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Do the Clinical Responses and Complications Following Etanercept or Infliximab Therapy Predict Similar Outcomes with the Other Tumor Necrosis Factor-a Antagonists in Patients with Rheumatoid Arthritis?

HERBERT T.S. ANG and SIMON HELFGOTT

ABSTRACT.

Objective.
To study a group of 29 patients with rheumatoid arthritis (RA) who have been treated with both tumor necrosis factor (TNF)-a antagonists, etanercept and infliximab and to determine the correlation of responses and complications seen in these patients.

Methods. Patients' responses to and complications from either treatment were reviewed retrospectively by determining the joint counts, acute phase reactants, as well as occurrences of infection, hypersensitivity, and cytopenia. The correlation of responses and complications was determined using phi coefficients and exact p values.

Results. There was no correlation between the joint count responses (exact p value for correlation coefficient, 0.70) and acute phase reactant responses (exact p value 0.14) with the use of etanercept and infliximab in the same patient. There was no correlation between the occurrences of drug hypersensitivity reactions (exact p value 0.20) or infectious complications (exact p value 1.00). However, the occurrence of anemia with the use of one TNF-alpha antagonist was correlated with a similar occurrence with the use of the other antagonist (exact p value 0.007).

Conclusion. Our study indicates that patients who fail to respond to one TNF-a antagonist can respond to the other antagonist. Furthermore, there appears to be no contraindication to using one TNF-a antagonist for patients who have developed hypersensitivity reactions to the other. The infections observed in our study were generally mild and did not necessarily recur with the use of the second antagonist. In contrast, anemia, when present with the use of one agent, was likely to occur with the use of the second agent. (J Rheumatol 2003;30:2315-8)

Key Indexing Terms:

RHEUMATOID ARTHRITIS
ETANERCEPT
INFLIXIMAB
CLASS EFFECT


From the Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital and the Division of Rheumatology, Allergy and Immunology, Brigham and Women's Hospital, Boston, Massachusetts, USA.

Supported by the National Research Service Award Grant No. AR07258-24 from the National Institutes of Health (H.T.S. Ang).

H.T.S. Ang, MD, MPH, Rheumatology Fellow, Massachusetts General Hospital; S. Helfgott, MD, Assistant Professor of Medicine, Harvard Medical School, and Rheumatologist, Brigham and Women's Hospital and Massachusetts General Hospital.

Address reprint requests to Dr. H.T.S. Ang, Division of Rheumatology, Harvard Vanguard Medical Associates/Department of Medicine, Brigham and Women's Hospital, 133 Brookline Ave, Boston, MA, 02215, USA. E-mail: Herbert_Ang@vmed.org

Submitted October 9, 2002; revision accepted March 20, 2003.




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