Case Reports

Arthritis, Infectious Tenosynovitis, and Tendon Rupture in a Patient With Rheumatoid Arthritis and Psoriasis

Fed Pract. 2015 February;32(2):31-35

Author(s):

References

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4. Galloway JB, Hyrich KL, Mercer LK, et al; BSR Biologics Register. Risk of septic arthritis in patients with rheumatoid arthritis and the effect of anti-TNF therapy: Results from the British Society for Rheumatology Biologics Register. Ann Rheum Dis. 2011;70(10):1810-1814.

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9. Bogliolo L, Alpini C, Caporali R, Scirè CA, Moratti R, Montecucco C. Antibodies to cyclic citrullinated peptides in psoriatic arthritis. J Rheumatol. 2005;32(3):511-515.

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Compared with monoarticular arthritis, polyarticular arthritis may yield an initially narrower differential diagnosis that focuses on systemic inflammatory conditions, such as rheumatoid arthritis (RA). Approximately 15% to 30% of septic arthritis is polyarticular, of which about 45% is associated with underlying RA.^1,2 Regardless of the number of joints involved, septic (infectious) arthritis is a valid consideration given the morbidity and mortality.

In a retrospective study in the United Kingdom (UK) between 1982 and 1991, the morbidity and mortality of septic arthritis was 31.6% and 11.5%, respectively, and 16% of the study population had RA.³ A review of the literature by Dubost and colleagues found that polyarticular septic arthritis (PASA) has a mortality of 31% to 42% compared with 4% to 8% for monoarticular septic arthritis, and RA was present in 67% of the PASA fatalities.¹

Rheumatoid arthritis and its treatment predispose patients to septic arthritis. Septic arthritis in the UK general population is 0.42 per 100 patient-years for patients with RA on antitumor necrosis factor therapy.^3,4 In a retrospective study in the U.S., the incidence of septic arthritis was 0.40 per 100 patient-years for patients with RA compared with 0.02 per 100 patient-years for patients without RA.⁵

Other complications of RA include infectious tenosynovitis and tendon rupture. The incidence and prevalence of infectious tenosynovitis and tendon rupture in RA are not firmly established in the literature.

We present a patient with RA and psoriasis who responded initially to acute management for RA but subsequently was diagnosed with culture-negative polyarticular arthritis and infectious tenosynovitis associated with beta hemolytic group G Streptococcus (GGS), a part of Streptococcus milleri (S. milleri). During surgery, he was also found to have bilateral extensor pollicus longus (EPL) tendon rupture. Given the possible morbidity, the authors believe this patient may be of interest to the medical community.

Case Presentation

A 69-year-old African American male presented with 3 to 4 days of swelling and pain of bilateral wrists, bilateral hands, and the left ankle with subjective, but resolved, fevers and chills. His medical history was significant for seropositive erosive RA, psoriasis, hypertension, hyperlipidemia, alcohol abuse, chronic tobacco use, osteoporosis, and glaucoma. He did not have diabetes, reported no IV drug abuse, and except for the immunosuppressive effects of his medications, was not otherwise immunocompromised.

For 2 years in the outpatient setting, the rheumatology clinic had been managing the patient’s rheumatoid factor (RF) positive and anti-cyclic citrullinated peptide (CCP) antibody positive erosive RA with etanercept 25 mg subcutaneously twice a week. The RA affected his hands, wrists, shoulders, and ankles bilaterally but was successfully controlled. The dermatology clinic was managing the patient’s psoriasis with calcipotriene cream 0.005% twice a week and clobetasol ointment 0.05% twice a week. Psoriatic plaques were noted on bilateral elbows, bilateral dorsal hands, and bilateral dorsal feet.

Initial Evaluation

At evaluation, the patient’s vital signs revealed a temperature of 36.3°C (97.3°F), pulse of 102 beats per minute, respiratory rate of 16 breaths per minute, oxygen saturation of 99% on room air, and blood pressure of 102/70 mm Hg. He was found to have edema, tenderness, and erythema of the wrists bilaterally and left metacarpophalangeal joints (MCPs) and edematous right MCPs and left medial ankle.

The patient had been nonadherent with etanercept for 5 monthsand restarted taking the medication only 2 weeks before presentation. He had noticed worsening arthritis for at least 1 month. His last RA flare was approximately 1 year before presentation. Additional symptoms included 4 days of nausea, nonbloody and nonbilious emesis, left lower quadrant pain, and diarrhea without melena or hematochezia.

Initial laboratory studies found 3.2 k/μL white blood cells (WBCs) with a differential of 11.9% lymphocytes, 4.2% monocytes, 83.3% neutrophils, 0.5% eosinophils, and 0.1% basophils; 165 k/μL platelets; 96 mm/h erythrocyte sedimentation rate (ESR); and 45 mg/dL C-reactive protein. The patient was diagnosed with viral gastroenteritis and RA flare and was admitted for inpatient management secondary to limited ability to care for himself.

The patient was started on prednisone 40 mg orally once a day (for 5 days) for empiric treatment of an RA flare and continued on etanercept. The inpatient rheumatology service was consulted. Further evaluation later that day found involvement of the proximal interphalangeal joints and elbows and tenderness of the tendons of the dorsal hand bilaterally. Over the next 2 days, the patient remained afebrile and WBCs were within normal limits. Edema, erythema, and tenderness of the involved joints somewhat improved, but tenderness along the tendons of the dorsal hand worsened, which concerned the managing teams for infectious tenosynovitis.