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The ability of antimalarials to moderate severe disease activity in systemic lupus erythematosus (SLE) is plausible but undemonstrated. We evaluated the long-term effectiveness of maintaining treatment with hydroxychloroquine sulphate (HCQ) to prevent major flares in quiescent SLE. Forty-seven patients with quiescent SLE who had been randomized to take HCQ (n = 25) or placebo (n = 22) as part of a 24-week withdrawal trial were evaluated for an additional 3 years. The primary outcome was time to a major flare of SLE which resulted in either the institution of or an increase in the current dosage of prednisone of 10 mg/day or more, or institution of therapy with immunosuppressive agents. Secondary outcomes included the specific subtype of these major flares (glomerulonephritis, vasculitis or other) and hospitalization for an exacerbation of SLE. An intent-to-treat analysis was conducted. Over the 42 months of study, 11 of 22 (50%) patients randomized initially to placebo, and seven of 25 (28%) patients randomized to continue treatment experienced a major flare. The relative risk of major flare for those randomized to continue HCQ compared with controls was 0.43 (95% CI: 0.17, 1.12). The relative risks for subtypes of flares were 0.26 (95% CI: 0.03, 2.54) for nephritis, 0.51 (95% CI: 0.09, 3.08) for vasculitis and 0.65 (95% CI: 0.17, 2.41) for flares characterized by other symptoms. The relative risk of hospitalization for major flare for patients randomized to continue hydroxychloroquine was 0.58 (95% CI: 0.13, 2.60). While the results are not statistically significant, they are compatible with the clinical belief that HCQ has a long-term protective effect against major disease flares in SLE and suggest that on average, HCQ use reduces major flares by 57% (95% CI: 83% reduction to 12% increase).

Mice immunized with B lymphocytes obtained from patients who had had well-documented rheumatic fever in the past yielded 2 monoclonal antibodies, termed 83819.23 and 256810, which identified certain alloantigens present on the B cells of these patients. The frequency of the B cell marker detected by clone 83S19.23 in rheumatic fever patients was found to be 59%, 77%, and 74% in India, New Mexico, and New York, respectively. Monoclonal antibody 256810 identified 75% of those rheumatic fever patients who were nonreactive to clone 83819.23. Thus, the 2 antibodies identify approximately 92% of all rheumatic fever patients and suggest the presence of a diallelic genetic marker for susceptibility to rheumatic fever.The possibility that genetic factors might play a role in susceptibility to rheumatic fever was first suggested in 1889 by Dr. W. B. Cheadle (1). Since that time,, a number of investigators have reexamined this question (2-4). However, with the exception of a slightly increased frequency of Lewis blood group antigen secretors among rheumatic fever patients (9, identification of a definite genetic marker for susceptibility to rheumatic fever has remained controversial. The possibility that rheumatic fever susceptibility might be associated with or linked to HLA loci was tested, but a clear relationship between any HLA haplotype and rheumatic fever or rheumatic heart disease could not be found (6).More recently, a new B cell alloantigen, called 883, which correctly identified 70-75% of all rheumatic fever subjects from different geographic areas, was identified. The discovery of this alloantigen, which was recognized by a serum obtained from a multiparous woman in Bogota, Colombia (7), has rekindled interesl in the genetic aspects of the pathogenesis of rheumatic fever. Unfortunately, the supply of the single human serum used in the original studies was limited and the search for other equally efficacious human sera proved to be difficult. Thus, many important questions concerning the relationshp between the 883 B cell marker and the rheumatic fever disease process were left unanswered.In the present paper we describe the production of 2 hybridoma-derived monoclonal antibodies prepared against B cells of rheumatic fever patients. The first antibody exhibits the same specificity as the original human B cell alloantiserum. The second antibody appears to identify the majority of rheumatic fever patients not identified by the original 883 B cell alloantiserum.

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This case suggests a possible aetiological role for gold in the pathogenesis of constrictive bronchiolitis obliterans, or alternatively an association between psoriatic arthritis and this inflammatory airway condition.