In a population based study of 68 individuals with atopic dermatitis and 94 control individuals it was not possible to demonstrateany significant associations between the disease and gene frequencies of HLA-ABC, ABO, MN, Rhesus, Kell, Duffy, Hp, Gc, Gm, Km/Inv, PGM, AcP, GPT, EsD, GLO, AK, PGD, ADA, and GALT/Gt.
In a population based study of 68 individuals with atopic dermatitis and 94 control individuals it was not possible to demonstrateany significant associations between the disease and gene frequencies of HLA-ABC, ABO, MN, Rhesus, Kell, Duffy, Hp, Gc, Gm, Km/Inv, PGM, AcP, GPT, EsD, GLO, AK, PGD, ADA, and GALT/Gt.
In a population based study of 68 individuals with atopic dermatitis and 94 control individuals it was not possible to demonstrateany significant associations between the disease and gene frequencies of HLA-ABC, ABO, MN, Rhesus, Kell, Duffy, Hp, Gc, Gm, Km/Inv, PGM, AcP, GPT, EsD, GLO, AK, PGD, ADA, and GALT/Gt.
In a population based study of 68 individuals with atopic dermatitis and 94 control individuals it was not possible to demonstrateany significant associations between the disease and gene frequencies of HLA-ABC, ABO, MN, Rhesus, Kell, Duffy, Hp, Gc, Gm, Km/Inv, PGM, AcP, GPT, EsD, GLO, AK, PGD, ADA, and GALT/Gt.
In a population based study of 68 individuals with atopic dermatitis and 94 control individuals it was not possible to demonstrateany significant associations between the disease and gene frequencies of HLA-ABC, ABO, MN, Rhesus, Kell, Duffy, Hp, Gc, Gm, Km/Inv, PGM, AcP, GPT, EsD, GLO, AK, PGD, ADA, and GALT/Gt.
From this and other previous works, we can conclude that an individual whose right hand tda angle reaches values near 75%, and with a MZ phenotype of alpha 1 antitrypsin, has a greater possibility of pertaining to one of the groups of asthma, atopic dermatitis and rhinitis symptomatology.
In an attempt to determine whether IL-5 is generated by eosinophils in atopic dermatitis we have used i) in situ hybridization with 35S-labeled IL-5 RNA probe combined with immunohistochemistry using a monoclonal antibody (MoAb) (EG2) directed against the activated form of Eosinophil Cationic Protein (ECP) and ii) double-immunostaining with anti-IL-5 MoAb and polyclonal anti-ECP antibody.