Previous studies have indicated that CMA1 promoter polymorphism rs1800875 may be involved in regulating immunoglobulin E (IgE) levels in patients with eczema, and it is associated with the progression of immunoglobulin A nephropathy.
While the CMA1 promoter SNP (rs1800875) was not associated with DHF/DSS, the homozygous form of α-tryptase allele was associated with DSS patients in Vinh Long and the Philippines (OR=3.52, p<0.0001; OR=3.37, p<0.0001, respectively) and with DHF in Ho Chi Minh City (OR=2.54, p=0.0084).
While the CMA1 promoter SNP (rs1800875) was not associated with DHF/DSS, the homozygous form of α-tryptase allele was associated with DSS patients in Vinh Long and the Philippines (OR=3.52, p<0.0001; OR=3.37, p<0.0001, respectively) and with DHF in Ho Chi Minh City (OR=2.54, p=0.0084).
While the CMA1 promoter SNP (rs1800875) was not associated with DHF/DSS, the homozygous form of α-tryptase allele was associated with DSS patients in Vinh Long and the Philippines (OR=3.52, p<0.0001; OR=3.37, p<0.0001, respectively) and with DHF in Ho Chi Minh City (OR=2.54, p=0.0084).
To further investigate, we analyzed CMA1 promoter SNP (rs1800875) and TPSAB1 gene alleles, which encode the Human Chymase and α- and β- tryptase 1 enzymes respectively, for susceptibility to Dengue Hemorrhagic Fever (DHF) and Dengue Shock Syndrome (DSS) in patients from hospitals in Vietnam (Ho Chi Minh City and Vinh Long) and the Philippines.
The frequency of AA/AG genotypes of CMA rs1800875 and CC/CT genotype of CMA rs1800876 were significantly higher in patients with progressive disease course than in those with stable course (53.2 vs. 38.6%, p = 0.029; 89.6 vs. 78.3%, p = 0.031, respectively).
Previous studies have indicated that CMA1 promoter polymorphism rs1800875 may be involved in regulating immunoglobulin E (IgE) levels in patients with eczema, and it is associated with the progression of immunoglobulin A nephropathy.
The frequency of AA/AG genotypes of CMA rs1800875 and CC/CT genotype of CMA rs1800876 were significantly higher in patients with progressive disease course than in those with stable course (53.2 vs. 38.6%, p = 0.029; 89.6 vs. 78.3%, p = 0.031, respectively).
The frequency of AA/AG genotypes of CMA rs1800875 and CC/CT genotype of CMA rs1800876 were significantly higher in patients with progressive disease course than in those with stable course (53.2 vs. 38.6%, p = 0.029; 89.6 vs. 78.3%, p = 0.031, respectively).
The frequency of AA/AG genotypes of CMA rs1800875 and CC/CT genotype of CMA rs1800876 were significantly higher in patients with progressive disease course than in those with stable course (53.2 vs. 38.6%, p = 0.029; 89.6 vs. 78.3%, p = 0.031, respectively).
Results confirm previous observations of a significant association between the CMA1 promoter polymorphism rs1800875 and atopic eczema, but not with serum IgE levels, and support the hypothesis that CMA1 serves as candidate gene for atopic eczema.