Please use this identifier to cite or link to this item: http://hdl.handle.net/20.500.12323/3685
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dc.contributor.authorNasrullayeva, Gulnara Mahammadali-
dc.contributor.authorMammadova, Vafa Rustam-
dc.contributor.authorKhalilova, Afaq Vladimr-
dc.contributor.authorShahgeldiyeva, Shabnam Eldar-
dc.date.accessioned2017-11-30T04:13:26Z-
dc.date.available2017-11-30T04:13:26Z-
dc.date.issued2017-
dc.identifier.issn2333-9721-
dc.identifier.issn2333-9705-
dc.identifier.urihttp://hdl.handle.net/20.500.12323/3685-
dc.description.abstractBackground: Agammaglobulinemia (AGM) is a genetic immune system disorder in which the body could not produce antibodies. There are two types of this disease: X-linked AGM (XLA) and autosomal forms. X-linked agammaglobulinemia results from a mutation in the gene for Bruton’s tyrosine kinase (BTK), found on the X chromosome. Mutations in BTK result in lack of mature B-cells and immunoglobulins of all classes. There are 8 types of autosomal forms which are reflected in different defective genes. 7-year-old male patient at the age of 1 - 6, was encountered the recurrent broncho-pulmonary and gastro-intestinal infections, furunculosis and recurrent otitis. Also, because of the strain, pain and swelling on the 4th finger of the right hand it was suspected that the patient had rheumatoid arthritis. On immunological investigation, we have found out of absent of B lymphocyte. Level of IgG was 10 times less; IgA, IgM and IgE levels were 3 to 8 times less than the norm. Quantity of T-lymphocytes: absolute number of CD4+ lymphocytes increased, CD3+ and CD8+ lymphocytes were also high. Phagocyte activity in NBT, absolute number of NK cells and IRI index were 2 times lower than the norm. Genetically analysis has discovered the presence of abnormal homozygous BLNK gene.en
dc.language.isoenen
dc.publisherOALib Journalen
dc.relation.ispartofseriesVol. 4;-
dc.subjectBLNK Geneen
dc.subjectRheumatoid Arthritisen
dc.subjectAgammaglobulinemiaen
dc.titleThe Novel Patient with BLNK Gene Type of Agammaglobulinemiaen
dc.typeArticleen
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