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DQB.1780360301 in Felty's syndrome

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43 1
In summary, fluorescent lamps, especially those that
are new, emit surprisingly high levels of UV-B radiation.
Although not erythemogenic, the photons emitted are photochemically active and for that reason have potential for
toxicity in patients with SLE. Standard commercial diffusers
effectively block these UV-B wavelengths and, to a lesser
extent, UV-A wavelengths. We thank Dr. Sontheimer for his
excellent letter and data, which have prompted us to further
analyze our observations and helped us to explain them
more fully.
Hugh McGrath, Jr., MD
Louisiana State University
Medical Center
New Orleans, L A
1. Kobza A, Ramsay CA, Magnus IA: Photosensitivity due to the
“sunburn” ultraviolet content of white fluorescent lamps. Br J
Dermatol 89:351-359, 1973
2. Noonan FP, de Fabo EC: Ultraviolet-B dose-response curves for
local and systemic immunosuppression are identical. Photochem
Photobiol 52:801-810, 1990
3. Norval M, Simson TJ, Bardshiri E, Crosby J: Quantification of
urocanic acid isomers in human stratum corneum. Photodermatol
Photoimmunol Photomed 5:179-186, 1988
DQB*0301 in Felty’s syndrome
To the Editor:
We wish to respond to the challenge of Olerup et a1 in
the last sentence of their reply (Olerup 0, Wallin J, Strom H:
Reply [letter]. Arthritis Rheum 35:845-846, 1992) to our
Second-Line Agents in the Treatment of Rheumatic Diseases.
Inflammatory Diseuse and Therapy Series, Volume 9 . Edited
by Jonathan S . Dixon and Daniel E . Furst. New York,
Marcel Dekker, 1992. 648 p p . Illustrated. Indexed. $165.00.
This volume, the ninth in the series on Inflammatory
Disease and Therapy, reviews second-line (diseasemodifying or slow-acting) drug therapy in rheumatoid arthritis (RA) and other rheumatic diseases. Corticosteroids are
discussed in chapters on systemic lupus erythematosus
(SLE) and systemic vasculitis, but nonsteroidal antiinflammatory drugs are mentioned only briefly in order to contrast
their actions with those of second-line agents (SLAs). The
chapter authors are recognized authorities from the US, UK,
other European countries, Canada, and Australia.
The first of 4 sections is devoted to clinical trial
methodology, monitoring procedures, and prediction of risk
and response. These issues are usually not awarded dedicated space in standard rheumatology textbooks. The chapter by Bulpitt and Paulus is an excellent, concise review of
Arthritis and Rheumatism, Vol. 36,No. 3 (March 1993)
letter concerning DR-DQ variants in Felty ’ s syndrome
(Grennan DM, Hillarby MC: DR-DQ variants in rheumatoid
arthritis and Felty’s syndrome: comment on the article by
Wallin et a1 [letter]. Arthritis Rheum 353444345, 1992).
Their question concerns whether the increased frequency of
DQB*0301, which has been observed in Felty’s syndrome
(FS) patients as compared with rheumatoid arthritis (RA)
patients without extraarticular features, is dependent on a
primary association at the DRBl locus with DRB*0401. In
our patient population, we studied FS and non-FS RA
patients who were negative for DRB*0401, and found that 9
of 10 FS patients, as compared with 33 of 59 non-FS RA
patients, were DQB*0301 positive ( P = 0.0354 by Fisher’s
exact test). When we carried out the converse analysis on FS
and non-FS RA patients who were negative for DQB*0301,
4 of 5 FS patients and 34 of 59 non-FS patients typed positive
for DRB*0401 (P = 0.2517 by Fisher’s exact test).
Thus, among FS patients, there is a weak association
with DQB*0301 in those who are DRB*0401 negative, but no
association with DRB*0401 in those who are DQB*0301
negative. We interpret these findings as suggesting that HLA
variants outside the DRBl locus can influence susceptibility
to FS as discussed in our letter, and we believe it is more
likely that this reflects an effect of the B44;Bf*S;C4A3;
C4BQO;DR4;DQB*0301 haplotype as opposed to a primary
effect at DQB or another single locus within the HLA region.
D. M. Grennan, MD, PhD
M. C. Hillarby, PhD
University of Manchester
Salford, Englund
the basic elements and pitfalls of study design. The choice
and sequencing of agents in the US, UK, and Australia are
contrasted in separate chapters.
The second section deals with individual SLAs in
RA. A standard textbook format is used, but each chapter is
well-written and abundantly referenced.
The third section, on SLAs in other arthritides,
predictably includes seronegative polyarthritis, but rather
surprisingly devotes chapters also to osteoarthritis (OA),
SLE, crystal-induced synovitis, and vasculitis. All are wellorganized and informative. Most of this material has been
reviewed elsewhere in greater detail, however, the only
exception being a chapter on OA by Australian authors, to
which 10% of the volume is devoted. This chapter covers the
“chondroprotective” agents such as Arteparon, Rumalon,
and hyaluronic acid, none of which is currently available for
clinical use in the US. I found this chapter, which focuses on
cartilage physiology, animal studies, and human trials, quite
fascinating, with material that has seldom been compiled and
presented so well. The chapters on SLE and vasculitis
include virtually the full gamut of pharmacotherapy for these
disorders, while the discussion of crystal-induced synovitis
is a rather brief review of drug therapy for hyperuricemia.
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felt, syndrome, dqb, 1780360301
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