Journal of clinical immunology · 2002
Griscelli disease: genotype-phenotype correlation in an array of clinical heterogeneity.
СтатьяПоддержка исследования: вне правительства СШАНазвание 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.
Sanal Ozden, Ersoy Fúgen, Tezcan Ilhan, Metin Ayşe, Yel Leman, Ménasché Gaël, Gürgey Aytemiz, Berkel Izzet, de Saint Basile Geneviève
Аннотация
Griscelli disease is a rare autosomal recessive disorder characterized by diffuse pigmentary dilution and occurrence of acute phases of uncontrolled lymphocyte and macrophage activation, so-called "hemophagocytic syndrome" (HS) that leads to death. Recently, two closely linked genes located on human 15q21 region have been found to be responsible for the disease. We present clinical and laboratory findings of 13 unrelated patients with Griscelli disease as well as mutation analyses in an effort to define a genotype-phenotype correlation. Eight patients who showed RAB27A mutations presented with HS. In contrast, two patients who primarily presented with a neurological impairment in the absence of infection susceptibility or HS were found to have homozygous MYO5A mutations. No mutation in RAB27A could be detected in the other three patients. One of the latter developed HS at a rather late age, while the other two are free of HS at 12 and 15 years of age. Griscelli disease presents with a heterogeneous clinical picture that seems to reflect the involved gene defect. This genotype-phenotype correlation suggests that the natural course of the disease and outcome is dictated by the site and type of the genetic mutation.
Предметные рубрики MeSH
AdolescentChildChild, PreschoolChromosomes, Human, Pair 15FemaleGenes, RecessiveGenotypeHistiocytosis, Non-Langerhans-CellHumansHypopigmentationImmunologic Deficiency SyndromesInfantLymphocyte ActivationMacrophage ActivationMaleMutationMyosin Type VPhenotypeSyndromerab GTP-Binding Proteinsrab27 GTP-Binding Proteins