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Immune-mediated Polyarthritis

By: Dr. Douglas Brum

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Diagnosis In-depth

The diagnosis of immune-mediated polyarthritis is made in two parts. First, your veterinarian must establish a diagnosis of polyarthritis, which is often difficult. Once the polyarthritis is diagnosed, a cause needs to be determined. Since the diagnosis of immune-mediated polyarthritis is based on the exclusion of other causes, a significant work-up is usually required. Diagnostic tests include:

  • CBC. The CBC is an important test used in evaluating the white and red blood cell lines. Elevations in white blood cells may indicate an inflammatory response, signs of infection or a neoplastic (cancer) process. The red cell line is used to check for anemia, which may be seen with many infectious, neoplastic or immune-mediated processes. The platelets, which are the blood cells responsible for clotting, are also counted. Decreases in the platelet count may be seen with tick borne diseases, SLE or neoplastic disease.

  • Biochemical profile. Many internal metabolic conditions are monitored through the biochemical profile. Kidney function is assessed as SLE commonly can cause kidney damage. Occasionally kidney damage is also seen with the tick borne diseases. Liver disease may be noted, as inflammation of the liver may be present as a primary cause of reactive polyarthritis.

  • A urinalysis should always be done in the work-up for polyarthritis. A urinalysis is needed to assess kidney function, and to check for signs of infection. A culture is also generally recommended, since long-term immunosuppressive therapy may be required for treatment of the disease.

  • Arthrocentesis is needed to make a definitive diagnosis of polyarthritis. Multiple joints should be sampled and the fluid submitted for cytologic evaluation and culture. Analysis of immune-mediated joint fluid typically has an increased number of inflammatory cells. Other causes of polyarthritis may have different cytologic characteristics; however, tick borne diseases and other causes of immune-mediated diseases such as SLE will show similar cytologic findings as the idiopathic disease, and thus require different diagnostic tests to differentiate the conditions.

  • Radiographs of the affected joints are important to determine if the joint disease is causing an erosive arthritis that is sometimes seen in septic arthritis, and commonly seen in rheumatoid arthritis. Idiopathic immune-mediated disease is typically a non-erosive polyarthritis.

  • Chest and abdominal radiographs are useful to rule out underling diseases. Tumors, infections, foreign bodies and stones may all be a cause of chronic immune stimulation.

  • Immune profile. RF and ANA titers can be submitted to help diagnose rheumatoid arthritis and SLE. The tests, if positive, help in establishing a diagnosis but are not definitive.

  • Infectious disease titers for Lyme disease, ehrlichia and Rocky Mountain spotted fever are helpful in ruling out these causes of polyarthritis. Many times they are the only way to differentiate the idiopathic disease from infectious causes.

  • If indicated, an abdominal ultrasound, echocardiogram or blood culture might be required.

    Therapy In-depth

  • Prednisone. Prednisone is the most common and generally most effective drug used in the treatment of immune-mediated polyarthritis. When given at high dosages, it causes suppression of the immune response. Improvement of the clinical signs is usually seen quickly, within 48 hours. To induce remission, high doses are given at the start of therapy. If remission occurs, dosages are gradually decreased and eventually stopped, over 4 to 9 months. If remission is difficult to achieve, a relapse has occurred, or there are unwanted side effects from the prednisone, additional immunosuppressive drugs are required.

  • Azathioprine (Imuran). Imuran is usually the next immunosuppressive drug used in the treatment of the disease. It is usually used together with prednisone, allowing for lower prednisone dosages, but can be used as a maintenance drug. The drug requires 2 to 3 weeks to become effective. Azathioprine can cause bone marrow suppression, but used with caution, it can be very effective.

    Generally, prednisone and Imuran are the most effective drugs used to treat the disease. In refractory cases, the following drugs may be of benefit:

  • Cyclophosphamide (Cytoxan). This drug causes potent immunosuppression, but needs to be used with care due to potent bone marrow suppression.

  • Chrysotherapy (gold salt therapy). Gold containing compounds have anti-inflammatory properties that may be useful in treatment. Intramuscular injection (sodium aurothiomalate) or oral preparations (auranofin) are available, but the drug may take a month or more to be effective.

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