Photorefractive keratectomy and laser in situ keratomileusis: a word from the devil's advocate.
Arch Ophthalmol. 2000 Dec;118(12):1706-7.
At a time when there has been a significant improvement in the technology of treatment of refractive errors by laser in-situ keratomileusis (LASIK), this author has issued a very timely warning both to patients undergoing the procedure and to the people performing LASIK.
The procedure involves a laser beam at 193nm that evaporates part of the cornea, breaking cells and molecules to create the smooth corneal surface necessary for best optical results.
The creation of free radicals, is an inseparable part of the cornea reshaping process. Both photorefractive keratectomy (PRK) and LASIK are known to cause keratocyte apoptosis in the corneae of laboratory animals and hence, though there is no short-term damage, long-term damage must be considered.
These procedures are also known to have caused biochemical and ultrastructural modifications in the lens, both of which are markers of cataractogenesis. The vitreous base, located just posterior to the lens may be affected by the same process that affects the cornea, anterior chamber and the lens. Free radicals damage the vitreous collagen, leading to vitreous liquefaction. They have also been shown to promote tumours.
PRK might initiate a cascade of events leading to slowly developing abnormalities of the cornea, lens, vitreous retina and choroid.
On one hand there is a marked increase in the popularity of LASIK promulgated by massive advertisement. Hence there is an urgent need for intensive research into the potential threats to ocular function caused by LASIK which may occur in patients decades after the initial procedure, slowly but almost surely.