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Nonarteritic anterior ischemic optic neuropathy associated with chronic anemia: a case series of myelodysplastic syndrome patients

INTRODUCTION: We report on three cases of visual loss due to nonarteritic anterior ischemic optic neuropathy that developed during the course of refractory anemia, a subtype of myelodysplastic syndrome. PATIENTS AND METHODS: Patients underwent fundus, visual field examination, and fluorescein angiog...

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Detalles Bibliográficos
Autores principales: Brouzas, Dimitrios, Charakidas, Antonios, Ladas, Ioannis, Apostolopoulos, Michael
Formato: Texto
Lenguaje:English
Publicado: Dove Medical Press 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2709018/
https://www.ncbi.nlm.nih.gov/pubmed/19668557
Descripción
Sumario:INTRODUCTION: We report on three cases of visual loss due to nonarteritic anterior ischemic optic neuropathy that developed during the course of refractory anemia, a subtype of myelodysplastic syndrome. PATIENTS AND METHODS: Patients underwent fundus, visual field examination, and fluorescein angiography. A thrombophilic tendency investigation including prothrombin time, partial thromboplastin time, protein C, free protein S, and antithrombin III, polymerase chain reaction and hybridisation to allele-specific oligonucleotide probes and a bone marrow biopsy were also performed. RESULTS: Relative recovery of visual function was noted in two patients, a 58-year-old man and a 67-year-old woman, whereas the vision of the third patient, a 62-year-old man, showed only marginal improvement during the follow-up period. Two patients received vigorous blood transfusion during hospitalization, while dosage adjustment of the erythropoietin infusion was decided for the third one. Thrombophilic tendency was not identified in any patient. DISCUSSION: Chronic anemia, as presented in myelodysplastic syndrome’s refractory anemia subtype, probably in the presence of additional factors, such as hypotension, is likely to be complicated by optic neuropathy, possibly through a mechanism of anemic hypoxia and/or microvascular insufficiency.