43 1 BOOK REVIEWS 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 BOOK REVIEWS 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.