Limitations in the usefulness of the 28-joint countcomment on the article by Fuchs and Pincus and the editorial by the American College of Rheumatology.код для вставкиСкачать
1712 LETTERS The consensus report also suggests that renal dysfunction and hypertension are contraindications for CSA. We initially excluded patients who had renal dysfunction defined by the presence of a >2-fold rise in serum creatinine levels and those who had hypertension that was resistant to conventional therapy. Furthermore, it should be emphasized that side effects observed during the study period were tolerable and did not warrant discontinuation of CSA. Another question seems focused on the mildness or severity (or activity) of our patients’ diseases. Patients who had central nervous system or vascular system manifestations or serositis were excluded from our study. However, most rheumatologists may consider these manifestations to be life-threatening, necessitating prompt establishment of high-dose corticosteroid treatment. Some of our patients (patients 2, 3, and 7) did indeed have only immunologic abnormalities which had failed to respond to conventional immunosuppressive therapies. However, it is well known that immunologic abnormalities, including hypocomplementemia and a rise in anti-double-stranded DNA antibody levels, might reflect the disease activity of SLE and often precede disease exacerbations (2-4). This work is important since low-dose CSA combined with low-dose corticosteroids can effect both clinical and immunologic improvement, with probable safety when possible side effects are carefully monitored. We hope that a randomized trial will be undertaken with the objective of determining whether criteria could be established for the selection of patients most likely to derive benefit from low-dose CSA treatment. Studies to examine the possibility of establishing these criteria are in progress. Michiaki Tokuda, MD Noriyuki Kurata, MD Akihito Mizoguchi, MD Masayuki Inoh, MD Kunio Seto, MD Makoto Kinashi, MD Jiro Takahara, MD Kagawa Medical School Kagawa, Japan 1. Panayi GS, Tugwell P: An international consensus report: the use of cyclosporin A in rheumatoid arthritis. Br J Rheumatol32(suppl 1):1-3, 1993 2. Laitman RS, Glicklich D, Sablay LB, Grayzel AI, Barland P, Bank N: Effect of long-term normalization of serum complement levels on the course of lupus nephritis. Am J Med 87(2):132-138, 1989 3. Rauch J, Hazeltine M, Tannenbaum H , Danoff D, Isenberg DA, Wild J, Sampalis J, Esdaile JM: Association of anti-DNA idiotype markers with clinical and serological manifestations in patients with systemic lupus erythematosus. 3 Rheumatol 17(2): 178-185, 1990 4. Ter Borg EJ, Horst G, Hummel EJ, Limburg PC, Kallenberg CGM: Measurement of increases in anti-double-stranded DNA antibody levels as a predictor of disease exacerbation in systemic lupus erythematosus: a long-term, prospective study. Arthritis Rheum 33:634-643, 1990 Limitations in the usefulness of the 28-joint count: comment on the article by Fuchs and Pincus and the editorial by the American College of Rheumatology To the Editor: Fuchs and Pincus (1) and the accompanying editorial (2) in a recent issue of Arthritis and Rheumatism demonstrate evidence to support a major advance in rheumatoid arthritis (RA) assessment methodology. Its use should expedite controlled studies of RA, and it should facilitate international drug development strategies. I would add to the clinical caveats mentioned (the importance, clinically, of foot pathology in RA, including its use as an early radiographic marker, and the continued necessity for individualization of RA treatment in practice) another important methodologic point which may, I think, have potentially broad ramifications: guarding against allowing our vision of future therapeutics in RA to be overguided by “datadriven,” rather than “disease-driven,’’ methodologic innovations. The 28-joint count proposal is purely data-driven, its raison d’&trederived exclusively from the performance of treatments that have already been in use. Succumbing to the temptation to use this rather than the 66-joint count in all situations is tantamount to allowing research to be driven by methodology, rather than methodology driven by research. The 28-joint count can have a use in supporting claims of similarity among existing disease-modifying antirheumatic or nonsteroidal antiinflammatory drugs. However, the 28-joint count is clearly inappropriate for assessing claims of superiority. In fact, the rationale for the 28-joint count is itself diametrically opposed to the rational pursuit of superior, nonstandard therapies. For these pursuits, fully inclusive measures, reflecting the breadth of disease pathology, are needed. Kent Johnson, MD Bethesda. MD 1. Fuchs HA, Pincus T: Reducedjoint counts in controlled clinical trials in rheumatoid arthritis. Arthritis Rheum 37:47W75, 1994 2. American College of Rheumatology Committee on Outcome Measures in Rheumatoid Arthritis Clinical Trials: Reduced joint counts in rheumatoid arthritis clinical trials (editorial). Arthritis Rheum 37:463464, 1994 Reply To the Editor: We share Dr. Johnson’s concerns regarding possible inappropriate use of reduced joint counts. However, isn’t a joint count that is “data-driven,” whether the 28-joint count (1) or any other carefully analyzed joint count (2), more “disease-driven” than one that is simply empirically derived? The joints included in the 28-joint count were selected because they are likely to be involved in disease, responsive to therapeutic interventions, and reproducibly assessed (1). Inclusion of additional joints adds “noise” and dilutes effective measurement (more joints are not necessarily better). The 28-joint count, and counts with even fewer joints, have been shown to be as predictive of long-term mortality as more elaborate joint counts (3).