Central Retinal Vein Occlusion in Sickle Cell Disease

Hasan, Syed; Elbedawi, Mamoon; Castro, Oswaldo; Gladwin, Mark T.; Palestine, Alan G.

doi:10.1097/01.smj.0000100266.87750.f5

Cited by 6 publications

(8 citation statements)

References 12 publications

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“…Reprinted with permission from Nyffenegger et al 50 48 However, induction of iron deficiency in patients with SCD also raises concerns about an increased risk of thrombosis. [89][90][91][92] Until the effects of this experimental treatment on thrombosis risk are better characterized, it seems prudent to avoid enrolling patients with known thrombophilia or increased baseline risk of thrombosis.…”

Section: Animal Models For Treatment Of Scd With Iron Restrictionmentioning

confidence: 99%

Iron restriction in sickle cell disease: When less is more

Castro,

De Franceschi,

Ganz

et al. 2024

American J Hematol

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Primum non nocere! Can iron deficiency, an abnormality that causes anemia, benefit people with sickle cell disease (SCD) who already have an anemia? The published literature we review appears to answer this question in the affirmative: basic science considerations, animal model experiments, and noncontrolled clinical observations all suggest a therapeutic potential of iron restriction in SCD. This is because SCD's clinical manifestations are ultimately attributable to the polymerization of hemoglobin S (HbS), a process strongly influenced by intracellular HbS concentration. Even small decrements in HbS concentration greatly reduce polymerization, and iron deficiency lowers erythrocyte hemoglobin concentration. Thus, iron deficiency could improve SCD by changing its clinical features to those of a more benign anemia (i.e., a condition with fewer or no vaso‐occlusive events). We propose that well‐designed clinical studies be implemented to definitively determine whether iron restriction is a safe and effective option in SCD. These investigations are particularly timely now that pharmacologic agents are being developed, which may directly reduce red cell hemoglobin concentrations without the need for phlebotomies to deplete total body iron.

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Section: Animal Models For Treatment Of Scd With Iron Restrictionmentioning

confidence: 99%

Iron restriction in sickle cell disease: When less is more

Castro,

De Franceschi,

Ganz

et al. 2024

American J Hematol

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“…The search for risk factors for central retinal vein occlusion in this young patient revealed protein S deficiency and a history of iron deficiency. He was treated with anticoagulation therapy, and his vision improved gradually [11].…”

Section: Diagnosis Sickle Cell Retinopathy [10]mentioning

confidence: 99%

Retinal occlusion as an advanced complication of sickle cell disease

Alkhaibari¹

2016

New Front Ophthalmol

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Retinopathy is a one of the major clinical manifestation of Hemoglobinopathy. It is acquired secondary to another retinal disorder. Retinopathy especially retinal occlusions are painless loss of monocular vision it's from a vascular disorder. Ocular stroke caused by embolism in a retinal artery, that may emboli travel to distal branches of the retinal artery, causing loss of other section in the visual field. The manifestations of Sickle cell disease ocular manifestations came due to vascular occlusion, which may exist in the conjunctiva, iris, retina, and choroid. Because the ocular changes produced by SCD could be shown in other diseases, it's important to except other occlusions' causes, which have included central retinal vein occlusion, Eales disease, and retinopathy secondary to other chronic disorders. Other ocular changes cause that includes polycythemia vera, familial exudative vitreoretinopathy, talc and cornstarch emboli, and uveitis. Diagnosis of hemoglobenopathies is performed exclusively through Hb electrophoresis. The treatments and their results vary from one condition to the other.

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“…The patient was admitted to the local hospital where, other than his poor visual acuity, physical and neurological exams were within normal limits. Laboratory tests showed a hemoglobin of 7.4g/dL (normal 11.1-15.0g/dL), white count of 28,000/mm 3 (normal 3,400-9,600/mm 3 ), and platelet count of 461,000/mm 3 (normal 162-380,000/mm 3 ). Cranial computed tomography (CT) was normal.…”

Section: Introductionmentioning

confidence: 98%