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Jerry Sebag, MD, FRCOphth; Alfredo A. Sadun, MD, PhD
Los Angeles, Calif

Arch Ophthalmol. 1996;114(9):1158-1159.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

In a recent article in the ARCHIVES, Chang et al¹ ascribed photoreceptor cell degeneration in patients with traumatic retinal detachment as being due to apoptosis. They based this claim on terminal deoxynucleotidyl transferase-mediated biotinylated deoxyuridine triphosphate nick end labeling (TUNEL)-positive labeling of photoreceptor nuclei in 7 (46.7%) of 15 eyes that were enucleated within 2 days after trauma. Furthermore, they found nicked nuclear DNA as early as 8 hours after trauma. This is of great interest since apoptosis is thought to represent genetically programmed cell death, which may be triggered by a variety of biochemical and other physiological factors. If apoptosis is found to be an important mechanism of photoreceptor cell degeneration soon after traumatic retinal detachment in humans, then it may be impossible to reverse the consequent degeneration. This may serve as an indication for the need for very early intervention in trauma. Such information might have an . . . [Full Text PDF of this Article]

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