家兔PRK术后角膜的组织病理、免疫组化及超微结构的实验研究

目的 评价实验性家兔不同屈光度ＰＲＫ术后角膜创面愈合的过程及皮质类固醇对愈合的影响。方法 应用ＳＶＳ ＡＰＥＸ ＰＬＵＳ型准分子激光治疗系统对６只家兔双眼进行ＰＲＫ术,设定右眼－４．００Ｄ,左眼－８．００Ｄ。随机分为ＦＬＭ点眼组和ＣＭ点眼组,每组３只家兔,ＦＬＭ点眼组双眼滴皮质类固醇激素眼液（０．１％ｆｌｕｏｒｏｍｅｔｈｏｌｏｎｅ,ＦＬＭ,美国）;ＣＭ点眼组双眼滴０．２５％氯霉素眼液。分别于术后３     

准分子激光角膜切削术后皮质类固醇激毒的应用

比较准分子激光角膜切削术（ｐｈｏｔｏｒｅｆｒａｃｔｉｖｅｋｅｒａｔｅｃｔｏｍｙ，ＰＲＫ）后皮质 类固醇激光素的应用方法。方法应用ＮｉｄｅｋＥＣ５０００型准分子激光机对６００只近眼行ＰＲＫ，术后随机分为Ａ组和Ｂ组，分别采用不同的方法应用皮质类固醇激素，随访６个月。     

屈光性手术的最新进展

屈光性手术始于十九世纪下半叶 ,是当前眼科界发展最快的前沿领域之一 ,种类繁多。有放射状角膜切开术(ＲＫ)、准分子激光角膜切削术 (ＰＲＫ)、自动板层角膜成型术 (ＡＬＫ)、准分子激光角膜原位磨镶术 (ＬＡＳＩＫ)、角膜表面镜片术 (ＥＰ)、角膜内环植入术 (ＩＣＲＳ)等 ;晶     

准分子激光角膜切削术后并发皮质类固醇性高眼压或青光眼

目的探讨准分子激光角膜切削术（ＰＲＫ）后伴发皮质类固醇性高眼压或青光眼的临床意义。方法ＰＲＫ治疗近视１０９８眼，术后使用氟美龙（ＦＭＬ）点眼４～６个月，防止术后并发症发生。结果使用ＦＭＬ而诱致激素性高眼压或青光眼共３５例６７眼，发生率为６．１％。结论为减少该病发生：①术前详细检查，询问有无青光眼家族史；②术后注意眼压变化；③改进手术方式     

准分子激光角膜切削术后皮质类固醇激素的应用

比较准分子激光角膜切削术（ｐｈｏｔｏｒｅｆｒａｃｔｉｖｅｋｅｒａｔｅｃｔｏｍｙ，ＰＲＫ）后皮质类固醇激素的应用方法。方法应用ＮｉｄｅｋＥｃ５０００型准分子激光机对６００只近视眼行ＰＲＫ，术后随机分为Ａ组（２２８只眼）和Ｂ组（３７２只眼），分别采用不同的方法应用皮质类固酵激素，随６个月。结果术后６个月裸眼视力大于０．８、１·０者，Ａ组分别为９７．９％、９３．２％；Ｂ组为９８．６％、９３．５％；Ａ、Ｂ两组发生过性高眼压分别为２．２％、２·７％，差异无显著性（Ｐ＞０．０５）１级以上角膜雾状混浊（ｈａｚｅ）的发生率在Ａ、Ｂ两组分别为１８．４％、５·４％两者差异有非常显著性（Ｐ＜０．０５）。结论合理使用皮质类固醇激素能有效地降低ＰＲＫ后ｈａｚｅ的形成及其所引起的近视回退，早期使用强效皮质类固醇激素，后期使用低浓度的皮质类固醇激素能减少激素性高眼压的发生率。     

准分子激光角膜切削术后角膜创面的愈合及皮质类固醇对愈合的影响

目的研究准分子激光角膜切削术（ｐｈｏｔｏｒｅｆｒａｃｔｉｖｅｋｅｒａｔｅｃｔｏｍｙ，ＰＲＫ）后创面愈合过程及皮质类固醇对愈合的影响。方法６只猕猴双眼行ＰＲＫ后，右眼滴皮质类固醇激素眼液，左眼滴新霉素眼液。于术后４天、１、２周、１、３及６个月测量角膜厚度，并取角膜做免疫组化染色，检测Ⅲ、Ⅳ、Ⅶ型胶原、纤维连结蛋白和层粘连蛋白。结果术后１个月角膜Ⅶ型胶原的分布恢复正常状态；应用皮质类固醇可降低Ⅲ型胶原和纤维连结蛋白的沉积，且术后中央角膜厚度的变化较对照组更接近期望值。结论ＰＲＫ后角膜上皮细胞与基质可达到紧密的附着；皮质类固醇对减少术后角膜雾状混浊和屈光回退有一定作用。     

PRK术后局部使用艾氟龙或地塞米松安全性及疗效观察

目的评估准分子激光削融术（ＰＲＫ）后局部滴用艾氟龙（ｆｌｕｏｒｏｍｅｔｈｏｌｏｎｅ，ＦＭＬ）或地塞米松滴眼液（ｄｅｘａｍｅｔｈａｓｏｎｅ，ＤＥＸ）治疗后皮质类固醇性高眼压、角膜雾浊及屈光回退的发生率。方法追踪观察了ＰＲＫ治疗的１７７例患者（３４１眼）。患者自上皮愈合日始，随机分为滴０．１％艾氟龙或０．２５％地塞米松组。药物使用４次／ｄ，共１个月；从第２月始逐月每日减少１滴，总疗程４个月。随访时间分别在１０ｄ，１、２、３、４月。结果ＰＲＫ术后４月，皮质类固醇性高眼压发生率艾氟龙组为１４．８％，地塞米松组为３２．１％，差异有显著性（Ｐ＜０．０１）。角膜雾浊和屈光回退在两组间基本相似（Ｐ＞０．０５）。结论ＰＲＫ术后使用艾氟龙可有效降低皮质类固醇性高眼压的发生率，但对减轻角膜雾浊，防止屈光回退的效果两药相同。     

PRK与LASIK治疗PK术后残留近视的临床研究

目的 探讨准分子激光角膜切削术（ＰＲＫ）及准分子激光原位角膜磨镶术（ＬＡＳＩＫ）矫治角膜放射状切开术（ＲＫ）后残留近视的安全性、稳定性和可靠性。方法 采用美国ＣＯＭＰＡＫ－２００型准分子激光治疗仪帮ＳＣＭＤ公司的可调节器气动微型角膜刀,分别对ＲＫ后残留近视的３８眼和９眼行ＰＲＫ和ＬＡＳＩＫ术,并随访半年以上。ＰＲＫ组根据屈光状态分为３组：Ⅰ组〈－３．００Ｄ;Ⅱ组－３．００～５．７５Ｄ,Ⅲ组－６．０     

兔准分子激光角膜切削术后角膜血小板源性生长因子mRNA表达的变化

研究角膜上皮下混浊形成的发生机制,检测准分子激光屈光性角膜切削术后角膜上皮和基质血小板源性生长因子表达的变化。方法新西兰白兔施行ＰＲＫ后１,２,３月用裂隙灯显微镜观察ｈａｘｅ形成情况,并用原位酸分子杂交方法,检测角膜上皮和基质ＰＤＧＦ ｍＲＮＡ的表达。结果正常角膜上皮细胞有ＰＤＧＦ ｍＲＮＡ表达,基质层无表达;ＰＲＫ后角膜上皮细胞ＰＤＧＦｍＲＮＡ表达增加,术后２月表达最强,且基质中亦有轻微表达。上     

激光原位角膜磨镶术后层间感染1例

目前准分子激光原位角膜磨镶术（ＬＡＳＩＫ）较之准分子激光屈光性角膜切削术（ＰＲＫ），由于保留角膜上皮层和前弹力层，术后不易发生角膜混浊。但ＬＡＳＩＫ较ＰＲＫ复杂，更依赖于手术者的技术，ＬＡＳＩＫ术中、术后可能发生的并发症有：角膜瓣游离、角膜上皮层间植...     

多柔比星对兔眼准分子激光角膜切削术后角膜上皮下混浊（Haze)的影响

目的　通过动物实验初步观察应用多柔比星对准分子激光角膜切削术（photorefractive keratectomy,PRK）术后角膜上皮下混浊(Haze)的影响,评估其抑制PRK术后Haze的有效性和安全性,旨在探讨PRK术中多柔比星替代丝裂霉素C应用的可行性。方法　新西兰白兔10只（20眼）,其中右眼为多柔比星治疗的实验组,左眼为丝裂霉素C治疗的对照组,两组兔眼均行PRK激光切削校正-8.00 D后,分别用0.2 g·L^-1多柔比星或0.2 g·L^-1丝裂霉素C的棉片处理,分别于术后1 d、1周、2周、3周、4周在裂隙灯下观察角膜上皮愈合及Haze情况。结果　术后1周,两组所有兔眼角膜上皮均已完全愈合。实验组3眼术后1 d即出现角膜基质片状炎性浸润灶,其中2眼治疗后角膜基质炎性浸润灶消退,另1眼形成浅层斑翳;实验组其余7眼及对照组10眼均未见Haze。结论　多柔比星虽然可能引起角膜基质非感染性炎症反应,但在抑制PRK术后细胞增殖方面或具有与丝裂霉素C类似效果。     

Corneal power, thickness, and stiffness: results of a prospective randomized controlled trial of PRK and LASIK for myopia

PURPOSE: To compare the short-, medium-, and long-term changes in corneal optical power and corneal aberrations, central corneal thickness, and corneal "stiffness" assessed by pneumotonometry readings in patients having laser in situ keratomileusis (LASIK) or photorefractive keratectomy (PRK) for myopia. SETTING: Department of Ophthalmology, Arhus University Hospital, Arhus, Denmark. METHODS: One eye of each of 45 patients with myopia ranging from -6.00 to -8.00 diopters (D) (spherical equivalent spectacle refraction [SER]) was randomized to LASIK (n=25; mean SER -7.12 D +/- 0.57 [SD]) or PRK (n=20; mean SER -6.91 +/- 0.57 D). Data were collected prospectively before and 1, 3, 6, 12, and 36 months after surgery. Measurements included corneal topography (TMS-1, Tomey), corneal thickness (ultrasound pachymetry), and apparent intraocular pressure (IOP) (pneumotonometry). Retreatments were not performed during the first year, and retreated eyes were excluded from the 3-year follow-up. Changes in corneal power and aberrations, thickness, and apparent IOP were calculated in a pair-wise manner for 3 time periods: short term (preoperative to 1 month after surgery), medium term (1 to 12 months after surgery), and long term (1 to 3 years after surgery). RESULTS: In the short term, corneal power decreased equally in LASIK and PRK eyes. Spherical aberrations and coma-like aberrations increased equally, while corneal thickness decreased significantly less in LASIK eyes than in PRK eyes. The apparent IOP decreased more in LASIK eyes than in PRK eyes. In the medium term, corneal power increased significantly in both groups. Spherical aberrations decreased significantly in PRK eyes but not in LASIK eyes. From 1 to 12 months, corneal thickness increased more in PRK eyes than in LASIK eyes. During this period, the apparent IOP increased significantly in LASIK eyes. In the long term, corneal power and corneal aberrations did not change significantly in either group. Corneal thickness increased slightly but significantly in both groups. The apparent IOP increased significantly more in PRK eyes. CONCLUSIONS: Differences between LASIK and PRK related to time-dependent events affecting corneal shape and structural integrity were present. Peripheral changes in flap hydration in LASIK eyes and epithelial and/or stromal thickening in PRK eyes appeared to be the most important factors in optical power changes in the first year after treatment. The changes in apparent IOP suggest that some interlamellar healing occurred during the first year after LASIK. After LASIK and PRK, corneal bending stiffness seemed permanently decreased, although some restiffening may occur in PRK eyes in the long term.     

Mitomycin C alters corneal stromal wound healing and corneal haze in rabbits after argon-fluoride excimer laser photorefractive keratectomy.

PURPOSE: To investigate the effects of mitomycin C (MMC) on rabbit cornea wound healing after photorefractive keratectomy (PRK). MATERIALS AND METHODS: Rabbit corneas were stained with dichlorotriazinyl aminofluorescein immediately after PRK. MMC was applied to the right eye and phosphate-buffered salt solution (PBS) to the left. Corneal epithelial wound healing rate and corneal haze were examined. Ultrasound pachymetry was performed. Stromal collagen regeneration was evaluated by fluorescent microscopy. We used terminal deoxyribonucleotidyl transferase-mediated D-uridine 5'-triphosphated-digoxigenin nick-end labeling (TUNEL) assay and transmission electron microscopy (TEM) to evaluate keratocyte apoptosis. RESULTS: In eyes treated with MMC, there was no delay to the healing rate of corneal epithelial wound, and less haze 4 weeks after PRK. Ultrasound pachymetry showed thinner corneal thickness in MMC-treated eyes at week 4. Corneal stromal thickness regression was less in MMC-treated eyes observed by fluorescent microscope at week 4. Keratocyte apoptosis was noted in both MMC- and PBS-treated eyes by TUNEL assay and TEM observation. This study discovered the phenomenon that MMC prolongs keratocyte apoptosis. CONCLUSIONS: Applying MMC after PRK is an effective method to decrease haze formation and corneal stromal thickness regression in rabbit corneas. The effect may be related to MMC prolonging keratocyte apoptosis.     

Mitomycin C-induced reduction of keratocytes and fibroblasts after photorefractive keratectomy

PURPOSE: To investigate the effects of mitomycin C (MMC) on the number of keratocytes and the proliferation of fibroblasts after photorefractive keratectomy (PRK) and exposure to ultraviolet B (UV-B) irradiation. METHODS: The right eyes of New Zealand White rabbits in Groups 1, 2, and 3 (n = 18 each) underwent PRK to correct -10 diopters with 5 mm optical zone. Sponges soaked with 0.02% MMC were applied to the right eyes of Group 1 rabbits for 2 minutes. Antibiotic ointment was applied daily to all rabbits until the epithelium healed completely, after which 0.02% MMC eye drops were applied twice daily to the right eyes in Group 2 until 4 weeks after PRK. Three weeks after PRK, the right eyes of all the remaining rabbits were exposed to 100 mJ/cm2 C UV-B radiation. Corneal haziness was assessed biomicroscopically using the Fantes scale every 3 weeks. Six eyes of each group were each enucleated 3, 6, and 12 weeks after PRK, and tissue specimens were stained with hematoxylin and eosin and with TUNEL stain. The tissues were evaluated immunohistochemically with antibody to alpha-smooth muscle actin (SMA). Cellular changes in the anterior stroma and epithelial basement membrane were evaluated by electron microscopy. RESULTS: Corneal haze was observed after PRK and was aggravated by UV-B irradiation. A single intraoperative application of MMC immediately after PRK induced opacity and apoptosis of keratocytes. Twelve weeks after PRK, MMC significantly reduced corneal haze, the number of keratocytes, apoptotic cells, and fibroblasts, even after UV-B irradiation. Relatively large numbers of apoptotic and SMA-positive cells were found only in PRK-treated, non-MMC treated rabbits (Group 3), even after 12 weeks. Three weeks after PRK, dying stromal cells showed cell shrinkage, and chromatin condensation was observed in all treated groups by electron microscopy. Twelve weeks after PRK, fewer keratocytes and inflammatory cells were observed just beneath the epithelial layer in Group 1 than in any of the other groups. CONCLUSIONS: MMC is a potent inhibitor of corneal haze induced by PRK. MMC reduced the number of keratocytes and fibroblasts after PRK and UV-B irradiation. Although MMC would improve the clinical results of PRK, it has significant toxicity on corneal keratocytes, which did not disappear until 3 months after PRK.     

Comparison of wound healing after photorefractive keratectomy and laser in situ keratomileusis in rabbits.

PURPOSE: To evaluate and compare the corneal wound-healing process after photorefractive keratectomy (PRK) and laser in situ keratomileusis (LASIK). SETTING: Kangnam St. Mary's Hospital, Seoul, Korea. METHODS: Two surgical procedures, PRK with the VISX Star excimer laser and LASIK with a MicroTech microkeratome, were performed in 24 rabbit eyes. In the PRK group (n = 12 eyes), the rabbit cornea was treated with a 20 microns ablation. In the LASIK group (n = 12 eyes), a 20 microns laser ablation was performed after a 150 microns thick hinged corneal flap had been made. During both procedures, dichlorotriazinyl aminofluorescien (DTAF) dye was applied to the ablated stromal bed; in the LASIK group, the stromal side of the corneal flap was also stained with DTAF to differentiate regenerated collagen from normal stromal tissue. Corneal wound healing was evaluated postoperatively at 1, 4, 8, and 12 weeks using light, electron, and fluorescence microscopy. The amount of regenerated stromal tissue and the number of keratocytes were analyzed by an image-analysis system. RESULTS: In the PRK group, epithelial migration and regeneration were observed in the ablated area without any stromal regeneration 1 week postoperatively. However, newly regenerated, irregularly arranged stromal collagen, with epithelial hyperplasia in the ablated area, was observed 4 to 12 weeks postoperatively by light and fluorescence microscopy. The number of keratocytes in the surgical area was also increased. In ultrastructural observation using an electron microscope, the shape of keratocytes in the ablated area was changed, and the number of rough and smooth endoplasmic reticuli, ribosomes, mitochondria, and electron-dense vesicles in the cytoplasm were increased, suggesting that the cells were activated. In the LASIK group, there was no observed regenerated collagen between the corneal flap and the ablated stromal bed except in the wound margin. Lamellated, parallel collagen fibers in the cornealstroma were not disturbed. However, in the wound margin, corneal epithelial ingrowth between the flap and the stromal bed was observed, as was some regenerated stromal tissue. The amount of regenerated stromal tissue and the number of keratocytes in the wound area were statistically smaller than those in the PRK group (P < .05). Observation by electron microscopy showed no activated keratocytes, unlike in the PRK group. The collagen fibers in the wound area were parallel. CONCLUSION: Stromal wound healing in the LASIK group was minimal compared with that in the PRK group, except in the wound margin. These results may support the clinical findings of less corneal haze in the human cornea after LASIK.     

LASEK and photorefractive keratectomy for myopia: clinical and confocal microscopy comparison

PURPOSE: To compare postoperative visual acuity and corneal morphology after laser epithelial keratomileusis (LASEK) versus photorefractive keratectomy (PRK) in the correction of low to moderate myopia. METHODS: In a double-blind, randomized clinical trial, 50 myopic patients (mean: -4.5 +/- 1.35 diopters) were randomized to receive LASEK in one eye and PRK in the fellow eye. No mitomycin C eye drops were used in this study. Patients were observed daily for 4 days, then at 1 month and every 3 months up to 1 year. Uncorrected and best-corrected visual acuity (UCVA and BSCVA), manifest refraction, corneal epithelium healing time, postoperative pain, and corneal haze were evaluated. Corneal wound healing was quantified with corneal confocal microscopy. RESULTS: Refractive error, UCVA, and BSCVA were not statistically different between eyes treated with LASEK and PRK. Corneal epithelium healing time was 2.52 +/- 0.99 days in the eyes treated with PRK and 2.29 +/- 0.52 days in the eyes treated with LASEK (P=.22). The postoperative pain score was 2.17 +/- 0.87 in the eyes treated with PRK and 2.62 +/- 0.60 (P=.02) in the eyes treated with LASEK. Corneal confocal microscopy showed fewer stromal activated keratocytes and less extracellular matrix deposition in the eyes treated with LASEK than in the eyes treated with PRK at 1 month postoperatively (P=.003). CONCLUSIONS: LASEK is an effective and safe procedure for low to moderate myopia, but it seems more painful until full corneal reepithelization. In the early postoperative period, the corneal wound healing process is significantly less intense in eyes treated with LASEK than in eyes treated with PRK. The role of LASEK in corneal wound healing modulation remains controversial.     

Aberrant corneal nerve regeneration after PRK

PURPOSE: To report a case of aberrant corneal nerve regeneration after myopic photorefractive keratectomy (PRK). METHODS: One patient underwent bilateral PRK to correct a refractive error of -5.50 D in each eye. Thirteen months after the original PRK, the left eye underwent an uncomplicated PRK reoperation to correct a regression of -1.00 D. The central corneas were examined by confocal microscopy preoperatively in both eyes, at 1 and 2 years after the original PRK in the right eye, and before and 1 and 2 years after the PRK reoperation in the left eye. RESULTS: Aberrant anterior stromal nerves with a coiled course and irregular branching pattern were identified 22 micro m deep to the most anterior keratocyte layer at 1 year after the PRK reoperation in the left eye and remained unchanged 2 years after reoperation. No abnormal stromal nerves were identified in the left eye before the reoperation or at any time in the right eye. CONCLUSION: Aberrant regeneration of corneal stromal nerves may occur after myopic PRK reoperation.     

Corneal endothelial cell injury induced by mitomycin-C in photorefractive keratectomy: nonrandomized controlled trial

PURPOSE: To evaluate the effect of intraoperative use of mitomycin-C (MMC) on the corneal endothelium during excimer laser photorefractive keratectomy (PRK). SETTING: Vanak Eye Surgery Center, Tehran, Iran. METHODS: This nonrandomized trial comprised 81 patients (162 eyes) with bilateral low to moderate myopia and adequate corneal thickness to allow PRK (estimated postoperative residual stromal thickness >350 microm without considering epithelial thickness). The indication for intraoperative application of MMC 0.02% (0.2 mg/mL) was an ablation depth of 75 microm or more. Patients were divided into 3 groups: bilateral (both eyes treated with MMC), unilateral (only 1 eye treated with MMC), and untreated (no eye treated with MMC). Visual acuity, refraction, endothelial cell density (ECD), and corneal thickness were measured preoperatively as well as 1 week and 1, 3, and 6 months postoperatively. RESULTS: Overall, 76 eyes were treated with MMC. Eyes treated with MMC and untreated eyes were comparable in postoperative visual acuity and refraction. Preoperative to postoperative changes in ECD were statistically significantly greater in the treated eyes (-14.8%) than in untreated eyes (-5.1%) 6 months after PRK (P<.001). Longer MMC contact time (P<.001) and male sex (P= .04) were the only factors independently associated with greater endothelial cell loss. CONCLUSIONS: The prophylactic use of diluted intraoperative MMC 0.02% solution caused corneal endothelial cell loss. The rate of cell loss was correlated with the duration of MMC exposure.     

Confocal microscopy changes in epithelial and stromal thickness up to 7 years after LASIK and photorefractive keratectomy for myopia

PURPOSE: To determine the long-term changes in epithelial, stromal, and corneal thickness after LASIK and photorefractive keratectomy (PRK). METHODS: In two prospective observational case series, 11 patients (16 eyes) received LASIK and 12 patients (18 eyes) received PRK to correct myopia or myopic astigmatism. None of the corneas had retreatment procedures. Corneas were examined using confocal microscopy before and at 1 month, and at 1, 2, 3, 5, and 7 years after surgery. Central thicknesses were measured from reflected light intensity profiles recorded by confocal microscopy. Postoperative epithelial thickness was compared to preoperative, and postoperative stromal and corneal thicknesses were compared to thickness at 1 month after surgery. RESULTS: In LASIK, epithelial thickness at 1 month (51 +/- 4 microm, n = 11) was greater than before surgery (41 +/- 4 microm, n = 16; P < .001) and remained thicker through 7 years (52 +/- 6 microm, n = 13; P < .001). Stromal and corneal thickness did not change between 1 month and 7 years after LASIK. After PRK, corneal thickness at 1 year (464 +/- 44 microm, n = 17) was greater than at 1 month (442 +/- 39 microm, n = 15; P = .001) and remained thicker at 7 years after PRK (471 +/- 45 microm, n = 17; P > .001). CONCLUSIONS: The early increase in central epithelial thickness after myopic LASIK persists for at least 7 years and is probably the result of epithelial hyperplasia. Central corneal thickness increases during the first year after PRK and remains stable thereafter up to 7 years.     

Effects of topical vitamin E on corneal superoxide dismutase,glutathione peroxidase activities and polymorphonuclear leucocyte infiltration after photorefractive keratectomy

PURPOSE: Photorefractive keratectomy (PRK) induces free radical formation and polymorphonuclear (PMN) cell infiltration in the cornea. Vitamin E is a free radical scavenger and protects the cells from reactive oxygen species. We investigated the effects of topical vitamin E on corneal PMN cell infiltration and corneal antioxidant enzyme activities after PRK. METHODS: We studied four groups, each consisting of seven eyes. Group 1 were control eyes. In group 2 the corneal epithelium was removed by a blunt spatula (epithelial scrape). In group 3, corneal photoablation (59 micro m, 5 dioptres) was performed after epithelial removal (traditional PRK). In group 4 we tested the effects of topical Vitamin E after traditional PRK. Corneal tissues were removed and studied with enzymatic analysis (measurement of corneal superoxide dismutase and glutathione peroxidase activities) and histologically. RESULTS: Stromal PMN leucocyte counts were significantly higher after mechanical epithelial removal and traditional PRK (p < 0.05). Corneal superoxide dismutase and glutathione peroxidase activities decreased significantly after mechanical epithelial removal and traditional PRK (p < 0.05). In group 4, treated with vitamin E, corneal superoxide dismutase activity did not differ significantly from that in the medically non-treated groups, nor did corneal PMN cell infiltration after traditional PRK. The reduction of corneal glutathione peroxidase activity after PRK was reduced significantly after topical vitamin E treatment. CONCLUSIONS: Topical vitamin E treatment may be useful for reducing the harmful effects of reactive oxygen radical after epithelial scraping and PRK in that it increases corneal glutathione peroxidase activity.