M’estergren erythrocyte sedimentation rate was 122 mm/hr and urinalysis revealed 5-10 white blood cells and 2-3 red blood cells per high powered field. But the BUN, creatinine, and serum proteins were normal. Chest x-ray showed a small right pleural effusion with mild cardiomegaly. She was treated with irradiation for bleeding gastric ulcers in 1954. A state of partial hyperthyroidism was induced with lS’I as treatment for SLE. Cortisone (75 mg daily) and desiccated thyroid (60 mg daily) were prescribed through 1964. At that time she was hospitalized for severe back pain. T w o vertebral body compres- sion fractures of the thoracic spine were treated with bedrest and calcium dietary supplementation.

On the eve of the Easter holiday, 1969, while departing from a bus, she felt a sudden “pop” of her right knee as she shifted her weight to her right foot. To avoid falling, she quickly shifted her weight to her left leg which was partially flexed. As soon as her balance was established, she felt a second “pop” in her left knee and fell from the bus to the ground. She was unable to extend either knee and was taken to the University of Chicago Hospitals where complete rupture of the infrapatel- lar tendons bilaterally at their insertion into the tibia was found. After the edema had subsided, the tendons were repaired. Microscopic examination of the tendon material removed at surgery revealed

round cell infiltration of the tendon substance and perivascular lymphocytes. There was no lineal hem- orrhage.

One year later she was able to extend both knees fully and was walking without difficulty. In the following 5 years she had silastic implants of the second, third and fourth right MP joints and two hospitalizations for thrombophlebitis and cellulitis. The SLE has remained quiescent with borderline low total hemolytic complement levels, ANIF reac- tive at not greater than 1-20 and a creatinine clear- ance of 85 ml/min.

DISCUSSION Spontaneous rupture of a tendon is a rare

event (1,2). Most authors refer to the great tensile strength of normal tendons and pos- tulate rupture of the tendon only when a destructive or pathological process can be identified (1-3). Table 2 lists those processes which have been identified as associated with tendon ruptures.

The specific pathologic processes involv- ing the tendon in gout (4), tuberculosis, syphilis, tumor and acute suppuration (2,3) are well defined. In hyperparathyroidism the proposed mechanism is dystrophic calci- fication and a possible direct effect of PTH on the highly polymerized glycoprotein ma- trix (5,6). Most authors postulate a gradual weakening with age through partial tears or ruptures with secondary calcification and fibrosis. Complete rupture then occurs through attrition (3).

The majority of tendon ruptures in rheu- matoid arthritis occur over the roughened

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TENDON RUPTURES IN SLE

Table 2. Conditions Associated with Tendon Rupture

Disease Mechanism

Tumor Tuberculosis Acute Suppuration

Gout Syphilis Rheumatoid Arthritis

Hyperparathyroidism

Glucocorticoids Lupus erythematosus

Direct infiltration Caseating granuloma Bacterial necrosis

(eg, gonorrhea) Urate crystal deposition Gumma Attrition RA nodules Vascular occlusion Dystrophic calcification ? PTH effect Partial ruptures with

fibrosis Calcification Attrition ? ?

surface created by joint subluxation and bony erosion. The tendon ruptures both through direct involvement of its synovium and through attrition as it moves over the displaced roughened bone. Rheumatoid nodules within the tendon substance, or occlusion of the vascular supply by proli- ferative synovium, as described by Manner- felt and Norman, may also cause rupture (7).

The question mark regarding mechanism after steroids and SLE in Table 2 reflects the problem of separating what may be two distinct processes occurring simultaneously in the same tendon. Certainly the role of steroids in slowing the healing process has been well studied (S), but their actual part in creating tendon pathology is less clear. In every instance where steroids have been implicated as a cause of tendon rupture, the underlying condition for which they were used can be cited as causal, eg RA (9), SLE (10-14) or athletic trauma (15).

Cruickshank (16) has described fibrinoid degeneration of tendon sheaths associated with round cell infiltration in six of seven

cases of SLE. In the one case studied, he found marked disruption of collagen fibrils in the tendon proper. However, he did not state the course of therapy for any patient.

Lotem et a1 (12) have suggested that a differentiation can be made between lupus degeneration and the effect of steroids by the presence or absence of an inflammatory infiltrate, respectively. He believes that both his case and others cited were prima- rily steroid induced. If this were true, one would expect to find many reports of ten- don ruptures occurring in patients with asthma, regional enteritis, or ulcerative coli- tis, in whom steroids are often used in high dose for long periods of time. But the liter- ature reveals only one case of tendon rup- ture in an asthmatic patient receiving ster- oids (17). Here pathologic data were not given. In our case showing round cell infil- tration the cause of the tendon rupture is presumably SLE.

REFERENCES 1 . Gilcreest E: Ruptures and tears of muscles

and tendons in systemic lupus erythema- tows. JAMA 100:153-160, 1933

2. McMaster PE: Tendon and muscle ruptures. J Bone Joint Surg 15:705-721, 1933

3. Boyd W: Surgical Pathology. Fourth edition. Philadelphia, WB Saunders Company, 1938

4. Levy M, Seelenfreund M, Maor P, et al: Bilateral spontaneous and simultaneous rup- ture of the quadriceps tendons in gout. J Bone Joint Surg 53B:510-513, 1971

5. Preston FS, Adicoff A: Hyperparathyroidism with avulsion of three major tendons. N Engl J Med 266:968-971, 1962

6. Preston FS: Avulsions of both quadriceps tendons in hyperparathyroidism. JAMA 221 : 406-407, 1972

7. Mannerfelt L, Norman 0: Attrition rup- tures of the flexor tendons in rheumatoid arthritis caused by bony spurs in the carpal tunnel. A clinical and radiological study. J Bone Joint Surg 51B:270-275, 1969

Arthritis and Rheumatism, Vol. 17, No. 6 (November-December 1974) 1035

MORGAN AND McCARM

8. Ragan C: The physiology of the connective tissue. Annu Rev Physiol 14:51-72, 1952

9. Moberg E: Tendon grafting and tendon suture in rheumatoid arthritis. Am J Surg

10. Cowan MA, Alexander S: Simultaneous bi- lateral rupture of Achilles tendons due to triamcinolone. Br bled J 1: 1658, 1961

11. Lee MLH: Bilateral rupture of Achilles tendon. Br Med J 1:1829-1830, 1961

12. Loten M, Maor P, Levi M: Rupture of the extensor tendons of the hand in lupus ery- thematosus disseminatus. Ann Rheum Dis 32:457459, 1973

13. Martin JR, Wilson CL, Mathews WH: Bi-

109:375-380, 1965

lateral rupture of ligamenta patellae in a case of disseminated lupus erythematosus. Arthritis Rheum 6:548-552, 1958

14. Twining RH, Marcus WY, Carey JL: Ten- don rupture in systemic lupus erythema-

15. Sweetnam R: Corticosteroid arthropathy and tendon rupture. J Bone Joint Surg 51B:

16. Cruickshank B: Lesions of joints and ten- don sheaths in systemic lupus erythematosus. Ann Rheum Dis 18:111-119, 1959

17. Smaill GB: Bilateral rupture of Achilles tendons. Br Med J 1:1657-1658, 1961

tosus. JAMA 189:377-378, 1964

397-398, 1969

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