Favizm Olgu Sunumu ile Glukoz 6- Fosfat Dehidrogenaz Eksikliğine Yaklaşım
Özet
Referanslar
Sodeman WA Jr, Sodeman TM. Sodeman’s Pathologic Physiology Mechanism of Disease, 1985. Çev: kurul, Fizyopatoloji cilt-2, Ankara:Türkiye Klinikleri Yayınevi, 1991:720-724
Mason PJ, Bautista JM, Gilsanz F. G6PD deficiency: The genotypephenotype 16. association. Blood Rev 2007;21:267-83
Nathan DG, Orkin SH. Glucose-6-phosphate dehydrogenase deficiency and hemolytic anemia. In: Nathan and Oski’s hematology of infancy and childhood. 7th ed. Philadelphia: W. B. Saunders, 2009: 883-900.
Nkhoma ET, Poole C, Vannappagari V, Hall SA, & Beutler E. The global prevalence of glucose-6-phosphate dehydrogenase deficiency: a systematic review and meta-analysis. Blood Cells, Molecules, and Diseases. 2009;42(3): 267-278.
Altay Ç, Gümrük F. Red cell glucose-6- phosphate dehydrogenase deficiency in Turkey. Turk J Hematol. 2008;25(1):1-7.
Mehta AB. Glucose-6-phosphate dehydrogenase deficiency. Postgraduate Medical Journal. 1994; 70(830): 871-877.
Wajcman H, Galactéros F. Glucose 6-phosphate dehydrogenase deficiency: a protection against malaria and a risk for hemolytic accidents. Comptes Rendus Biologies, 2004; 327(8): 711-720.
Gómez-Manzo S, Marcial-Quino J, Vanoye-Carlo A, et al. Glucose-6-phosphate dehydrogenase: update and analysis of new mutations around the world. International Journal of Molecular Sciences. 2016; 17(12): 2069.
Beutler E. Glucose-6-phosphate dehydrogenase deficiency: a historical perspective. Blood. 2008; 111(1): 16-24.
Song M. Preventing favism by selecting faba bean mutants using molecular markers. STEM Fellowship Journal.2017; 3(1): 2-6.
Arese P, Gallo V, Pantaleo A, Turrini F. Life and death of glucose-6-phosphate dehydrogenase (G6PD) deficient erythrocytes–role of redox stress and band 3 modifications. Transfusion Medicine and Hemotherapy. 2012; 39(5): 328-334.
Ahmed SN. Do favic patients resume fava beans ingestion later in their life, a study for this, and a new hypothesis for favism etiology. Hematology/Oncology and Stem Cell Therapy.2013; 6(1): 9-13.
Referanslar
Sodeman WA Jr, Sodeman TM. Sodeman’s Pathologic Physiology Mechanism of Disease, 1985. Çev: kurul, Fizyopatoloji cilt-2, Ankara:Türkiye Klinikleri Yayınevi, 1991:720-724
Mason PJ, Bautista JM, Gilsanz F. G6PD deficiency: The genotypephenotype 16. association. Blood Rev 2007;21:267-83
Nathan DG, Orkin SH. Glucose-6-phosphate dehydrogenase deficiency and hemolytic anemia. In: Nathan and Oski’s hematology of infancy and childhood. 7th ed. Philadelphia: W. B. Saunders, 2009: 883-900.
Nkhoma ET, Poole C, Vannappagari V, Hall SA, & Beutler E. The global prevalence of glucose-6-phosphate dehydrogenase deficiency: a systematic review and meta-analysis. Blood Cells, Molecules, and Diseases. 2009;42(3): 267-278.
Altay Ç, Gümrük F. Red cell glucose-6- phosphate dehydrogenase deficiency in Turkey. Turk J Hematol. 2008;25(1):1-7.
Mehta AB. Glucose-6-phosphate dehydrogenase deficiency. Postgraduate Medical Journal. 1994; 70(830): 871-877.
Wajcman H, Galactéros F. Glucose 6-phosphate dehydrogenase deficiency: a protection against malaria and a risk for hemolytic accidents. Comptes Rendus Biologies, 2004; 327(8): 711-720.
Gómez-Manzo S, Marcial-Quino J, Vanoye-Carlo A, et al. Glucose-6-phosphate dehydrogenase: update and analysis of new mutations around the world. International Journal of Molecular Sciences. 2016; 17(12): 2069.
Beutler E. Glucose-6-phosphate dehydrogenase deficiency: a historical perspective. Blood. 2008; 111(1): 16-24.
Song M. Preventing favism by selecting faba bean mutants using molecular markers. STEM Fellowship Journal.2017; 3(1): 2-6.
Arese P, Gallo V, Pantaleo A, Turrini F. Life and death of glucose-6-phosphate dehydrogenase (G6PD) deficient erythrocytes–role of redox stress and band 3 modifications. Transfusion Medicine and Hemotherapy. 2012; 39(5): 328-334.
Ahmed SN. Do favic patients resume fava beans ingestion later in their life, a study for this, and a new hypothesis for favism etiology. Hematology/Oncology and Stem Cell Therapy.2013; 6(1): 9-13.
