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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.

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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).
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