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PubMed1993

Evaluation of secondary prophylactic schemes, based on benzathine penicillin G, for rheumatic fever in children.

Serum concentrations of penicillin were measured in children with rheumatic fever. The adequacy of the values after administration of 1.2 million units of benzathine penicillin G every 2 or 3 weeks was confirmed; the adequacy of a 4-week regimen was questionable. The administration of 0.6 million units every 3 weeks was found to be inadequate to maintain serum levels high enough for the secondary prophylaxis of rheumatic fever.

Adolescent↗

PubMed1956

Diagnosis of rheumatic fever and like conditions; evaluation of certain of the acute phase reactants in a single specimen of blood.

CERTAIN OF THE ACUTE PHASE REACTANT TESTS WERE PERFORMED ON THE SAME SPECIMEN OF BLOOD FROM PERSONS WITH THE FOLLOWING STATES: Normal, acute respiratory disease, streptococcosis, acute rheumatic fever, acute glomerulonephritis, acute rheumatoid arthritis, inactive rheumatic fever, lupus erythematosus, malignant disease, obesity, asthma, and allergic rhinitis. Of the tests performed, the mucoprotein-tyrosine and the antistreptolysin-0 titer when done together appeared to be the most discriminating. It is suggested that the performance of such tests on the same sample of blood might aid in differentiating mild acute rheumatic fever and acute rheumatoid arthritis from each other and also from other disease states.

Acute Disease↗

PubMed1995

[Autopsy of a patient with rheumatic fever, who initially presented with acute respiratory failure].

A 59-year-old man was admitted to the hospital because of dyspnea, fever, and general erythema. He had hypoxemia on admission. Chest X-ray film showed diffuse reticulonodular shadows in both lungs. Chest CT showed a diffuse increase in density, predominantly in both lower lobes. The respiratory failure had rapidly progressed, and the patient died only 40 hours after admission. Autopsy revealed diffuse alveolar damage in the lung, and Aschoff's bodies in the cardiac muscle. Aschoff's bodies are specific for rheumatic fever, and consist of Aschoff's cells with owl-eye-like or caterpillar-like nuclei. We diagnosed this patient's condition as rheumatic fever because of the presence of Aschoff's bodies. Rheumatic fever is generally seen as a disease of younger people, and these patients rarely present with respiratory signs, but this case shows that we have to recognize the possibility of rheumatic fever in adults with respiratory signs and skin lesions.

Acute Disease↗

PubMedDate not supplied

A study of HLA antigens in adults with acute rheumatic fever.

By use of a microlymphocytotoxic assay to detect 32 HLA antigens of the A and B series, we examined 49 Mexican-American adults with acute rheumatic fever and contrasted the findings with 100 ethnically identical controls. Eighty-nine percent of the total possible antigens were identified. Strong associations between HLA antigens from either locus and acute rheumatic fever were not detected. These findings serve to emphasize the importance of nongenetic factors in the pathogenesis of acute rheumatic fever and help clarify the role of HLA antigens in rheumatic diseases.

ABO Blood-Group System↗

PubMed1992

Pharmacokinetics of rheumatic fever prophylaxis regimens.

The pharmacokinetics of benzathine penicillin G (1,200,000 IU given intramuscularly), penicillin V (250 mg given orally twice daily), erythromycin stearate (250 mg given orally twice daily) and roxithromycin (150 mg given orally once daily) were investigated. The drugs were given prophylactically to prevent the recurrence of rheumatic fever to 20 patients attending a rheumatic fever clinic in a study of crossover design. Serum antibiotic concentrations were determined by microbiological assay at intervals of up to 28 days after intramuscular injection and immediately before and 1-2 h after the fifth oral dose. The concentrations of penicillin G in all serum samples obtained on day 28 after parenteral benzathine penicillin G administration were greater than 0.01 mg/dl. Most patients had no detectable penicillin V or erythromycin in blood samples drawn immediately before the fifth dose. The concentration of roxithromycin at 24 h after the dose was greater than 1.2 mg/dl in all patients. Based on the pharmacokinetic profiles, it is suggested that 1,200,000 IU benzathine penicillin G given every 4 weeks is an appropriate regimen for preventing the recurrence of rheumatic fever in Thai adults. Roxithromycin had much better pharmacokinetics than penicillin V and erythromycin stearate, and is probably the best alternative regimen to intramuscular penicillin G.

Adult↗

PubMed1984

Occurrence and prevention of rheumatic fever among ethnic groups of Hawaii.

To assess the occurrence of acute rheumatic fever (RF) among the ethnic groups of Hawaii, the case records of hospitalized children with RF in Oahu were reviewed for the period from October 1976 to September 1980. One hundred four of the records met the modified Jones criteria. Incidence rates per 100,000 children were as follows: Japanese, 0; white, 9; Filipino, 9.1; Hawaiian and part-Hawaiian, 27.2; and Samoan, 96.5. Carditis was most common among Samoan children; it occurred in nine of 18 children. A streptococcal, throat culture program for children with respiratory infections was in progress in 60% of Oahu's public schools during this period of time. Children with positive cultures were excluded from school until the start of treatment. However, RF occurred with equal frequency in participating and nonparticipating schools. Rheumatic fever continues to be a substantial problem among Polynesian children in Hawaii, and it is apparent that the school-based primary prevention program used in Hawaii to control streptococcal disease has not altered the frequency of RF among them.

Adolescent↗

PubMed1975

Salivary immunoglobulins and streptococcal antibodies in patients with acute rheumatic fever.

Evidence of a local immunologic response to recent pharyngeal infection with group A streptococci was sought in 23 patients with acute rheumatic fever. Salivas from these patients were examined and compared with salivas from control subjects. As assayed, both IgG and IgA values ranged between 8 and 170 mg. per 100 ml. in 10-fold concentrated samples of saliva. When these values were corrected for the concentration of the samples and for the use of serum IgA standards, the following mean values were obtained: for patients with acute rheumatic fever, IgG was 4.5 mg. per 100 ml. and IgA was 8.7 mg. per 100 ml.; for control subjects, IgG was 5.0 mg per 100 ml. and IgA was 9.9 mg. per 100 ml. IgM was present in amounts of 1 to 2 mg. per 100 ml. in 2 patients and 7 control subjects. Antistreptolysin O titers correlated with amounts of IgG in the saliva samples while antihyaluronidase, antigroup A carbohydrate, and antiteichoic acid titers did not. None of the antibody titers correlated with the IgA content of the saliva samples. Furthermore, saliva antibody titers did not differ between patients with acute rheumatic fever and control subjects.

Acute Disease↗

PubMed1992

[Cardiolipin antibodies in acute rheumatic fever].

The paper presented the results obtained in studying the patients with acute rheumatic fever for antibodies to cardiolipin (ACL). The study resulted in the establishment that the development of immunopathies in the presence of acute rheumatic fever combined with the acute streptococcal infection was accompanied by hyperproduction of ACL (more common IgG versus IgM isotypes). The phenomenon mentioned widened the spectrum of acute infectious diseases associated with an increase in ACL synthesis. It was also stated that increased ACL contents were closely related with the involvement of the cardiac valves. Authentic clinical and echocardiological signs of the heart disease were mainly revealed in the patients with high contents of IgG and IgM isotypes of ACL. A certain relationship between the laboratory activity of the disease and ACL hyperproduction was noted as well. The latter permitted the discussion on the impact of streptococcal infection initiating the development of acute inflammation on the hyperproduction of ACL.

Acute Disease↗

PubMed1951