نتایج جستجو برای: کمبود آنزیم g6pd

تعداد نتایج: 25849  

2011
Saorin Kim Chea Nguon Bertrand Guillard Socheat Duong Sophy Chy Sarorn Sum Sina Nhem Christiane Bouchier Magali Tichit Eva Christophel Walter R. J. Taylor John Kevin Baird Didier Menard

Development of reliable, easy-to-use, rapid diagnostic tests (RDTs) to detect glucose-6-phosphate dehydrogenase (G6PD) deficiency at point of care is essential to deploying primaquine therapies as part of malaria elimination strategies. We assessed a kit under research and development called CareStart™ G6PD deficiency screening test (Access Bio, New Jersey, USA) by comparing its performance to ...

Journal: :Journal of infection in developing countries 2015
Seyed Mehdi Tabatabaei Alireza Salimi Khorashad Mohammad Sakeni Ahmad Raeisi Zahra Metanat

INTRODUCTION Glucose-6-phosphate dehydrogenase deficiency (G6PD) is an X-linked genetic disorder with a relatively high frequency in malaria-endemic regions. It is an obstacle to malaria elimination, as primaquine administered in the treatment of malaria can cause hemolysis in G6PD-deficient individuals. This study presents information on the prevalence of G6PD deficiency in Sistan and Balouche...

Journal: :Haematologica 2005
Naif S Karadsheh Linda Moses Said I Ismail Joseph M Devaney Eric Hoffman

Molecular screening for glucose-6-phosphate (G6PD) mutations in two Jordanian populations revealed six different mutations and higher incidences of G6PD deficiency and G6PD A- (376A-->G + 202G-->A) mutation in Jordan Valley than in the Amman area. These observations may be explained by historically higher rates of malaria and African ancestral origins, respectively.

Journal: :Genetics 1988
P A Carter W B Watt

The polymorphic phosphoglucomutase (PGM) and glucose-6-phosphate dehydrogenase (G6PD) loci have been studied in parallel to experimental work on the phosphoglucose isomerase (PGI) polymorphism in Colias butterflies. PGI, PGM and G6PD are also autosomal in Colias. PGM and G6PD are loosely linked (and represent the first identified autosomal linkage group in Colias); they assort independently fro...

2017
Geraldine M Clarke Kirk Rockett Katja Kivinen Christina Hubbart Anna E Jeffreys Kate Rowlands Muminatou Jallow David J Conway Kalifa A Bojang Margaret Pinder Stanley Usen Fatoumatta Sisay-Joof Giorgio Sirugo Ousmane Toure Mahamadou A Thera Salimata Konate Sibiry Sissoko Amadou Niangaly Belco Poudiougou Valentina D Mangano Edith C Bougouma Sodiomon B Sirima David Modiano Lucas N Amenga-Etego Anita Ghansah Kwadwo A Koram Michael D Wilson Anthony Enimil Jennifer Evans Olukemi K Amodu Subulade Olaniyan Tobias Apinjoh Regina Mugri Andre Ndi Carolyne M Ndila Sophie Uyoga Alexander Macharia Norbert Peshu Thomas N Williams Alphaxard Manjurano Nuno Sepúlveda Taane G Clark Eleanor Riley Chris Drakeley Hugh Reyburn Vysaul Nyirongo David Kachala Malcolm Molyneux Sarah J Dunstan Nguyen Hoan Phu Nguyen Ngoc Quyen Cao Quang Thai Tran Tinh Hien Laurens Manning Moses Laman Peter Siba Harin Karunajeewa Steve Allen Angela Allen Timothy Me Davis Pascal Michon Ivo Mueller Síle F Molloy Susana Campino Angeliki Kerasidou Victoria J Cornelius Lee Hart Shivang S Shah Gavin Band Chris Ca Spencer Tsiri Agbenyega Eric Achidi Ogobara K Doumbo Jeremy Farrar Kevin Marsh Terrie Taylor Dominic P Kwiatkowski

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is believed to confer protection against Plasmodium falciparum malaria, but the precise nature of the protective effecthas proved difficult to define as G6PD deficiency has multiple allelic variants with different effects in males and females, and it has heterogeneous effects on the clinical outcome of P. falciparum infection. Here we report a...

2005
A. Morelli U. Benatti L. Lenzerini B. Sparatore F. S. Pontremoli A. De Flora

T HE MEDITERRANEAN variety of glucose-6phosphate dehydrogenase (G6PD) deficiency is characterized by severely decreased catalytic activity in the affected erythrocytes and is therefore classified as belonging to class II in the usual tabulations of G6PD variants.’ However, evidence has been provided that in Mediterranean countries there are several polymorphic G6PD variants sharing activity lev...

Journal: :Archives of disease in childhood 1981
K L Tan

Neonatal jaundice and its relationship to glucose-6-phosphate dehydrogenase (G6PD) status of healthy, term Chinese infants was evaluated in 220 G6PD-deficient infants, 26 intermediate infants who were observed for 3 weeks, and 116 normal (control) infants. Each infant was free of isoimmunisation, cephalhaematomas, or contusions. The mode of labour, method of delivery, and type of feeds had no a...

Journal: :Blood 1993
D T Chiu L Zuo L Chao E Chen E Louie B Lubin T Z Liu C S Du

The underlying DNA changes associated with glucose-6-phosphate dehydrogenase (G6PD)-deficient Asians have not been extensively investigated. To fill this gap, we sequenced the G6PD gene of 43 G6PD-deficient Chinese whose G6PD was well characterized biochemically. DNA samples were obtained from peripheral blood of these individuals for sequencing using a direct polymerase chain reaction (PCR) se...

2016
Pradeep Kumar Upendra Yadav Vandana Rai

G6PD deficiency; Hemolytic anemia; Meta-analysis; Prevalence Abstract Background: Glucose-6-phosphate dehydrogenase (G6PD) is a house keeping enzyme which catalyzes the first step in the hexose monophosphate pathway of glucose metabolism. G6PD deficiency is the commonest hemolytic X-linked genetic disease, which affects approximately 400 million people worldwide. The prevalence rate of G6PD def...

Journal: :Blood 2000
A Rovira M De Angioletti O Camacho-Vanegas D Liu V Rosti H F Gallardo R Notaro M Sadelain L Luzzatto

Many mutations of the housekeeping gene encoding glucose-6-phosphate dehydrogenase (G6PD) cause G6PD deficiency in humans. Some underlie severe forms of chronic nonspherocytic hemolytic anemia (CNSHA) for which there is no definitive treatment. By using retroviral vectors pseudotyped with the vesicular stomatitis virus G glycoprotein that harbor the human G6PD (hG6PD) complementary DNA, stable ...

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