Toxic endothelial degeneration in ocular surface disease treated with topical medications containing benzalkonium chloride

We examined a 56-year-old man with keratoconjunctivitis sicca and marked ocular surface disease in whom the prolonged frequent use of topical medications containing the preservative benzalkonium chloride was associated with corneal endothelial damage requiring corneal transplantation in one eye. The histopathologic findings on examination of the excised button were consistent with toxic endothelial disease. Postoperatively, the patient's symptoms continued until the preservative-containing medications were substituted with nonpreserved saline eyedrops.     

Dose-dependent benzalkonium chloride toxicity imparts ocular surface epithelial changes with features of dry eye disease

PurposeInclusion of the preservative benzalkonium chloride (BAC) in ophthalmic solutions is prevalent, despite the noted potential for exacerbating dry eye disease (DED). Whilst studies incorporating BAC have assessed its’ effects as a mouse model of DED, the impact on limbal epithelia is under-studied. Our investigation aimed to comprehensively assess the impact of different BAC dosing regimens and their suitability as a mouse model of DED.MethodsC57BL/6J mice (n = 72) were administered topical BAC (0.05–0.2%) over 7 days. Fluorescein staining, corneal smoothness index, and immuno-histological analyses were applied to determine architectural and cellular changes on the ocular surface following BAC treatment. The effect of BAC (0.0001–0.01%) on cultivated primary mouse corneo-limbal epithelial cells (CLECs) (n = 6) was examined using morphological and functional assays.ResultsWhilst 0.2% BAC induced severe corneal epithelial defects, 0.1% BAC dispensed once daily over 7 days, induced punctate fluorescein staining without detriment to corneal smoothness. Histochemical staining revealed disorganized basal corneal epithelial cells with enlarged cytoplasmic halos. Furthermore, PAS⁺ goblet cells were decreased. BAC treatment also modulated K14 expression and distribution within the limbus. In cultured CLEC, BAC triggered cell contraction and vacuolation, increased LDH release and elevated cell necrosis by 4.1-fold. Concentrations of BAC as low as 0.0001% decreased colony formation.ConclusionsThis study describes how exposing C57BL/6 mice to BAC induce some clinicopathological features of DED seen in humans, and therefore provides the foundations to explore the consequences on the ocular surface, particularly on limbal epithelia and its’ stem cells.     

The effect of benzalkonium chloride on the electropotential of the rabbit cornea.

The effect of benzalkonium chloride on the electropotenial of the cornea has been examined. The anterior surface of the in vivo or in vitro cornea was exposed to various concentrations of the surfactant, from 0.005% to 0.02%, for either 1 or 2 min. The initial effect is a hyperpolarization lasting up to 30 sec, followed by a rapid fall in potential difference with a subsequent recovery. The degree of potential difference decrease and the recovery rate was dependent upon both the concentration of the detergent, and the exposure time. There is excellent correlation between the previous anatomical and physiological studies on tracer penetration across the in vivo and in vitro cornea and our present work. The data indicate that benzalkonium chloride acts by breaking down the physiological and anatomical diffusion barrier to solute and solvent which is located in the outer layer of the epithelium.     

聚乙二醇滴眼液对拉坦前列腺素眼表毒性的中和作用

背景 减少局部抗青光眼药物的眼表毒性、提高患者对药物治疗的依从性已经成为青光眼药物治疗过程中亟待解决的问题.聚乙二醇是一种新型的人工泪液,其是否可以减轻抗青光眼药物局部应用后的眼表毒性尚待研究. 目的 探讨聚乙二醇对拉坦前列腺素滴眼液中防腐剂苯扎氯胺所致眼表毒性的影响.方法 采用随机数字表法将30只新西兰大白兔分为3个组,每组10只,正常对照组兔眼不给予任何干预,PBS处理组给予质量分数0.005％拉坦前列腺素联合PBS溶液连续点眼60 d,聚乙二醇处理组给予0.005％拉坦前列腺素联合聚乙二醇滴眼液点眼60 d.分别于用药前及用药后第31天和第61天行兔眼基础泪液分泌试验、角膜荧光素染色评分、角膜结膜虎红染色评分和结膜印迹细胞学检查,并于第61天获取角膜及球结膜组织标本行扫描电子显微镜和透射电子显微镜观察. 结果 对照组、PBS处理组及聚乙二醇处理组在实验第31天和第61天的角膜荧光素染色评分差异均有统计学意义(H=25.265、29.426,P＜0.001);3个组在实验第31天和第61天角膜球结膜虎红染色评分差异均有统计学意义(H=26.167、29.212,P＜0.001);各组不同时间点基础泪液分泌量的差异有统计学意义(F交互作用=4.746,P＜0.05),各组不同时间点球结膜杯状细胞密度的差异有统计学意义(F=18.055,P＜0.001).与对照组比较,PBS处理组第61天角膜荧光素染色评分[0(0,1.0) vs.3(2.0,3.0)]及虎红染色评分[0(0,1)vs.2(2,3)]均明显升高,差异均有统计学意义(P＜0.001);PBS处理组第61天基础泪液分泌量和结膜上皮杯状细胞密度均明显低于对照组[(5.18±0.46)mmVs.(9.43±0.57)mm;(53.04±2.98)个/高倍视野vs.(87.73±2.34)个/高倍视野],差异均有统计学意义(P＜0.01);扫描电子显微镜和透射电子显微镜下可见PBS处理组第61天角膜和结膜上皮细胞表面微绒毛及细胞器明显损伤.与PBS处理组比较,聚乙二醇处理组第61天角膜荧光素染色评分[3(2.0,3.0) vs.1(0.5,1.0)]及角膜结膜虎红染色评分[2(2,3) vs.1(0,1)]明显下降,差异均有统计学意义(P＜0.001);聚乙二醇处理组第61天兔眼基础泪液分泌量明显多于PBS处理组[(7.00±0.71)mm vs.(5.18±0.46) mm],差异有统计学意义(P＜0.05);聚乙二醇处理组第61天结膜上皮杯状细胞密度值高于PBS处理组[(63.88±3.32)个/高倍视野vs.(53.04±2.98)个/高倍视野],差异有统计学意义(P＜0.05);球结膜印迹细胞学评分改善,角膜和结膜上皮细胞微绒毛及细胞器等超微结构完整. 结论 聚乙二醇可以减少含苯扎氯胺的拉坦前列腺素滴眼液所致的兔眼表毒性,改善青光眼局部用药所致的眼表损伤.     

Confocal microscopic studies of living rabbit cornea treated with benzalkonium chloride.

The effects of benzalkonium chloride (BAK) on the living rabbit cornea were studied by in vivo Tandem scanning confocal microscopy (TSCM) and confirmed by conventional scanning electron microscopy (SEM). Two drops of saline or phosphate-buffered saline (PBS) containing BAK in concentrations of 0.02, 0.01, and 0.005% was applied to rabbit eyes 15 times at 5-min intervals. The solutions were pH 5.5-5.9 (saline) and pH 7.5 (PBS), and osmolarity was 275-280 (saline) and 300-307 mOsm (PBS). Immediately after application of 0.02 and 0.01% BAK, no normal corneal superficial epithelial cells could be imaged by in vivo TSCM. No swelling of the superficial epithelial cells was observed for the control solution without BAK; however, there was a small amount of desquamation. Application of as little as 0.005% BAK caused the superficial epithelial cells to swell and desquamate. The observed desquamation of corneal superficial epithelial cells increased with higher BAK concentrations applied to the eye. One hour after final drug application, inflammatory cells appeared on the surface of the cornea treated with 0.02% BAK. These findings were correlated with SEM observations. Based on the results of this study, we believe that BAK used frequently can produce clinical corneal toxicity and that the cytotoxicity of any topical ophthalmic solutions can be evaluated by in vivo TSCM.     

Effect of benzalkonium chloride on the stability of the precorneal tear film in rabbit and man.

Benzalkonium chloride, a surface-active preservative commonly used in eyedrop preparations, has been shown to hasten the drying of the precorneal tear film. In the rabbit, 0.01 per cent benzalkonium (the concentration usually employed as a preservative) shortened the time required for the appearance of dry spots on the corneal surface by a factor of about four. In man, an approximately twofold hastening was demonstrated. This effect is thought to preclude the use of this substance as a preservative in eyedrop preparations for use as local anaesthetics.     

Effects of benzalkonium chloride on growth and survival of Chang conjunctival cells

PURPOSE: The aim of this study was to investigate the action of benzalkonium chloride (BAC), used as a preservative in most ophthalmic topical solutions, on epithelial conjunctival cells in vitro. METHODS: A continuous human conjunctival cell line (Wong-Kilbourne derivative of Chang conjunctiva) was exposed to BAC solutions at various concentrations (0.1%-0.0001%) during a period of 10 minutes. Cells were examined before treatment and 3, 24, 48, and 72 hours later, after reexposure to normal cell culture conditions. Cell number and viability were assessed with crystal violet and 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyl tetrazolium bromide colorimetric assays. The expression of the apoptotic marker Apo 2.7, nuclear antigen p53, membrane proteins Fas and Fas ligand, and DNA content was studied by flow cytometry. Morphologic aspects of cell nuclei were analyzed on slides with a nucleic acid-specific dye, 4',6'-diamidino-2-phenylindole dihydrochloride. Cytoskeleton was labeled with a monoclonal anti-pancytokeratin antibody. In addition, apoptosis was measured by DNA electrophoresis assays in agarose gel. RESULTS: Cell exposure to 0.1% and 0.05% BAC induced cell lysis immediately after treatment. All cells (100%) treated with 0.01% BAC died in a delayed manner within 24 hours, with most of the characteristics of apoptosis (chromatin condensation and DNA fragmentation, reduction in cell volume, expression of the apoptotic marker Apo 2.7, and apoptotic changes in DNA content). Aliquots of 0.005%, 0.001%, 0.0005%, and 0.0001% BAC induced growth arrest and apoptotic cell death in a dose-dependent manner between 24 and 72 hours after treatment. The expressions of Fas and p53 did not vary after BAC treatment. Fas ligand was always negative. CONCLUSIONS: These results suggest that BAC induces cell growth arrest and death at a concentration as low as 0.0001%. The mode of BAC-induced cell death is dose-dependent. Cells die by necrosis after BAC treatment at high concentrations and by apoptosis if low concentrations of BAC are applied. This new aspect of in vitro toxicity of BAC could in part explain some ocular surface disorders observed in patients undergoing long-term topical treatments with preservative-containing drugs.     

Permeability of rabbit corneal epithelium to horseradish peroxidase after the influence of benzalkonium chloride.

A tight barrier against permeation of horseradish peroxidase into the corneal epithelium exists at the corneal surface adjacent to the tear film. The present light and transmission electron microscopic study reveals that the cationic surfactant, benzalkonium chloride, which is commonly added to eye drops as a preservative, breaks down this barrier. Lysis of the cell membranes was demonstrated, resulting in a leakage of the tracer into and underneath the superficial cells. The grade of cellular destruction caused by benzalkonium chloride was dependent upon the concentration and exposure time of the drug.     

苯扎氯铵对人结膜上皮细胞黏蛋白MUC1表达的影响

目的 探讨防腐剂苯扎氯铵(BAC)对体外培养的人结膜上皮细胞黏蛋白MUC1表达的影响及毒性作用.方法 采用培养的3～5代人结膜上皮细胞,将不同浓度(0.0100%、0.0050%、0.0010%、0.0005%、0.0001%)的BAC单次作用于结膜上皮细胞15 min,分别于处理细胞后0、6、12、24、48、72 h提取RNA及蛋白,采用RT-PCR及Western杂交方法检测MUC1表达水平.结果 0.0100%和0.0050%BAC作用后12～72 h可观察到结膜上皮细胞MUC1基因表达下调,0.0010%和0.0005%BAC作用后,24～48 h出现MUC1基因表达的下调,72 h恢复.0.0100%BAC作用后6～72 h检测到MUC1蛋白表达下降,而0.0050%BAC作用后12～72 h MUC1蛋白表达下降,0.0010%BAC作用后72 h MUC1蛋白表达减少.结论 BAC具有下调人结膜上皮细胞MUC1表达的作用,其下调作用具有时间依赖性和剂量依赖性.     

A rabbit dry eye model induced by topical medication of a preservative benzalkonium chloride

PURPOSE: To establish a rabbit dry eye model with topical medication of the ocular preparation preservative benzalkonium chloride (BAC). METHODS: Sixteen white rabbits were used. One eye of each rabbit was chosen randomly for topical administration of 0.1% BAC twice daily for 14 days. The other untreated eyes served as controls. Schirmer test, fluorescein, and rose bengal staining were performed before and after BAC treatment on days 3, 5, 7, and 14. Conjunctiva impression cytology specimens were collected on days 0, 7, and 14. The rabbits were killed after day 14. Immunofluorescence staining was performed to detect mucin-5 subtype AC (MUC5AC) on conjunctival cryosections. Cornea and conjunctiva structures were evaluated by light and electron microscopy. RESULTS: Compared with untreated controls, BAC-treated eyes showed significant decreases in Schirmer scores (P = 0.01) and increases in fluorescein scores (P < 0.001) on days 5, 7, and 14. A significant increase in rose bengal scores was noticed as early as day 3 (P = 0.001). Decreases in goblet cell density occurred on days 7 and 14 (P = 0.001). Decreased MUC5AC and histopathologic and ultrastructural disorders of the cornea and conjunctiva were also observed in the BAC group. CONCLUSIONS: These findings demonstrated that an ophthalmic preservative, benzalkonium chloride, induced a dry eye syndrome in rabbits with damage to the cornea and conjunctiva, decreased aqueous tear basal secretion, goblet cell loss, and MUC5AC deficiency. This rabbit model was consistent with human dry eye syndrome in both aqueous tear and mucin deficiency and may be appropriate for studying dry eye syndrome.     

Effects of environment pollution on the ocular surface

The twenty-first century is fraught with dangers like climate change and pollution, which impacts human health and mortality. As levels of pollution increase, respiratory illnesses and cardiovascular ailments become more prevalent. Less understood are the eye-related complaints, which are commonly associated with increasing pollution. Affected people may complain of irritation, redness, foreign body sensation, tearing, and blurring of vision. Sources of pollution are varied, ranging from gases (such as ozone and NO₂) and particulate matter produced from traffic, to some other hazards associated with indoor environments. Mechanisms causing ocular surface disease involve toxicity, oxidative stress, and inflammation. Homeostatic mechanisms of the ocular surface may adapt to certain chronic changes in the environment, so affected people may not always be symptomatic. However there are many challenges associated with assessing effects of air pollution on eyes, as pollution is large scale and difficult to control. Persons with chronic allergic or atopic tendencies may have a pre-existing state of heightened mucosal immune response, hence they may have less tolerance for further environmental antigenic stimulation. It is beneficial to identify vulnerable people whose quality of life will be significantly impaired by environmental changes and provide counter measures in the form of protection or treatment. Better technologies in monitoring of pollutants and assessment of the eye will facilitate progress in this field.     

防腐剂对眼表的损伤

眼科用防腐剂的毒性问题越来越受到人们的重视，本文介绍了眼科常用防腐剂的种类、防腐剂对眼表损伤的机制、防腐剂对眼表损伤的诊断与治疗、防腐剂的联合应用、含防腐剂与无防腐剂药物的比较、防腐剂对眼表损伤研究的动物模型及方法。     

Effect of benzalkonium chloride on transscleral drug delivery

PURPOSE: To investigate the effect and safety of benzalkonium chloride on transscleral drug delivery in the rabbit after continuous intrascleral administration. METHODS: Betamethasone 21-phosphate (BP) aqueous solutions, with or without benzalkonium chloride (BAK), were continuously administered to albino rabbit sclera with an osmotic pump for 1 week. The BP concentrations in the aqueous humor, vitreous, and retina-choroid were measured by high-performance liquid chromatography (HPLC). To investigate the effect of BAK on scleral permeability of BP in vitro, penetration of BP aqueous solution with or without BAK across the rabbit sclera was evaluated using a two-chamber Ussing apparatus. To determine the effects of BAK on transscleral delivery of large molecules, 20- and 70-kDa fluorescein isothiocyanate (FITC)-dextran (FD-20 and -70, respectively) aqueous solutions, with or without BAK, were continuously administered to the sclera by an osmotic pump. The intensity of fluorescence in the aqueous humor, vitreous, and retina-choroid was measured by fluorescence spectrophotometry at 1 week after implantation of the pump. The retinal toxicity of BAK was evaluated electrophysiologically and histologically. RESULTS: BAK increased concentrations of BP in the vitreous and retina-choroid compared with the control. BP was not detected in the aqueous humor. In the in vitro study, BAK did not increase the scleral permeability of BP. In the retina-choroid, BAK significantly increased concentrations of FD-20 but did not increase those of FD-70. The addition of BAK did not increase concentrations of FD-20 or -70 in the vitreous. No substantial toxic reactions were observed in the retina in electrophysiological or histologic examinations after the addition of BAK. CONCLUSIONS: The results of this study demonstrate that BAK may improve the ocular penetration of a drug in a transscleral drug delivery system without producing toxic reactions.     

An ultrastructural study of rabbit ocular surface transdifferentiation

When debridement of the rabbit cornea is followed by re-epithelialization from the conjunctiva, a process of transdifferentiation of the endothelium occurs. Goblet cells appear peripherally 1 week after healing of the epithelial defect, are widespread at 2 weeks, and disappear centrally at 3 to 4 weeks. Six weeks after closure of the defect, the epithelium has reverted to the customary corneal appearance. The morphology of the regenerating epithelium was studied by light, transmission and scanning electron microscopy. The precursor cells for the goblet cells were identified in stage 1, before PAS-positive cells were present, as pairs of cells with dark cytoplasm and prominent Golgi. Subsequently, goblet cells were present in pairs, indicating that goblet cells are derived from non-goblet epithelial cells, and that they do not simply migrate onto the cornea. At the time of transdifferentiation, loss of goblet cells was shown to occur both by desquamation from the surface and by in situ cell death.     

Effects of a 0.9% sodium chloride ophthalmic solution on the ocular surface of symptomatic contact lens wearers

BACKGROUND: Ocular surface-related discomfort is the main reason for stopping contact lens wear. We carried out a study to evaluate the efficacy of preservative-free artificial tears containing 0.9% sodium chloride on ocular surface signs and symptoms in contact lens wearers experiencing discomfort and its possible influence on the duration of contact lens wear. METHODS: We studied 49 contact lens wearers experiencing discomfort who had normal results of slit-lamp biomicroscopy, a fluorescein tear film break-up time (BUT) of 10 seconds or more, and wetting greater than 5 mm in 5 minutes on the Schirmer 1 test with and without anesthesia. Twenty-nine subjects (16 men and 13 women with a mean age of 32.5 years [standard deviation (SD) 8.7 years]) received one instillation of the 0.9% sodium chloride solution four times daily in the lower conjunctival fornix for 21 days. Twenty subjects (12 men and 8 women with a mean age of 35.1 [SD 6.2] years) received no drops and served as a control group. The overall comfort and duration of contact lens wear, results of tear film analysis and adverse events were recorded on days 7 and 21. Patients rated their symptoms (while not receiving any medications or hydrating solutions) on a 100-mm visual analogue scale with "Excellent (lenses not felt)" at the left and "Very uncomfortable (lenses cause irritation or discomfort)" at the right. Measurement of corrected visual acuity, slit-lamp examination, determination of the tear film BUT, the Schirmer 1 test with and without anesthesia, and assessment of the colour and surface of the lens were performed at baseline and at day 21. We analysed the data for the more uncomfortable eye or, if the eyes were equally uncomfortable, the right eye. RESULTS: Significant lessening of ocular discomfort was observed in the treatment group during the study: the mean rating on the visual analogue scale at baseline was 60.2 mm (SD 12.7 mm), compared with 35.8 mm (SD 18.0 mm) at day 21 (p < 0.001, Student's t test). The duration of contact lens wear was significantly longer at day 21 than at baseline (7.0 [SD 2.6] hours vs. 6.4 [SD 2.6] hours, p < 0.05, Student's t test), and the proportion of subjects with conjunctival hyperemia was significantly lower at day 21 (48.3% vs. 82.8%, p < 0.05, chi2 test). No statistically significant changes were observed in tear film BUT, results of the Schirmer 1 test, corneal punctate staining by fluorescein or results of tear film analysis. The treatment was well tolerated by all patients. No significant differences in any of the variables studied were observed in the control group. INTERPRETATION: Treatment with a preservative-free 0.9% sodium chloride ophthalmic solution reduced ocular surface discomfort and extended the duration of contact lens wear without interfering with the tear film or contact lens materials. Long-term studies are needed to confirm the role of this solution in reducing discomfort experienced by contact lens wearers.     

Effects of vitamin A deficiency on the ocular surface

Vitamin A deficiency remains an important cause of ocular morbidity among patients with chronic liver disease and lipid malabsorption, and is a major cause of blindness in developing countries. Early ocular surface changes include keratinization of the conjunctiva and development of superficial punctate keratopathy. More severe deficiency results in corneal keratinization, ulceration, and necrosis. Vitamin A is necessary for normal differentiation of nonsquamous epithelium; keratinization is a direct consequence of its deficiency. Exposure exacerbates the process and surface phenomena, especially localized drying from loss of mucus-secreting goblet cells, reduced aqueous tear production, and irregularities of the keratinized surface may all contribute to stromal melting, which can occur in the absence of inflammatory infiltration or bacterial invasion. Surface abnormalities respond rapidly to systemic vitamin A. Significantly, corneal changes disappear long before the reappearance of goblet cells. Inflammation sometimes masks or reverses the xerotic process.     

芳香化酶抑制剂对眼表微环境影响的分析

目的：分析芳香化酶抑制剂(AIs)对服用者眼表微环境的影响。

方法：横断面观察性研究。研究对象为2022-11/2023-05我院乳腺科就诊的接受AIs治疗的药物绝经后的女性,根据AIs的种类分为甾体组和非甾体组。对照组为年龄相匹配的职业健康体检女性。所有参与者都进行了眼表疾病指数(OSDI)问卷评分,详细的眼科检查包括：最佳矫正视力、眼压、眼轴、角膜曲率、泪河弯曲面的曲率半径、泪液渗透压、泪膜破裂时间、角膜荧光素钠染色评分、泪液分泌试验(SchirmerⅠ试验)、睑板腺红外线评分。

结果：对照组与甾体组、非甾体组的年龄、最佳矫正视力、眼压、眼轴、角膜曲率比较均无差异(P>0.05); 甾体组和非甾体组的药物服药时长比较无差异(P>0.05)。对照组与甾体组、非甾体组的OSDI评分、泪河弯曲面的曲率半径、泪液渗透压、泪膜破裂时间、角膜荧光素钠染色评分、SchirmerⅠ试验、睑板腺红外线评分比较均有差异(P<0.05); 甾体组和非甾体组SchirmerⅠ试验结果比较有差异(P<0.05),其余数据之间均无差异(P>0.05)。

结论：接受AIs治疗的药物绝经后女性患者,眼表微环境改变明显,干眼的发生既有泪液分泌不足,也存在泪液蒸发过强。特别是接受非甾体类AIs者主泪腺分泌减少更明显。     

Effects of topical antiglaucoma medications on the ocular surface

The side effects of topical antiglaucoma medications and their preservatives range from ocular discomfort to sight-threatening alterations of the ocular surface. Conjunctival hyperemia, decreased tear production and function, and superficial punctate keratitis are among the most common signs seen on routine clinical examination. Squamous cell metaplasia and changes in cell morphology have been demonstrated by impression cytology studies and evaluation of biopsy specimens, and inflammatory effects are documented by the presence of inflammatory markers. The adverse effects of topical antiglaucoma eyedrops interfere with the treatment of glaucoma on two levels: first, the discomfort produced by the eye drops discourages patient compliance; and, second, long-term treatment with eyedrops is associated with a higher failure of filtration surgery. The detailed mechanism of inflammatory response and/or direct toxicity of eye drops has yet to be determined, but it may vary with the different classes of eye drops, different preservatives, and durations of treatments. Upcoming multicenter trials for new antiglaucoma eye drops should specifically evaluate ocular surface effects.     

长期单眼配戴角膜塑形镜对眼表的影响

目的：探讨持续单眼配戴角膜塑形镜对眼表的影响。

方法：回顾性研究2013-01/2015-12在无锡市101医院眼科门诊就诊的单眼近视眼(对侧眼为正视眼)持续配戴角膜塑形镜6mo以上的患者。观察戴镜眼和非戴镜眼在戴镜前和戴镜后各时间点(1wk,1、3、6mo)的泪膜破裂时间、泪液基础分泌量、角膜中央厚度、角膜内皮细胞密度、结膜充血、角膜上皮荧光素染色的情况。

结果：单眼持续配戴角膜塑形镜患者共53例,年龄10.43±1.70岁,等效球镜度-3.37±1.50D。戴镜眼戴镜1wk泪膜破裂时间缩短,戴镜后1wk与戴镜后1、3、6mo泪膜破裂时间相比,差异无统计学意义(P>0.05); 非戴镜眼泪膜破裂时间各时间点无明显差异(P>0.05)。戴镜眼和非戴镜眼戴镜后各时间点泪液基础分泌量与戴镜前相比,差异均不明显(P>0.05)。戴镜后各时间点角膜中央厚度和角膜内皮细胞密度与戴镜前比较,差异均无统计学意义(P>0.05)。戴镜眼角膜上皮染色主要为Ⅰ级点染,Ⅰ级点染在戴镜后1wk,1、3、6mo分别为10眼(19%)、6眼(11%)、8眼(15%)、6眼(11%),Ⅱ级点染分别为1眼(2%)、0眼、0眼、1眼(2%)。10例患者戴镜后会出现结膜充血(评分1分)。所有病例在及时停戴、使用抗生素及角膜修复剂后,角膜上皮点状染色均消失,结膜充血消退。非戴镜眼观察期内未见明显结膜充血,角膜上皮染色均为0级。

结论：持续配戴角膜塑形镜会引起泪膜稳定性的下降,结膜、角膜上皮会出现不同程度的影响,但对泪液分泌、角膜厚度和角膜内皮细胞无明显影响。非戴镜眼无明显眼表损害。