Poststreptococcal reactive arthritis in children: a potential predecessor of rheumatic heart disease.

OBJECTIVE: To report several cases of arthritis seen in children after infection with Group A beta-hemolytic Streptococcus (GABHS) which were not associated with carditis or other major manifestations of the Jones Criteria for acute rheumatic fever (ARF); and to analyze the literature to determine these patients' potential risks for the subsequent development of rheumatic heart disease. METHODS: A retrospective chart review was performed of all patients seen in a pediatric rheumatology clinic from January, 1990 to December, 1992. RESULTS: Four patients were identified with poststreptococcal reactive arthritis (PSReA) and no carditis. Their arthritis had an acute onset, tended to have a longer duration than the arthritis typically seen in ARF, and in most instances did not respond promptly to therapy with aspirin or nonsteroidal antiinflammatory agents. In some patients, there was no history of sore throat or fever. Diagnosis of PSReA was made by serologic testing. Cardiac evaluation in all 4 patients was negative. CONCLUSION: PSReA should be considered in the differential diagnosis for any pediatric patient with the acute onset of arthritis, whether the arthritis is the classic migratory polyarthritis typically seen in ARF or not. Throat culture and serologic testing for streptococcal infection should be performed on these patients. If recent GABHS infection is confirmed, cardiac evaluation, including echocardiogram, is warranted. Both ARF and PSReA occur after GABHS infection, but the precise relationship between these 2 entities is unclear. Longterm follow up of pediatric patients with PSReA in previous reports have shown that a certain percentage of them upon subsequent GABHS infection develop carditis. Until the specific risk factors (either host or bacterial characteristics) for developing subsequent carditis are better delineated, antibiotic prophylaxis similar to that used in ARF should be considered in patients with PSReA.

Activation of human B lymphocytes by nanogram concentrations of anti-IgM-dextran conjugates.

Surface immunoglobulin (sIg) cross-linking on B lymphocytes by high concentrations of anti-Ig antibody has been used to mimic antigen-stimulated B cell activation. In order to develop a system to study sIg-mediated T cell-independent B cell activation using low concentrations of anti-Ig antibody that more closely resemble the concentrations of antigen that are achieved under in vivo conditions, we conjugated monoclonal anti-human IgM antibody (anti-mu) to dextran (molecular weight 2 X 10(6)) thereby increasing its valency. This dextran conjugate (anti-mu-Dex) stimulated comparable levels of thymidine incorporation and B cell size increases as were seen with unconjugated anti-mu but at 100- to 1000-fold lower concentrations. Anti-mu-Dex also stimulated increases in intracellular ionized calcium ([Ca2+]i) in a higher percentage of cells, of greater magnitude and of longer duration than that stimulated by unconjugated anti-mu. Interestingly, there was no direct correlation between the increases in [Ca2+]i that were stimulated by anti-mu-Dex and its ability to stimulate B cell proliferation. The concentrations of anti-mu-Dex (10 micrograms/ml) that led to the highest increase in [Ca2+]i resulted in thymidine incorporation that was no greater than that of medium control, whereas 0.01 to 0.1 microgram/ml stimulated significant thymidine incorporation with 50% lower levels of stimulation of [Ca2+]i. These data demonstrate that anti-mu-Dex is a potent activator of human B lymphocytes, is effective even at ng/ml concentrations which over a 2-h time period do not induce detectable modulation of sIg, and its stimulation of B cells into G1 and S may not be directly related to its ability to stimulate increases in levels of [Ca2+]i.