Treatment of Experimental Siderosis Bulbi, Vitreous Hemorrhage, and Corneal Bloodstaining With Deferoxamine
- 1 May 1966
- journal article
- research article
- Published by American Medical Association (AMA) in Archives of Ophthalmology (1950)
- Vol. 75 (5), 698-707
- https://doi.org/10.1001/archopht.1966.00970050700023
Abstract
The retention of an iron foreign body within an eye almost always results in progressive iron deposition throughout the eye, cataract formation, glaucoma, and eventually atrophy of all the intraocular tissues. This condition is known as siderosis bulbi.1 To prevent it, any intraocular iron particle must be removed surgically, if possible, even if the surgery itself may result in loss of the eye. Once siderosis is established, surgery seldom helps.2 Furthermore, as in two patients seen at the Wilmer Clinic recently, small iron particles may oxidize to nonmagnetic rust which cannot be localized or surgically extracted. Medical therapy of siderosis has been attempted using galvanic deactivation,3 intravenous edetic acid,4,5 and subconjunctival edetic acid or adenosine triphosphate.6,7 Edetic acid (formerly known as edathamil), the principal agent studied, has shown a number of toxic effects in humans receiving chronic systemic therapy.8,9 In 1960, Bickel et alThis publication has 4 references indexed in Scilit:
- Desferrioxamine in the Treatment of Acute Toxic Reaction to Ferrous GluconateJAMA, 1963
- Treatment of Primary and Secondary Hemochromatosis and Acute Iron Poisoning with a New, Potent Iron-Eliminating Agent (Desferrioxamine-B)New England Journal of Medicine, 1963
- INHIBITION OF COUPLED PHOSPHORYLATION IN BRAIN HOMOGENATES BY FERROUS SULFATE1948
- Histochemical Demonstration of Acid Polysaccharides in Animal TissuesNature, 1946