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CASE OF THE MONTH

Diagnostic challenges from your case files

Erich Fogg, PA-C, MMSc, department editor; Sima Terebelo, RPA-C

CASE

In July 2000, Mr. F., a 57-year-old computer programmer, presented with bilateral ankle pain aggravated by weight bearing and exercise, as well as some morning stiffness. On physical exam, he had ankle joint and subtalar joint findings of 2+ swelling and 2+ tenderness bilaterally, with full (but painful) range of motion. He had a C-reactive protein level of 12.1 mg/dL (normal, 0.00-0.80 mg/dL) and a rheumatoid factor (RF) of 158 IU/mL (normal, 0-20 IU/mL). Antinuclear antibodies (ANA) and uric acid levels were within normal limits, as was the erythrocyte sedimentation rate (ESR). Initial radiographs and subsequent CT scans of the feet and ankles were read as normal. At that point, Mr. F. was treated for degenerative joint disease.

In November 2000, the patient returned complaining of right ankle swelling, left knee pain, bilateral metacarpophalangeal (MCP) and wrist pain, and morning stiffness lasting longer than 1 hour. At this point, the patient fulfilled the American College of Rheumatology criteria for rheumatoid arthritis (RA); in January 2001, he was started on hydroxychloroquine (Plaquenil), 200 mg twice daily, as a disease-modifying antirheumatic drug (DMARD). Mr. F. remained well controlled and had no further symptoms, but in May 2002, visual field defects were found on an ophthalmology exam and hydroxychloroquine was promptly discontinued.

Current clinical dilemma At the next follow-up visit, the patient was asymptomatic and reluctant to take further DMARDs. At this point, Mr. F. was assigned to my care. Did this patient have a case of mild RA that would never progress, or would destructive joint changes develop if DMARD therapy was not instituted? The lack of symptoms, negative physical exam findings, and low-normal ESR pointed toward quiescent disease, but the high RF suggested the possibility of more active disease.

According to hospital radiologists, radiographs done in July and December 2002 showed only mild osteopenia. But when I reviewed the December films in clinic with the attending rheumatologist, we noted right MCP II and III erosions and signs of periarticular osteopenia. We started Mr. F. on methotrexate, 7.5 mg weekly increased to 10 mg weekly, to prevent further articular damage.

Mr. F. remained asymptomatic and tolerated the methotrexate. Radiographs done in December 2003 showed joint space narrowing and the previously seen erosions, so we decided to gradually increase the methotrexate to 15 mg weekly. When the official radiography report came in saying that the patient's joints were completely normal, I wanted to explore alternative imaging techniques to resolve this issue.

Imaging Based on studies showing that MRI is significantly more sensitive in detecting joint erosions and other pathologic signs,^1,2 I ordered MRI of the hands and wrists. The MRI conclusively showed erosions of MCP II and III in the right hand (see Figure 1). With the treatment plan finally validated, the methotrexate dosage remained at 15 mg weekly, and the patient was instructed to return monthly for monitoring.

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DISCUSSION

In RA, irreversible joint damage can occur within months of disease onset and lead to daily pain, increased morbidity, increased mortality, work disability, and significant health care costs. Much of this disability arises from the inflammatory-mediated joint destruction, most of which begins within the first 2 years of disease onset. Studies have shown that disability can be lessened or even avoided by timely institution of DMARDs.

Treatment options include methotrexate, hydroxychloroquine, sulfasalazine (Azulfidine), azathioprine (Imuran), and gold. These agents decrease the inflammation and joint destruction associated with RA by downregulating the immune system. They typically take a long time to work, and their efficacy must be monitored by clinical parameters as well as by radiographic change. Newer agents include biologics such as adalimumab (Humira), anakinra (Kineret), etanercept (Enbrel), infliximab (Remicade), and leflunomide (Arava). These agents are more specific for RA, as they target cytokines involved in mediating the inflammatory reaction. They typically have a quicker onset of action and less toxicity than the older agents, but their cost is high.

Clinical decisions, including whether to treat, how aggressively to treat, and whether or not DMARDs are working effectively, all rely on accurate imaging of affected joints to monitor for progression of joint damage.

REFERENCES

1. Hermann KG, Backhaus M, Schneider U, et al. Rheumatoid arthritis of the shoulder joint: comparison of conventional radiography, ultrasound, and dynamic contrast-enhanced magnetic resonance imaging. Arthritis Rheum. 2003;48:3338-3349.

2. Ostergaard M, Hansen M, Stoltenberg M, et al. New radiographic bone erosions in the wrists of patients with rheumatoid arthritis are detectable with magnetic resonance imaging a median of two years earlier. Arthritis Rheum. 2003;48:2128-2131.

Ms. Terebelo works in the Department of Clinical Trials and in the rheumatology clinic, State University of New York Downstate Medical Center, Brooklyn, NY. The author has indicated no relationships to disclose relating to the content of this article. Mr. Fogg is Assistant Professor in and Program Director of the Physician Assistant Program at the College of Health Professions, University of New England, Portland, Me.