Disease relevance of Rheumatic Fever

• Orally administered clindamycin and penicillin were compared for effectiveness in preventing streptococcal infections in 202 randomly assigned patients with previous rheumatic fever (RF) [1].
• Serological data with acute poststreptococcal glomerulonephritis (APSGN) and acute rheumatic fever sera indicated that the protein reacts preferentially with APSGN sera [2].
• The cost-effectivness of preventing primary acute rheumatic fever attacks by oral or benzathine penicillin treatment was analyzed for both epidemic and endemic streptococcal pharyngitis situations [3].
• Prevention of Bacterial Endocarditis. A statement for health professionals by the Committee on Rheumatic Fever and Infective Endocarditis of the Council on Cardiovascular Disease in the Young [4].
• In our study overlapping synthetic peptides copying the entire sequence of PepM5 protein were used to map the myosin cross-reactive epitopes of streptococcal M protein recognized by mouse and human mAb and affinity purified myosin-specific antibodies from acute rheumatic fever and rheumatic heart disease sera [5].

Psychiatry related information on Rheumatic Fever

• Patient compliance with prophylactic benzathine penicillin for rheumatic fever [6].
• D8/17 and CD19 expression on lymphocytes of patients with acute rheumatic fever and Tourette's disorder [7].
• The authors investigated obsessive-compulsive behavior, obsessive-compulsive disorder (OCD), and attention deficit and hyperactivity disorder (ADHD) in 50 healthy subjects, 50 patients with rheumatic fever without chorea, and 56 patients with Sydenham chorea [8].

High impact information on Rheumatic Fever

• Decreased serum salicylate concentrations in children with rheumatic fever treated with antacid [9].
• To determine if the common practice of giving antacids to patients on salicylate therapy has an effect on serum salicylate concentrations, we gave a widely used antacid, aluminum and magnesium hydroxide, and aspirin concomitantly to three children with rheumatic fever [9].
• Ibuprofen and aspirin in acute rheumatic fever [10].
• In the late 1960s and the 1970s, studies showed that in private practice settings with counseling as to the need to take oral penicillin for a full ten days to prevent rheumatic fever, good compliance with results equal to intramuscular penicillin G benzathine could be achieved [11].
• This study shows that serotype M3 and M18 S. pyogenes isolated during outbreaks of rheumatic fever have the unique capability to bind and aggregate human basement membrane collagen type IV [12].

Chemical compound and disease context of Rheumatic Fever

• In areas where rheumatic fever is still prevalent, particularly in poor and crowded inner-city populations where medical care is episodic, follow-up may be lacking, and compliance in taking oral penicillin cannot be relied on, treatment with intramuscular penicillin G benzathine remains preferred [11].
• Anti-streptococcal antibodies cross-reactive with N-acetyl-betaD-glucosamine (GlcNAc) and myosin are present in the sera of patients with rheumatic fever (RF) [13].
• A 12-15-h incubation of lymphocytes at 37 degrees C in 5% CO2-air showed persistence of CRP binding in substantial proportions of cells particularly in acute rheumatic fever [14].
• The story of the prevention of rheumatic fever has a large cast of characters, but special recognition must be given to Coburn for his observations confirming the role of the hemolytic streptococcus published in 1931 and showing the prophylactic value of sulfanilamide published in 1939 [15].
• However, the effect of fluoride on group A streptococci that causes rheumatic fever and acute poststreptococcal glomerulonephritis is not known [16].

Biological context of Rheumatic Fever

• These data provide evidence that fluoride causes decreased expression by S. pyogenes proteins used to respond to stress, virulence factors, and implicated in non-suppurative complications of S. pyogenes, including glomerulonephritis and rheumatic fever [16].
• Molecular mimicry or epitope similarity between group A streptococcal M proteins and myosin may contribute to the presence of heart reactive antibodies in acute rheumatic fever [5].
• In conclusion, it was found that exposure to pharyngeal infection with group A beta haemolytic streptococci may lead to acute rheumatic fever in those with an inherited recessive gene responsible for high responsiveness to the streptococcal polysaccharide antigen of the cell wall [17].
• This observation increases the significance of the previously observed sequence homology between streptococcal M protein and rabbit skeletal tropomyosin and may have relevance to the pathogenesis of rheumatic fever [18].
• The aim of the present study was to evaluate the DNA damage in children receiving one dose of 1.2 million units benzathine penicillin every 4 weeks over a long period to prevent recurrences of rheumatic fever [19].

Anatomical context of Rheumatic Fever

• CRP-binding lymphocytes may represent a marker for immunologically committed cells in acute rheumatic fever [14].
• Low density neutrophils in patients with systemic lupus erythematosus, rheumatoid arthritis, and acute rheumatic fever [20].
• The relative frequency of rheumatic fever has decreased and the most common cause is now primary mitral valve prolapse (PMVP) which accounts for 60% of all patients [21].
• Detection of antibodies to muramyl dipeptide, the adjuvant moiety of streptococcal cell wall, in patients with rheumatic fever [22].
• Failure to eradicate streptococci from patients can occasionally lead to rheumatic fever and rarely to glomerulonephritis. beta-lactamase-producing strains of aerobic and anaerobic bacteria in inflamed tonsils have been associated with increased failure rates of penicillins in the eradication of these infections [23].

Gene context of Rheumatic Fever

• DRB1, DQA1, DQB1 genes in Turkish children with rheumatic fever [24].
• IL-7 concentrations remained unchanged during different stages of rheumatic fever [25].
• Plasma interleukin-7 (IL-7) and IL-8 concentrations in acute rheumatic fever and chronic rheumatic heart disease [25].
• Plasma concentrations of inflammatory cytokines (IL-1 alpha, IL-1 beta, IL-6, IL-8 and TNF alpha) 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 [26].
• The DRB1 genotyping results were compared with those in 33 patients with rheumatic fever and 190 normal individuals [27].

Analytical, diagnostic and therapeutic context of Rheumatic Fever

• METHODS: Echocardiography and assessment of cardiac troponin I (cTnI) blood levels were systematically performed in 95 consecutive patients with acute rheumatic fever, who were divided into three groups [28].
• Sera of patients with suspected rheumatic fever and elevated titers of antibody to streptolysin O were examined by an immunoblotting technique [29].
• The occurrence of IgE and IgG antibodies to penicillin G and V in children on long-term treatment with penicillin as secondary prophylaxis for rheumatic fever was studied using Phadebas RAST (Pharmacia Diagnostics, Uppsala, Sweden) and ELISA respectively [30].
• Evaluation of DNA damage using the comet assay in children on long-term benzathine penicillin for secondary prophylaxis of rheumatic fever [19].
• 2. High levels of immune complexes, observed in the sera of patients with rheumatic fever, reduced markedly following plasmapheresis [31].

References