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PubMed2003

Angiotensin-converting enzyme genotype predicts valve damage in acute rheumatic fever.

BACKGROUND AND AIM OF THE STUDY: The genetic basis for host susceptibility to subsequent valve damage and scarring is not well defined in patients with a history of acute rheumatic fever (ARF). A high angiotensin-converting enzyme (ACE) activity has been demonstrated in valve tissue; hence, the study aim was to determine whether the ACE-DD genotype was a predisposing factor to heart valve damage after ARF attack. METHODS: A total of 165 patients diagnosed previously (16 +/- 5 years ago) with ARF was evaluated. Diagnoses were conducted according to Jones' criteria, and all received similar treatment and remain on regular penicillin prophylaxis. The ACE genotype was determined using polymerase chain reaction methods. RESULTS: Echocardiography showed that 39 patients (11 males, 28 females; mean age 25 +/- 6 years) had completely normal valves, and 126 patients (38 males, 88 females; mean age 21 +/- 6 years) had valve disease. The mitral valve was involved in 93% of patients (stenosis 86%, regurgitation 69%), and the aortic valve in 50% (stenosis 19%, regurgitation 48%). The ACE-DD genotype is associated with a significantly greater risk of valve involvement (risk ratio 2.7, 95% CI 1.15-6.5, p = 0.02). The distribution of genotypes was similar between aortic and mitral valve involvement. CONCLUSION: In patients with acute rheumatic fever the ACE-DD genotype is associated with an increased risk of subsequent heart valve damage.

Adolescent↗
PubMedDate not supplied

[Rheumatic fever--exacerbation or decline? Analysis of patients admitted to a medical service within a period of 20 years].

The authors revised 116 clinical files of patients admitted to a Medicine ward with Rheumatic Fever in the years 1959-63 and 1979-83, in order to detect a possible recrudescence of the disease. The following parameters were analysed: age, sex, length of hospital stay, clinical manifestations, ancillary exams, therapeutics and evolution. It was found an impressive decline in the incidence of the disease (90 cases vs 26) and also a very significant decrease of the period of hospitalization in the recent group of patients (p less than 0.0005); Carditis and relapses of Rheumatic Fever were more frequent in the old group of patients.

Adolescent↗
PubMed1987

Presumptive evidence for an immunosuppressor susceptibility gene, linked to HLA, in rheumatic fever.

In a study of rheumatic carditis, 135 members of 21 multiplex families have been investigated, along with 60 normal unrelated control individuals. Circulating T-lymphocytes were reduced (as a percentage of total blood mononuclear cells) in all 'rheumatic' individuals, in 7 of 40 normal parents, and in 8 of 49 normal sibs. An immune response characterized by an increase in the proportion of suppressor T cells occurs in most individuals affected by rheumatic carditis and this change persists for a long time. Genetic analysis revealed three important points: 1. increased HLA haplotype sharing amongst the affected sib-pairs; 2. the possibility of using low circulating T-cell percentage as a marker of susceptibility; 3. presumptive evidence for a recessive susceptibility gene linked to HLA and responsible for the suppressor cell response.

Female↗
PubMed1989

Evidence for two distinct classes of streptococcal M protein and their relationship to rheumatic fever.

The antigenic relatedness of surface-exposed portions of M protein molecules derived from group A streptococcal isolates representing more than 50 distinct serotypes was examined. The data indicate that the majority of serotypes fall into two major classes. Class I M protein molecules share a surface-exposed, antigenic domain comprising the C repeat region defined for M6 protein. The C repeat region of M6 protein is located adjacent to the COOH-terminal side of the pepsin-susceptible site. In contrast, Class I M proteins display considerably less antigenic relatedness to the B repeat region of M6 protein, which lies immediately NH2-terminal to the pepsin site. Surface-exposed portions of Class II M proteins lack antigenic epitopes that define the Class I molecules. Studies in the 1970s demonstrated that M protein serotypes can be divided into two groups based on both immunoreactivity directed to an unknown surface antigen (termed M-associated protein) and production of serum opacity factor. These two groups closely parallel our current definition of Class I and Class II serotypes. Both classes retain the antiphagocytic property characteristic of M protein, and Class II M proteins share some immunodeterminants with Class I M proteins, although the shared determinants do not appear to be exposed on the streptococcal surface. Nearly all streptococcal serotypes associated with outbreaks of acute rheumatic fever express M protein of a Class I serotype. Thus, the surface-exposed, conserved C repeat domain of Class I serotypes may be a virulence determinant for rheumatic fever.

Antigens, Bacterial↗
PubMed1981

[Liver changes in acute rheumatic fever].

Following the course of disease in a 19 year old patient with acute rheumatic fever we report the reaction of the liver parenchyma: on histological examination besides a marked steatosis several "unspecific" granulomas were seen. Nutritional and toxic factors were excluded aetiologically. Difficulties in diagnosis and differential diagnosis of acute mono/poly-arthritis as a leading symptom are discussed.

Acute Disease↗