Defining Response in Systemic Lupus Erythematosus: A Study by the Systemic Lupus International Collaborating Clinics Group

SEAN J. WOLLASTON, VERNON T. FAREWELL, DAVID A. ISENBERG, CAROLINE GORDON, JOAN T. MERRILL, MICHELLE A. PETRI, and KENNETH C. KALUNIAN, for the Systemic Lupus International Collaborating Clinics (SLICC)

ABSTRACT.

Objective. In a preliminary attempt to develop a drug responder index for patients with systemic lupus erythematosus (SLE), 2 validated disease activity instruments were studied for their responsiveness and compared to a physician visual analog scale (VAS) assessment of disease activity. We attempted to determine whether these validated instruments were useful components in characterizing response in the setting of a clinical trial.

Methods. Eighty paper patients were assessed using the British Isles Lupus Assessment Group (BILAG) and Systemic Lupus Disease Activity Index (SLEDAI) and by physician's assessment of global activity. The cases were arranged in random order and divided into groups of 20 patients and each group was assessed by 20 lupus experts; change in disease activity was recorded at 3 and 6 months compared to baseline using a physician VAS.

Results. Four different lupus experts assessed disease activity in all 80 patients at baseline and 3 and 6 months after initiation of therapy using the BILAG and SLEDAI instruments. BILAG and SLEDAI scores correlated well over time; however, in a regression analysis where average physician VAS were chosen as the outcome variable, a significant amount of variation in the average physician VAS not related to the SLEDAI and BILAG scores was noted.

Conclusion. The physician VAS may be too blunt to assess response in SLE, because even among experienced lupus assessors, there were considerable differences in what influenced scoring decisions. (J Rheumatol 2004;31:2390-4)

Key Indexing Terms:

SYSTEMIC LUPUS ERYTHEMATOSUS
RESPONSE INDEX

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From the Division of Rheumatology, David Geffen School of Medicine at UCLA, Los Angeles, California; MRC Biostatistics Unit, University of Cambridge, Cambridge, UK; Centre for Rheumatology, University College London, London, UK; University of Birmingham, Birmingham, UK; Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma; and Division of Rheumatology, Johns Hopkins University, Baltimore, Maryland, USA.

Supported by a grant from the American College of Rheumatology.

S.J. Wollaston, MD, Division of Rheumatology, David Geffen School of Medicine at UCLA; V.T. Farewell, PhD, MRC Biostatistics Unit, University of Cambridge; D.A. Isenberg, MD Centre for Rheumatology, University College London; C. Gordon, MD, University of Birmingham; J.T. Merrill, MD, Oklahoma Medical Research Foundation; M.A. Petri, MD, MPH, Division of Rheumatology, Johns Hopkins University; K.C. Kalunian, MD, UCSD School of Medicine, La Jolla, CA.

Address reprint requests to Dr. K.C. Kalunian, UCSD Center for Innovative Therapy, 9320 Campus Point Drive #227, La Jolla, CA 92037.

Submitted April 28, 2003; revision accepted June 29, 2004.

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