120 LETTERS

Tables 1 and 2 show these new evaluations and the original evaluation of our results to date. As illustrated, our original observations hold true in the expanded populations. It is noteworthy that Benson and coworkers also noticed the absence of the BB genotype in their JRA + A group. Interestingly, we also did not find a significant association between the B allele and amyloidosis in adult patients with rheumatoid arthritis (n = 14).

We conclude that the meaning of the results for BB genotype is obscure at present. Further analysis of the DNA sequence of the 2 SAP genotypes is in progress.

In summary, we believe that the statistical method- ology of Harats and coworkers is inappropriate. However, the possibility that the gene pool from each study is different cannot be ruled out. Therefore, we await the report of an extended study with comparable control groups.

D. J. Faulkes, BSc Hon P. Woo, PhD, MRCP Medical Research Council Clinical Research Centre Harrow, UK

Reply To the Editor:

The letter by Faulkes and Woo correctly notes an error in the table legends of the article by Harats et a1 (Harats N , Kluve-Beckerman B, Skinner M, Passo M, Quinn L, Benson MD: Lack of association of a restriction fragment length polymorphism for serum amyloid P gene with reactive amyloidosis. Arthritis Rheum 32: 1325-1327, 1989). Unfortunately, in both Table 1 and Table 2 of that article, the phrase, “by Fisher’s exact test,” was inadvert- ently printed after values which were obtained by chi-square analysis. The data were analyzed using Fisher’s exact test and chi-square analysis, but of course, the comparison of 3 variables had to be by chi-square analysis.

The article is the result of a combined study from Indiana University School of Medicine and Boston Univer- sity School of Medicine that was undertaken mainly to evaluate the contention in Woo et al’s article that this polymorphic Msp I site “may well be associated with amyloidosis complicating more common conditions such as rheumatoid arthritis or chronic infections” (Woo P, O’Brien J , Robson M, Ansell BM: A genetic marker for systemic amyloidosis in juvenile arthritis. Lancet II:767-769, 1987). Our data did not support that statement and evidently Faulkes and Woo have now found that they “did not find a significant association between the B allele and amyloidosis in adult patients with rheumatoid arthritis (n = 14).” Unfor- tunately. the reader is unable to evaluate the new data presented by Faulkes and Woo because only the P values are reported, and not the allele frequency data.

Statistics aside, it would appear cogent to reserve final opinion about this polymorphism in a noncoding region of the serum amyloid P (SAP) gene until we see if it is linked to some objective factor in amyloid pathogenesis. Evalua- tion of this hypothesized association might begin with inves- tigations of possible linkage to a polymorphism in the coding region of SAP or investigations of gene expression of SAP at either the messenger RNA or protein level in juvenile

rheumatoid arthritis patients with and without AA amyloi- dosis.

Merrill D. Benson, MD Indiana University School of Medicine Indianapolis, IN

Comment on the article by Cush et a1

To the Editor: The article by Cush et a1 (Cush JJ, Lipsky PE,

Postlethwaite AE, Schrohenloher RE, Saway A, Koopman WJ: Correlation of serologic indicators of inflammation with effectiveness of nonsteroidal antiinflammatory drug therapy in rheumatoid arthritis. Arthritis Rheum 33: 19-28, 1990) raises several questions. How could 30 patients with what, by description of mean values, is serious, active rheumatoid arthritis (rheumatoid factor > 1,300; erythrocyte sedimenta- tion rate 51 mdhour ; 24 active joints; morning stiffness >2 hours) be treated for 3 months without disease-modifying antirheumatic drugs or corticosteroid drugs? Is this the usual treatment by rheumatologists?

What does the phrase “informed consent” mean in this context? Were the patients told that their minimal nonsteroidal antiinflammatory drugs (NSAIDs) would have to be discontinued for 2 weeks to be replaced by a drug which, by every study of the last 15 years, had no likelihood of being any better than the drug they stopped?

Cumulative experience should by now convince even the most optimistic that despite chemical differences, all the NSAIDs are equally impotent drugs in the treatment of rheumatoid arthritis; none is more effective than aspirin. While such studies will continue to be proposed by pharma- ceutical manufacturers, should they be published in the journal of the American College of Rheumatology?

L. A. Healey, MD The Mason Clinic Seattle, W A

To the Editor: We appreciate the interest and views expressed by

Dr. Healey and recognize that our results challenge conven- tional dogma, but, in truth, these traditional beliefs are not well supported by scientific evidence. Dr. Healey’s distress is apparently similar to that portrayed in Brecht’s Galileo (1). When faced with Galileo’s new observations that chal- lenged standard dogma, the question was posed, “Why should we go out of our way to look for things that can only strike a discord in the ineffable harmony?” We believe the answer is that the puvose of scientific investigation is to test hypotheses that may advance knowledge. If rheumatology is to advance as a scientifically based discipline, we must insist that our beliefs be supported by sound data.

Dr. Healey’s letter focuses on 3 main issues. The first has to do with whether “the usual treatment by rheumatol- ogists” is so grounded in fact that no additional information need be sought. Second, he questions whether patients who