The distribution of HLA-A, -B and -DR antigens as well as blood groups and secretor status was studied in sporadic, North Indian patients of rheumatic fever and rheumatic heart disease.
We studied the frequencies of red cell enzyme types, AcP, PGM1 and EsD in 213 patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), rheumatic heart disease (RHD), scleroderma (Scl) and psoriatic arthropathy (PsA).
Considering that in this investigation only RHD patients were included, further studies are necessary in order to clarify whether C4A6 is a marker for the cardiac form or for the disease itself.
Considering that in this investigation only RHD patients were included, further studies are necessary in order to clarify whether C4A6 is a marker for the cardiac form or for the disease itself.
Considering that in this investigation only RHD patients were included, further studies are necessary in order to clarify whether C4A6 is a marker for the cardiac form or for the disease itself.
To determine whether genetic factors could be involved in the pathogenesis of rheumatic heart disease (RHD), we analyzed the distribution of HLA-A, HLA-B, and HLA-DR antigens in Turkish patients with chronic rheumatic heart disease.
To determine whether genetic factors could be involved in the pathogenesis of rheumatic heart disease (RHD), we analyzed the distribution of HLA-A, HLA-B, and HLA-DR antigens in Turkish patients with chronic rheumatic heart disease.
HPA-1, HPA-3 and HPA-5 platelet phenotypes using PCR-RFLP and RhD phenotypes using amplification-refractory mutation system PCR were assessed in amniotic fluid and compared with those of fetal (15 times) or newborn (9 times) blood and with parental phenotypes (46 blood samples).
In three groups: acute rheumatic fever patients (no evidence of previous attacks of rheumatic fever), patients with chronic rheumatic heart disease and normal controls from the same population, we found a greater discriminating ability of PGI/MNII MAb to identify Indian RF/RHD patients than with the D8/17 MAb.
In three groups: acute rheumatic fever patients (no evidence of previous attacks of rheumatic fever), patients with chronic rheumatic heart disease and normal controls from the same population, we found a greater discriminating ability of PGI/MNII MAb to identify Indian RF/RHD patients than with the D8/17 MAb.
In three groups: acute rheumatic fever patients (no evidence of previous attacks of rheumatic fever), patients with chronic rheumatic heart disease and normal controls from the same population, we found a greater discriminating ability of PGI/MNII MAb to identify Indian RF/RHD patients than with the D8/17 MAb.
DQ alleles in linkage disequilibrium with DR alleles appear to influence risk/protection effect: whereas the DRB1*13-DQA1*0501-3-DQB1*0301 haplotype showed a trend toward risk, the DRB1*13-DQA1*0103-DQB1*0603 haplotype was absent in the RHD sample.
DQ alleles in linkage disequilibrium with DR alleles appear to influence risk/protection effect: whereas the DRB1*13-DQA1*0501-3-DQB1*0301 haplotype showed a trend toward risk, the DRB1*13-DQA1*0103-DQB1*0603 haplotype was absent in the RHD sample.
DQ alleles in linkage disequilibrium with DR alleles appear to influence risk/protection effect: whereas the DRB1*13-DQA1*0501-3-DQB1*0301 haplotype showed a trend toward risk, the DRB1*13-DQA1*0103-DQB1*0603 haplotype was absent in the RHD sample.
Rheumatic heart disease (RHD) is considered to be an autoimmune disorder mediated by group A streptococcal (GAS) M protein-specific T cells and antibodies that cross-react with cardiac antigens and epitopes of the GAS M protein.
The data demonstrate that RHD is associated with TNF-alpha polymorphisms in the Mexican population; however, these polymorphisms do not have relation with the valve damage.
A significant difference was seen in the distribution of allelic frequency between patients with RHD and control patients for TGF-beta1T869C polymorphism (P =.04).
The results were then compared with the RHD fetal genotype determined on amniotic cells and/or the RhD phenotype of the red blood cells of the infants at birth.