[Biochemical and molecular diagnosis of Gaucher disease in Tunisia].

نویسندگان

  • A Dandana
  • S Ferchichi
  • S Khedhiri
  • L Chkioua
  • Z Jaidane
  • K Monastiri
  • S Ben Khelifa
  • R Ben Mansour
  • I Maire
  • R Froissart
  • V Bonnet
  • S Laradi
  • A Miled
چکیده

Our study was carried out at a family from the Sahel (Tunisia). The father (index case) and his two children (son and daughter). The father beta-glucocerebrosidase (GCB) activity showing a deficit. These biochemical analyses are supplemented by molecular studies: enzymatic digestion and the direct sequencing. Two mutations were analysed, the p.Asn 370 Ser and the p.Leu 444 Pro. The DNA sequencing confirmed the presence of the homozygous genotype of this p.Asn 370 Ser in the father DNA and the heterozygous one in the two children DNA. It has no detection of the 55 pb deletion in exon 9 among all the specimens of DNA treated. The mutation p.Asn 370 Ser is associated with Gaucher disease type 1 correlated of a total absence of neurological involvements.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Report of Four Children with Gaucher Disease and Review of Literature

Gaucher Disease (GD) is the most common type of Lysosomal Storage Disorder and it is divided into three distinct subtypes. The authors here report four different cases of Gaucher Disease, with varying clinical manifestations, and the diagnosis of each established by the low level of Beta-Glucosidase enzyme as well as genetic DNA testing. The study also highlights the importance of early diagnos...

متن کامل

P-111: An Attempt to Facilitate the Production of Transgenic Mouse As A Model for Gene Therapy of Gaucher Disease

Background: Gaucher disease is an autosomal recessive inherited lysosomal storage disorder that affects many of the body's organs and tissues by defective function of the catabolic enzyme β-glucocerebrosidase. Gene therapy is one of the efficient ways for treatment of this disease. Due to the lack of appropriate animal models, in the field of gene therapy little progress has been done.Mate...

متن کامل

Substrate reduction therapy as a new treatment option for patients with Gaucher disease type 1: A review of literatures

of glucosylceramide and glucosylsphingosine in lysosomes of tissue macrophages and consequently leads to multisystemic manifestations. Clinical symptoms of GD1 include hepatosplenomegaly, anemia, thrombocytopenia, pulmonary diseases, immune dysfunction and bone disease. The diagnosis of GD1 is confirmed by demonstrating decreased activity of acid β-glucosidase in leukocytes and/or by molecular ...

متن کامل

Comparative study on glucocerebrosidase in spleens from patients with Gaucher disease.

In Gaucher disease (glucosylceramide lipidosis), deficiency of glucocerebrosidase causes pathological storage of glucosylceramide, particularly in the spleen. A comparative biochemical and immunological analysis has therefore been made of glucocerebrosidase in spleens from normal subjects (n = 4) and from Gaucher disease patients with non-neuronopathic (n = 5) and neuronopathic (n = 5) phenotyp...

متن کامل

Mutational Analysis and Genotype Investigation of Less Known Gaucher Mutations through Haplotype Analysis in Iranian Gaucher patients

Gaucher's disease (GD) is the most frequent lysosomal storage disorder resulting from a deficiency of the enzyme glucocerebrosidase (GBA) which causes the accumulation of glucocerebroside. More than 500 mutations have been reported on the GBA gene so far. In this study, we aimed to investigate more on the genotype of less known mutations through haplotype analysis to explain their disease-causi...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Annales de biologie clinique

دوره 65 6  شماره 

صفحات  -

تاریخ انتشار 2007