Clinical laboratory · 2012
Complement and mannose-binding lectin 2 polymorphism in meningococcal disease.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Lima Filho Alberto, Carmo Rodrigo, Cavalcanti Maria, Vasconcelos Luydson, Moura Patricia, Silva Almerinda, Sarinho Emanuel
Аннотация
BACKGROUND: Meningococcal disease is a leading cause of death due to infection in children. Differences in susceptibility and disease progression between children are unknown. The complement system plays a key role in the innate immunity against N. meningitides and could explain that differences in the response of individuals. The aim of this study was to evaluate the occurrence of complement system deficiencies and MBL2 polymorphism in patients with previous meningococcal disease.
METHODS: We evaluated 40 children with confirmed previous diagnosis of any form of meningococcal disease and performed quantification analysis of the complement system; C3, C4, and CH50, as well the analysis of the polymorphism of the MBL2 gene.
RESULTS: The major deficiency was found for C4 (27.5%) followed by C3 and CH50 (2.5%). Genotyping of MBL2 showed 21 cases of homozygous wild type allele named AA, (55.3%), 14 cases heterozygous, AO (36.8%), and 3 homozygous variant alleles, OO, (7.9%).
CONCLUSIONS: Complement deficiency and polymorphism in the MBL2 gene are possible explanations for the development of meningococcal disease in some patients. Evaluation of complement could be suggested for individuals affected by this serious disease.
METHODS: We evaluated 40 children with confirmed previous diagnosis of any form of meningococcal disease and performed quantification analysis of the complement system; C3, C4, and CH50, as well the analysis of the polymorphism of the MBL2 gene.
RESULTS: The major deficiency was found for C4 (27.5%) followed by C3 and CH50 (2.5%). Genotyping of MBL2 showed 21 cases of homozygous wild type allele named AA, (55.3%), 14 cases heterozygous, AO (36.8%), and 3 homozygous variant alleles, OO, (7.9%).
CONCLUSIONS: Complement deficiency and polymorphism in the MBL2 gene are possible explanations for the development of meningococcal disease in some patients. Evaluation of complement could be suggested for individuals affected by this serious disease.