Anticardiolipin antibodies in patients with rheumatic diseases

Recent attention has focused on the presence of anticardiolipin (ACL) antibodies and their possible role in recurrent thrombosis and abortions in patients with systemic lupus erythematosus. We analyzed ACL antibodies in 243 consecutive patients to determine their frequency in patients with different rheumatic disorders. A significantly elevated frequency was found in patients with systemic lupus erythematosus (38%), rheumatoid arthritis (33%), and psoriatic arthritis (28%). No correlation could be found between ACL antibody levels and recurrent thrombosis. In patients with rheumatoid arthritis there was a significant correlation between ACL antibodies and a history of repeated abortions. No significant association was found between ACL antibodies and other autoantibodies except in patients with rheumatoid arthritis; ACL antibody-positive rheumatoid arthritis patients were much more likely to be antinuclear antibody-positive (P less than 0.0002).     

Anticardiolipin antibodies are not associated with rheumatic heart disease.

The aim of this study was to examine the prevalence of anticardiolipin antibodies in rheumatic valve heart disease. Serum samples of 31 consecutive patients with rheumatic heart disease and documented valve involvement, as well as six patients with acute rheumatic fever were tested for IgG anticardiolipin antibodies by a validated ELISA. No anticardiolipin antibodies were found when a cut-off point set at mean +/- 5 s.d. was applied. We can conclude that anticardiolipin antibodies are not present in rheumatic heart disease patients and, as suggested by several observations, these antibodies do not appear to have a pathogenic role in this particular disease.     

Echocardiographic abnormalities in acute rheumatic fever.

The echocardiographic velocity of circumferential fiber shortening and left atrial dimension were measured serially in two groups of children with acute rheumatic fever: Group I, six patients with valve regurgitation without congestive heart failure, and Group II, seven patients with regurgitation and congestive heart failure. In Group I, the initial velocity of circumferential fiber shortening was increased to 1.90 +/- 0.31 circumferences per second (circ/sec) (mean +/- standard deviation). In group II, it was decreased (1.18+/-0.25). In group I velocity of circumferential fiber shortening subsequently decreased but remained above the normal level; in Group II it increased to exceed the expected normal value. Concurrent changes in left atrial dimension were observed in both groups. The initial left atrial dimension of Group I (2.2 +/- 0.75 cm/m2) was slightly increased and returned to normal (1.70 +/- 0.32) on follow-up study. The left atrial dimension of Group II was greatly increased initially (2.70 +/- 0.81 cm/m2) and remained large (2.50 +/- 0.67). Three patients in Group II experienced rebound during corticosteroid withdrawal. In each the velocity of circumferential fiber shortening decreased, suggesting impaired cardiac contractility. The echocardiogram thus facilitates serial assessment of the severity of carditis in acute rheumatic fever.     

Agalactosyl IgG, antibodies to heat shock proteins, and acute rheumatic fever.

In rheumatoid arthritis an increased proportion of the N-linked oligosaccharides on serum IgG terminate with N-acetylglucosamine (agalactosyl IgG). It has recently been shown that group A streptococcal cell wall peptidoglycan/polysaccharide complex may be used to raise monoclonal antibodies which bind to this glycoform of IgG. Patients with rheumatoid arthritis also have increased levels of antibody to the 65 kD and 70 kD families of heat shock proteins, particularly to a bacterial (Mycobacterium bovis) homologue of heat shock protein hsp65. Streptococci must contain similar heat shock proteins. Acute rheumatic fever follows infection with group A streptococci, and these organisms might theoretically evoke antibody to heat shock proteins or changes in the levels of agalactosyl IgG, which is antigenically cross reactive with their cell walls. It is shown here that serum samples from patients with acute rheumatic fever do not differ from those from normal children by these criteria.     

QT dispersion in acute rheumatic fever

BACKGROUND: Disturbances of conduction are well known in the setting of acute rheumatic fever. The aim of this study is to investigate the QT dispersion as seen in the surface electrocardiogram of children with acute rheumatic fever. METHODS: QT dispersion was quantitatively evaluated in 88 children with acute rheumatic fever. Patients were divided into two groups based on the absence or presence of carditis. As a control group, we studied 36 healthy children free of any disease, and matched for age with both groups. Repeat echocardiographic examinations were routinely scheduled in all patients at 3 months after the initial attack to study the evolution of valvar lesions. RESULTS: The mean QT dispersion was significantly higher in children with rheumatic carditis. But there was no statistical difference between children without carditis and normal children. Among the children with carditis, the mean dispersion was higher in those with significant valvar regurgitation. Dispersion of greater than 55 milliseconds had a sensitivity of 85%, and specificity of 70%, in predicting rheumatic carditis, while a value of 65 milliseconds or greater had sensitivity of 81% specificity of 85% in predicting severe valvar lesions in acute rheumatic carditis. At follow-up examination, a clear reduction on the QT dispersion was the main finding, reflecting an electrophysiological improvement. CONCLUSIONS: These observations suggest that QT dispersion is increased in association with cardiac involvement in children with acute rheumatic fever.     

Treatment of acute rheumatic fever and acute rheumatic heart disease

The treatment of acute rheumatic fever and acute rheumatic heart disease with failure was discussed in this morning's seminar. The efficacy of chemotherapy in the prevention of rheumatic recurrences was questioned. Massive salicylate therapy for acute rheumatic fever was considered effective in changing the course of rheumatic polyarthritis and early carditis. The benefits derived from sanatorium type of care for the protracted case of rheumatic disease were described and the principles underlying the aims of this type of care were delineated. Digitalis in the treatment of acute rheumatic carditis with failure was considered of limited value. Finally, the use of high concentrations of oxygen in the treatment of acute carditis was discussed. It was pointed out that while oxygen therapy may not influence the duration of rheumatic activity, it seems to lessen the cardiac disability resulting from carditis. Some of the physiologic principles responsible for the salutory effects of oxygen therapy were presented.     

Aortic valve replacement during acute rheumatic fever.

Emergency aortic valve replacement was performed during an attack of acute rheumatic fever in a 12-year-old black boy. He had an uneventful recovery and has remained asymptomatic 27 months after operation. In the light of this experience and that of others, one might conclude that the decision to operate on these patients should be based on the severity of the haemodynamic derangement rather than on the state of activity in the rheumatic process.     

Lymphocyte subsets in acute rheumatic fever and rheumatic heart disease

Lymphocyte subsets in 53 patients with acute rheumatic fever and 78 patients with chronic rheumatic heart disease were compared with 20 normal control subjects and 39 patients suffering from uncomplicated streptococcal pharyngitis to obtain information about the pathogenesis of the disease. Twenty patients with rheumatic fever were followed for 24 weeks to evaluate changes occurring over the course of the disease. Total leukocyte and lymphocyte counts were increased in patients with rheumatic fever and to a lesser extent in those with rheumatic heart disease, when compared with controls. The difference between the two groups was significant. Patients with acute rheumatic fever had an increased number of B cells and a smaller increase in total T and T-helper-inducer (CD-4) cells. The proportion of B cells increased, while that of T-suppressor-cytotoxic (CD-8) cells fell. An increased number and proportion of B cells was also seen in patients with rheumatic heart disease. Total T and T-helper lymphocyte percentages and numbers were significantly higher in patients with rheumatic fever compared with those of patients with rheumatic heart disease. Follow-up studies at 6, 12, and 24 weeks revealed no significant differences from the entry point studies, although there was a trend toward reduction in the degree of derangement from normal values. Patients with uncomplicated streptococcal pharyngitis, however, did not show perturbations in the T-cell and T-subset counts. Our study suggests that the immunoregulatory defect in acute rheumatic fever is characterized by a relative reduction of suppressor T cells with an absolute increase in helper T cells and B cells, resulting in an increased cellular as well as humoral immune response.(ABSTRACT TRUNCATED AT 250 WORDS)