Cytokines in acute rheumatic fever

 Plasma concentrations of inflammatory cytokines (IL-1α, IL-1β, IL-6, IL-8 and TNFα) were determined by ELISA in 27 patients with acute rheumatic fever (RF), 12 with only arthritis (RFA) and 15 with rheumatic heart disease (RHD), before, during and after treatment. Altogether, significant increases in TNFα, IL-8 and IL-6 levels were observed in the acute phase as compared to the data found during and after treatment. No significant differences were observed for the other cytokines. Elevations of one or more of the inflammatory cytokines were observed in 9 of 12 patients with RFA, and 12 of 15 with RHD. Increase of TNFα (6/9) and IL-8 (5/9) levels were higher in RHD patients with cardiac failure. These cytokines were below the detection limits on day 7 of treatment in all 22 patients, except in two, and in all 10 days after treatment. Conclusions These findings suggest that inflammatory cytokines, as TNFα, IL-8 and IL-6, may play a patho‐genic role in rheumatic fever. Received: 10 October 1995 / Accepted: 2 July 1996     

Cytokines in acute rheumatic fever

Plasma concentrations of inflammatory cytokines (IL-1α, IL-1β, IL-6, IL-8 and TNFα) were determined by ELISA in 27 patients with acute rheumatic fever (RF), 12 with only arthritis (RFA) and 15 with rheumatic heart disease (RHD), before, during and after treatment. Altogether, significant increases in TNFα, IL-8 and IL-6 levels were observed in the acute phase as compared to the data found during and after treatment. No significant differences were observed for the other cytokines. Elevations of one or more of the inflammatory cytokines were observed in 9 of 12 patients with RFA, and 12 of 15 with RHD. Increase of TNFα (6/9) and IL-8 (5/9) levels were higher in RHD patients with cardiac failure. These cytokines were below the detection limits on day 7 of treatment in all 22 patients, except in two, and in all 10 days after treatment. Conclusions?These findings suggest that inflammatory cytokines, as TNFα, IL-8 and IL-6, may play a patho‐genic role in rheumatic fever.     

Management of acute rheumatic fever

Management of rheumatic fever is outlined. It is emphasized that prevention of rheumatic fever is more important than treating the disease. Aspirin and steroids suppress the rheumatic inflammation but do not cure it. In the presence of cardiac involvement we prefer to use steroids as compared to aspirin. If congestive cardiac failure is present, the management must include steroids since aspirin treated patients have a higher morality.     

Resurgence of acute rheumatic fever

Rheumatic fever has been disappearing in the United States, especially during the past two decades. In the past two years, however, there have been 40 patients seen at the Columbus (Ohio) Children's Hospital diagnosed as having acute rheumatic fever. In marked contrast to the infrequency during the preceding ten years. Twenty of the 40 patients had carditis. Five of these patients were suffering from heart failure, and there was one death. The cause for this outbreak has not yet been found, but some possible causes are discussed. A possible nationwide resurgence of this disease may be heralded by our experience and that of others.     

Pneumonia associated with acute rheumatic fever

Pulmonary involvement in acute rheumatic fever is rare. Clinical and laboratory findings in rheumatic pneumonia are non-specific. Most of the cases of rheumatic pneumonia described in recent years have had a fulminant course often resulting in death. Autopsy findings are suggestive of but not specific for rheumatic pneumonia. In this article a case of pneumonia associated with acute rheumatic fever is described. Pneumonia and carditis occurred simultaneously in a 10-year-old boy treated without steroids, which resulted in recovery. The clinical spectrum of rheumatic pneumonia can range from mild to fulminant.     

Childhood acute rheumatic fever in Ankara, Turkey

Patients with acute rheumatic fever (ARF) admitted to a tertiary hospital in Ankara between January 1999 and July 2002 were studied cross-sectionally to verify the clinical profile and were followed during the acute period. All patients were investigated for throat culture, streptococcal serologic study, C-reactive protein, and erythrocyte sedimentation rate, and telecardiograms, electrocardiograms and echocardiographic study were done. During the study period, 129 attacks of ARF were observed: 118 were initial attacks and 11 were recurrences. Age on admission was 11.2 +/- 2.73 years (mean +/- SD, range: 6-21 years). Polyarthritis alone was present in 42 cases (33%), carditis alone in 33 (25%), combined carditis and polyarthritis in 36 (28%), combined carditis and chorea in 15 (12%) and chorea alone in 3 (2%). Nineteen (14%) patients with isolated arthritis and pure chorea had silent mitral and/or aortic regurgitation. Carditis was a dominant presenting manifestation, but appeared to be mild or moderate. The present study indicates that ARF is still a significant problem in Turkey. The observation that 8.5% of the attacks were recurrent reaffirms the need for more effective secondary prevention programs.     

Outbreak of acute rheumatic fever in northeast Ohio

An outbreak of acute rheumatic fever in 23 patients was seen in northeastern Ohio in 1986, with polyarthritis (78%) and carditis (30%) the major manifestations. Results of a questionnaire completed by the parents of all 23 patients indicated that they were generally nonindigent, with good access to medical care, and from a nonurban setting. Records of inpatients with acute rheumatic fever were reviewed for the 10 years prior to 1986. The clinical manifestations in inpatients from 1976 to 1985 were not significantly different from those of inpatients seen during 1986. Similar outbreaks have been reported elsewhere, and physicians should be aware of a possible resurgence of classic acute rheumatic fever and ensure compliance with an adequate course of therapy for patients with streptococcal pharyngitis.     

Atypical Cogan syndrome mimicking acute rheumatic fever

Cogan syndrome is a syndrome of non-syphilitic interstitial keratitis associated with vestibuloauditory deficits. We report a 10 year-old male child who presented with fever, acute polyarthritis, and unilateral red eye and was diagnosed as acute rheumatic fever. Subsequently unilateral hearing loss was detected and the child was diagnosed to have atypical Cogan syndrome.