Changes in higher-order aberrations after scleral buckling surgery for rhegmatogenous retinal detachment.

PURPOSE: To evaluate changes in higher-order aberrations (HOAs) after scleral buckling surgery for the treatment of rhegmatogenous retinal detachment (RD). DESIGN: Prospective observational comparative case series. PARTICIPANTS: The study included 67 eyes of 67 rhegmatogenous RD patients undergoing scleral buckling surgery, and the fellow normal eyes comprised the control group. Twenty-seven eyes were treated with the segmental buckling procedure and 40 eyes received the encircling buckling procedure alone. METHODS: Hartmann-Shack wavefront analysis was performed at 2 weeks, 1 month, and 3 months postoperatively. MAIN OUTCOME MEASURE: Time course of changes in HOAs. RESULTS: Scleral buckling surgery significantly increased HOAs at 2 weeks (P<0.0001), 1 month (P<0.0005), and 3 months (P<0.05) postoperatively as compared with the control group. At 3 months postoperatively, the HOAs were significantly lower in the encircling group than in the segmental buckling group (P<0.05). The vertical coma (Zernike Z(3)(-1)) became negative (significantly lower than zero, P<0.01) in patients who received segmental buckling in the upper quadrant. The ocular HOAs and logarithm of the minimum angle of resolution best-corrected visual acuity significantly correlated at 3 months postoperatively (third-order root mean square [RMS]: r = 0.445, P<0.0005; fourth-order RMS: r = 0.489, P<0.0001). CONCLUSIONS: Scleral buckling surgery significantly increased HOAs. The segmental buckling procedure increased the HOAs to a greater extent and for a longer duration than the encircling procedure. The direction of coma aberration corresponded to the location of the segmental buckle. The increase in HOAs can be one of the factors responsible for visual disturbances after scleral buckling surgery.

Molecular basis of ocular abnormalities associated with proximal renal tubular acidosis.

Proximal renal tubular acidosis associated with ocular abnormalities such as band keratopathy, glaucoma, and cataracts is caused by mutations in the Na(+)-HCO(3)(-) cotransporter (NBC-1). However, the mechanism by which NBC-1 inactivation leads to such ocular abnormalities remains to be elucidated. By immunological analysis of human and rat eyes, we demonstrate that both kidney type (kNBC-1) and pancreatic type (pNBC-1) transporters are present in the corneal endothelium, trabecular meshwork, ciliary epithelium, and lens epithelium. In the human lens epithelial (HLE) cells, RT-PCR detected mRNAs of both kNBC-1 and pNBC-1. Although a Na(+)-HCO(3)-cotransport activity has not been detected in mammalian lens epithelia, cell pH (pH(i)) measurements revealed the presence of Cl(-)-independent, electrogenic Na(+)-HCO(3)-cotransport activity in HLE cells. In addition, up to 80% of amiloride-insensitive pH(i) recovery from acid load in the presence of HCO(3)(-)/CO(2) was inhibited by adenovirus-mediated transfer of a specific hammerhead ribozyme against NBC-1, consistent with a major role of NBC-1 in overall HCO(3)-transport by the lens epithelium. These results indicate that the normal transport activity of NBC-1 is indispensable not only for the maintenance of corneal and lenticular transparency but also for the regulation of aqueous humor outflow.

Changes in corneal topography after 25-gauge transconjunctival sutureless vitrectomy versus after 20-gauge standard vitrectomy.

PURPOSE: To evaluate the changes in regular and irregular corneal astigmatism after 25-gauge transconjunctival sutureless vitrectomy and 20-gauge standard vitrectomy. DESIGN: Prospective observational comparative case series. PARTICIPANTS: Thirty-two eyes of 32 patients undergoing 25-gauge transconjunctival sutureless vitrectomy and 25 eyes of 24 patients undergoing 20-gauge standard vitrectomy. METHODS: Corneal topography was obtained preoperatively and at 2 weeks and 1 month postoperatively. MAIN OUTCOME MEASURES: The dioptric data of the central 3-mm zone of the cornea were decomposed using Fourier harmonic analysis into spherical power, regular astigmatism, asymmetry, and higher-order irregularity. RESULTS: None of the 4 Fourier indices changed throughout the observation period in the 25-gauge group. In the 20-gauge group, regular astigmatism, asymmetry, and higher-order irregularity were increased significantly at 2 weeks after vitrectomy (P<0.05, Wilcoxon signed-ranks test) and returned to preoperative levels by 1 month. The spherical power in the 20-gauge group did not change after surgery. For regular astigmatism, asymmetry, and higher-order irregularity, the 20-gauge group showed significantly greater surgically induced changes than the 25-gauge group (P<0.05, Mann-Whitney U test). CONCLUSIONS: Twenty-five-gauge transconjunctival sutureless vitrectomy does not induce significant changes in corneal topography and exerts little influence on the optical quality of the cornea.

Clinical evaluation of cornea pseudoguttata.

AIM: To report on cornea pseudoguttata which occurred in 44 eyes from 40 patients. METHODS: In 3521 consecutive patients seen at a local eye clinic, eyes were examined with a slit-lamp biomicroscope in specular illumination. When guttate appearance was found, specular microscopy was performed. RESULTS: Cornea pseudoguttata was found in 44 eyes of 40 patients (1.1%). All patients had some form of anterior-segment ocular diseases, including keratitis (corneal infiltration) with contact lens wear (n = 16), epidemic keratoconjunctivitis (n = 8), corneal epithelial defect (n = 6), superficial punctate keratitis (n = 4), corneal foreign body (n = 3), keratitis of unknown causes (n = 3), corneal ulcer (n = 2), herpetic keratitis (n = 1), and iritis (n = 1). Six eyes were lost to follow-up, but in the remaining 38 eyes, cornea pseudoguttata completely resolved as the primary anterior-segment diseases subsided. Specular microscopy, measured after resolution of cornea pseudoguttata, showed that corneal endothelial cell density was not different between the affected and contralateral healthy eyes. CONCLUSION: Cornea pseudoguttata is commonly found in cases with corneal infiltration and inflammation. These results indicate that cornea pseudoguttata is reversible in its nature and resolves completely without any damage to the corneal endothelial cells.

Advanced glycation end product deposits in climatic droplet keratopathy.

BACKGROUND: Climatic droplet keratopathy (CDK), known as spheroid degeneration of the cornea, is one of the most frequent degenerative corneal disorders affecting visual function. However, the histochemical nature of the deposits seen in CDK is still unclear. AIM: To investigate the pathogenesis of CDK, we investigated the immunohistochemical localisation of advanced glycation end products (AGEs) in surgical specimens of CDK. METHODS: Immunohistochemical localisation of N(epsilon)-(carboxymethyl)-l-lysine (CML), N(epsilon)-(carboxyethyl)-l-lysine (CEL), pyrraline, pentosidine and imidazolone was examined in three corneas with CDK, six corneas with bullous keratopathy and three corneas without any corneal diseases. RESULTS: In all the specimens with CDK, immunoreactivity was strong in CML, moderate in pyrraline and pentosidine, and weak in imidazolone. Immunoreactivity was absent in CEL. In contrast, no immunoreactivity to CML, pyrraline, pentosidine, imidazolone or CEL was detected in corneas with bullous keratopathy, or in corneas without any corneal diseases. CONCLUSIONS: CDK is caused by an aggregation of AGE-modified proteins. The result is consistent with etiological findings that ultraviolet irradiation and ageing, both of which are accelerators of AGE formation, are closely related to the development of CDK.

Influence of tilt and decentration of scleral-sutured intraocular lens on ocular higher-order wavefront aberration.

AIM: To investigate the influence of tilt and decentration of scleral-sutured intraocular lenses (IOLs) on ocular higher-order wavefront aberrations. METHODS: In 45 eyes of 36 patients who had undergone scleral suture fixation of posterior chamber IOL, tilt and decentration of IOLs were determined by Scheimpflug videophotography, and higher-order aberration for a 4-mm pupil was measured using the Hartmann-Shack aberrometer. In another 100 eyes of 100 patients after standard cataract surgery with posterior chamber IOL implantation, ocular higher-order aberration was measured. RESULTS: In eyes with scleral-sutured IOL, the mean (SD) tilt angle and decentration were 4.43 degrees (3.02 degrees ) and 0.279 (0.162) mm, respectively. Ocular coma-like aberration in the sutured IOL group was 0.324 (0.170) microm, which was significantly greater than that of the standard cataract surgery group (0.169 (0.061) microm, p<0.001, Student's t test). No significant difference was found in ocular spherical-like aberration between the sutured IOL group (0.142 (0.065) microm) and standard surgery group (0.126 (0.033) microm; p = 0.254). In the sutured IOL group, IOL tilt significantly correlated with ocular coma-like aberration (Pearson's correlation coefficient r = 0.628, p<0.001), but no significant correlation was found between IOL tilt and ocular spherical-like aberration (r = 0.222, p = 0.175). The IOL tilt did not correlate with corneal coma-like (r = 0.289, p = 0.171) and spherical-like (r = 0.150, p = 0.356) aberrations. The IOL decentration did not correlate with any higher-order aberrations. CONCLUSION: In eyes with scleral-sutured posterior chamber IOL, tilting of the lens induces considerable amount of ocular coma-like aberrations.

Retention and removal of a new viscous dispersive ophthalmic viscosurgical device during cataract surgery in animal eyes.

AIMS: To assess the retention and removal properties of a new viscous dispersive ophthalmic viscosurgical device (OVD), DisCoVisc, in comparison with those of cohesive (Provisc), dispersive (Viscoat), and viscoadaptive (Healon5) OVDs. METHODS: In 20 porcine eyes, cataract surgery was simulated using one of the four OVDs which were stained with fluorescein for better visualisation. Three parameters were measured. Firstly, the presence/absence of OVDs in the chamber at the completion of phacoemulsification was recorded. Secondly, the time until the OVDs were completely removed from the anterior chamber using the phaco needle was measured. Thirdly, after intraocular lens (IOL) implantation, the time needed to completely remove the OVDs from the chamber with irrigation/aspiration tip was recorded. RESULTS: At the completion of phacoemulsification, the OVDs retained in 0% (0/5) for Provisc, 80% (4/5) for Healon5, 100% (5/5) for DisCoVisc, and 100% (5/5) for Viscoat. The retention of OVDs during phacoemulsification was greatest with Viscoat followed by, in descending order, DisCoVisc, Healon5, and Provisc. The removal of OVDs after IOL implantation took longest with Viscoat followed by Healon5, DisCoVisc, and Provisc. CONCLUSION: The viscous dispersive DisCoVisc showed excellent retention during phacoemulsification, while its removal after IOL implantation was very easy. When compared with the viscoadaptive Healon5, DisCoVisc was retained better in the chamber and was easier to remove. These features of DisCoVisc should be highly advantageous when considering covering the entire cataract surgery procedure with a single OVD.

Time course of changes in aqueous protein concentration and flow rate after oral acetazolamide.

The coefficient of plasma protein entry into the aqueous humor, kin, was calculated in the human eyes from the aqueous protein concentration measured with a flare-cell meter and from the aqueous flow rate determined with fluorophotometry. The value of kin averaged 3.47 +/- 0.25 x 10(-5) min-1 (mean +/- SEM) in 12 eyes of six normal young volunteers. The time course of changes in aqueous protein concentration after oral administration of 500 mg acetazolamide was measured with a flare-cell meter in 24 eyes of 12 subjects. Aqueous protein concentration significantly increased from 2-10 hr postadministration with a maximum increase of 41 +/- 7% (mean +/- SEM) at 6 hr postadministration. Assuming that kin is not affected by the drug treatment, we calculated the time change of aqueous flow rate from that of aqueous protein concentration using the value of kin above. The calculated flow rate after the administration of acetazolamide decreased between 1.25 and 8 hr, with a maximum reduction of 40 +/- 11% at 1.75 hr postadministration. These measurements obtained with the flare-cell meter corresponded well to those obtained by fluorophotometry in a separate group of volunteers given the same treatment. It was shown that oral acetazolamide increases aqueous protein concentration, and that the time change of its effect on aqueous flow rate can be monitored by measuring aqueous protein concentration.

Effects of pilocarpine and tropicamide on blood-aqueous barrier permeability in man.

The time courses of changes in the effects of topical pilocarpine and tropicamide on the index of the blood-aqueous barrier permeability to plasma protein (Pin) were determined in normal volunteers. Before and after drug instillation in one eye, protein concentration in the anterior chamber (Ca) was determined from aqueous flare intensity with a laser flare-cell meter and from aqueous flow by fluorophotometry. The Pin was calculated from the Ca, plasma protein concentration, and aqueous flow. One percent pilocarpine produced a maximum increase of 21 +/- 10% in the Ca (mean +/- SEM, n = 10), no significant change in the aqueous flow (n = 5), and a maximum increase of 29 +/- 10% in the Pin (n = 10). Three percent pilocarpine produced a maximum increase of 55 +/- 11% in the Ca (n = 8), a maximum increase of 34 +/- 13% in the aqueous flow (n = 5), and a maximum increase of 74 +/- 18% in the Pin (n = 8). Tropicamide (0.4%) produced a maximum decrease of 17 +/- 7% in the Ca (n = 8), a maximum decrease of 15 +/- 11% in the aqueous flow (n = 8), and a maximum decrease of 24 +/- 13% in the Pin (n = 8). The results indicated that pilocarpine increased the blood-aqueous barrier permeability to plasma protein in a dose-dependent manner and that tropicamide reduced it.

Quantitative evaluation of irregular astigmatism by fourier series harmonic analysis of videokeratography data.

PURPOSE: To assess quantitatively corneal irregular astigmatism in association with best spectacle-corrected visual acuity. METHODS: Refractive powers on a mire ring measured with computerized videokeratography were decomposed, using the Fourier series harmonic analysis. Extracting spherical and regular astigmatic components, the remaining irregular astigmatic component was quantified on rings 2 through 9. A weighted average was calculated by using the Stiles-Crawford effect on the basis of the radius of each ring of each eye and was used as an index of the irregular astigmatic component. Data analyses were carried out in 108 eyes, including 53 normal eyes, 34 eyes with keratoconus, and 21 eyes that had undergone penetrating keratoplasty for keratoconus. Keratoconic eyes and eyes after keratoplasty were included in the study only if visual acuity, corrected with a hard contact lens, was 20/20 or better. Logarithm of best spectacle-corrected visual acuity, age, type of disease, refractive astigmatism, irregular astigmatic component, surface regularity index, and surface asymmetry index were analyzed. RESULTS: In results of multiple regression analysis, the irregular astigmatic component was significantly correlated with best spectacle-corrected visual acuity (r = -0.744; adjusted R2 = 0.549; P < 0.001), whereas other explanatory variables showed no correlation with best spectacle-corrected visual acuity. CONCLUSIONS: This model of the irregular astigmatic component seems to be an efficient, quantitative means of describing corneal irregular astigmatism.

Changes in corneal wavefront aberrations with aging.

PURPOSE: To investigate whether corneal wavefront aberrations vary with aging. METHODS: One hundred two eyes of 102 normal subjects were evaluated with videokeratography. The data were decomposed using Taylor and Zernike polynomials to calculate the monochromatic aberrations of the cornea for both small (3-mm) and large (7-mm) pupils. RESULTS: For a 3-mm pupil, the amount of total aberrations (Spearman rank correlation coefficient r(s) = 0.145; P = 0.103) and spherical-like aberrations (r(s) = -0.068; P = 0.448) did not change with aging, whereas comalike aberrations exhibited a weak but statistically significant correlation with age (r(s) = 0.256; P = 0.004). For a 7-mm pupil, total aberrations (r(s) = 0.552; P < 0.001) and comalike aberrations (r(s) = 0.561; P < 0.001) significantly increased with aging, but spherical-like aberrations showed no age-related changes (r(s) = 0.124; P = 0.166). Simulated pupillary dilation from 3 mm to 7 mm caused a 38.0+/-28.5-fold increase in the total aberrations, and the extent of increases significantly correlated with age (r(s) = 0.354; P < 0.001). Pupillary dilation influenced the comalike aberrations more in the older subjects than in the younger subjects (r(s) = 0.243; P = 0.006), but such age dependence was not found for spherical-like aberrations (r(s) = 0.141; P = 0.115). CONCLUSIONS: Comalike aberrations of the cornea correlate with age, implying that the corneas become less symmetrical along with aging. Spherical-like aberrations do not vary significantly with aging. Pupillary dilation markedly increases wavefront aberrations, and those effects are more prominent in older subjects than in younger subjects.

Expression regulation of hyaluronan synthase in corneal endothelial cells.

PURPOSE: Our previous study showed that hyaluronan synthase (HAS), the enzyme protein of hyaluronan (HA) biosynthesis, is expressed in ocular tissues including the corneal endothelium. In the current study, the mechanism that regulates HAS expression in bovine corneal endothelial cells (BCECs) was investigated. METHODS: Cultured BCECs were used. HAS expression in BCECs at the mRNA level was detected by reverse transcription-polymerase chain reaction (RT-PCR) and Northern blot analysis. The effects of transforming growth factor (TGF)-beta and platelet-derived growth factor (PDGF)-BB on HAS expression were examined by quantitative RT-PCR. The involvement of the Smad family (intracellular signal transducer of TGF-beta) was also investigated. The expression of HAS in BCECs at the protein level was confirmed by immunocytochemistry and Western blot analysis. RESULTS: Three HAS isoforms in BCECs were expressed at the mRNA level. The transcriptional sizes of each HAS in BCECs were 4.9 kb for HAS1, 2.8 kb for HAS2, and 1.6 kb for HAS3. The expression of HAS2 at the mRNA level was stimulated by TGF-beta1 and/or PDGF-BB treatment. In contrast, HAS1 and HAS3 expression was not affected by these growth factors. The additive effects of TGF-beta1 and PDGF-BB were observed in the stimulation of the expression levels of HAS2. HAS2 upregulation by these growth factors was also detected by Western blot analysis. The stimulation of the expression of HAS2 at the mRNA level by TGF-beta was accelerated by the overexpression of Smad2, Smad3, and Smad4 and inhibited by that of Smad7, all of which were confirmed to be involved in the signal transduction from TGF-beta through HAS expression. CONCLUSIONS: Although three HAS isoforms were expressed in the corneal endothelial cells, the expression of HAS2 was upregulated by TGF-beta1 and/or PDGF-BB. HAS2 expression was regulated by TGF-beta through Smad family members.

Advanced glycation end products in diabetic corneas.

PURPOSE: Corneal complications are often associated with diabetes mellitus and can be vision threatening. Corneas in diabetic patients are exposed to increased glucose concentration despite cornea's avascular property, and this condition may contribute to the accumulation of advanced glycation end products (AGEs). The focus of this study was to examine the role of AGEs in the pathogenesis of diabetic keratopathy. METHODS: An anti-AGE monoclonal antibody (6D12), which recognizes a N(epsilon)-carboxymethyl lysine (CML)-protein adduct as an epitope, was prepared. Immunohistochemical localization of CML was examined in human age-matched diabetic and nondiabetic corneas (8 of each). In vitro, type I collagen-, type IV collagen-, or laminin-coated 96-well plates were glycated by glucose-phosphate. In some experiments, aminoguanidine was present in the incubation mixture. The amounts of CML-protein adducts in the extracellular matrix (ECM) were determined by enzyme-linked immunosorbent assay using 6D12. SV40-immortalized human corneal epithelial cells were seeded onto modified or unmodified ECM in 96-well plates and allowed to attach for 3 hours. Attached cells were fixed, and the areas of attached cells in each condition were measured. Attached cells without fixation were removed, and cell number was counted. RESULTS: In all of the 8 diabetic corneas, CML immunoreactivity was observed in the epithelial basement membrane, whereas CML immunoreactivity was not found in the corresponding area in 7 of 8 nondiabetic corneas. In vitro, nonenzymatic glycation of laminin on the culture dish attenuated adhesion and spreading of corneal epithelial cells. The presence of amninoguanidine in the incubation mixture during glycation inhibited CML formation and promoted the adhesion and spreading of corneal epithelial cells in a dose-dependent manner. CONCLUSIONS: The accumulation of AGEs on the basement membrane, particularly on laminin, may play a causative role in the corneal epithelial disorders of diabetic patients.

Effect of bunazosin hydrochloride on intraocular pressure and aqueous humor dynamics in normotensive human eyes.

We investigated the effects of topical administration of bunazosin hydrochloride, a new selective alpha 1-adrenergic antagonist, on intraocular pressure and aqueous humor dynamics in normal human eyes. In the single-dose study, all concentrations of bunazosin (0.025%, 0.05%, 0.1%, and 0.2%) significantly lowered intraocular pressure in a concentration-dependent manner. Administration of multiple doses of 0.1% bunazosin revealed no occurrence of tachyphylaxis after 1 week. Single application of 0.1% bunazosin had no significant influence on aqueous flow rate, tonographic outflow facility, or episcleral venous pressure, suggesting that bunazosin reduces intraocular pressure by increasing uveoscleral outflow. Aqueous protein concentration was found to be unaltered by bunazosin, indicating that blood-aqueous barrier permeability to protein molecules remained unchanged. We conclude that bunazosin may be a possible new antiglaucoma agent with a mechanism of action different from those currently in use for treating ocular hypertension.

Ocular adverse effects of neuropsychiatric agents. Incidence and management.

Neuropsychiatric agents may adversely affect the eye in various ways. The more frequently encountered effects include corneal oedema and pigmentary changes in the lens and cornea which are induced by phenothiazine derivatives; thioridazine-induced retinopathy; tricyclic antidepressant-induced accommodation interference and glaucoma; and lithium carbonate-induced exophthalmos and papilloedema. Several adverse effects, such as corneal oedema, retinopathy and glaucoma, are vision-threatening, and patients often fail to describe their symptoms properly. A more precise understanding of these conditions is essential for prompt diagnosis and appropriate treatment.

Glycemic control and lens transparency in patients with type 1 diabetes mellitus.

PURPOSE: To assess quantitatively the cumulative effect of hyperglycemia on lens transparency in patients with juvenile type 1 diabetes mellitus. METHODS: Subjects were 30 patients (30 eyes) with type 1 diabetes mellitus who had well-documented records on the duration of diabetes mellitus and condition of glycemic control from the onset. They were 35 years of age or younger (mean, 26.0 years), had a history of type 1 diabetes mellitus at least 5 years (mean, 8.4 years), had corrected visual acuity of 20/20 or better, and showed no clinically apparent cataract on slit-lamp examination. Twenty-one eyes of 21 subjects served as age-matched normal controls. They were 35 years of age or younger (mean, 25.7 years), had no diabetes mellitus, had corrected visual acuity of 20/20 or better, and showed no signs of cataract on slit-lamp examination. The degree of lens opacity was quantified using the anterior eye segment analysis system based on the Scheimpflug principle. An index was created to represent the cumulative effect of long-term glycemic control (hyperglycemic accumulation) by multiplying the average hemoglobin A(1c) value and the number of months from the onset. RESULTS: The patients with diabetes mellitus exhibited significantly greater degree of lens opacity than the normal controls (P =.017, Mann-Whitney U-test). Among the patients with diabetes mellitus, the lens opacity was greater in eyes with retinopathy than those without retinopathy (P =.011). Multiple regression analysis revealed that only the index of hyperglycemic accumulation significantly correlated with the degree of lens opacity (P =.042). CONCLUSION: Accumulated effect of hyperglycemia is related to the lens transparency in patients with diabetes.

Chronic clinical course of two patients with severe corneal dystrophy caused by homozygous R124H mutations in the betaig-h3 gene.

PURPOSE: To report the chronic clinical course of two patients with homozygous R124H mutations in the betaig-h3 gene. METHODS: Case reports. RESULTS: Two patients with homozygous R124H mutations in the betaig-h3 gene developed severe juvenile corneal opacities that required keratoplasty. After surgery, corneal opacities recurred and limited the recovery of visual acuity in the chronic follow-up. CONCLUSION: In patients with homozygous R124H mutations in the betaig-h3 gene, recurrence of corneal opacities after keratoplasty limits the recovery of visual acuity in the chronic follow-up.

Influence of rapid glycemic control on lens opacity in patients with diabetes mellitus.

PURPOSE: To report the influence of rapid glycemic control on lens opacity in patients with diabetes mellitus. METHODS: In a prospective study, nine patients with adult onset diabetes mellitus and glycosylated hemoglobin values over 9% were divided into two groups, rapid glycemic control and slow glycemic control groups, based on the time course of glycosylated hemoglobin values after the initiation of glycemic control. The lens thickness and opacity were measured using the anterior eye segment analysis system. RESULTS: One week after onset of treatment, the lens in rapid glycemic control group became significantly thicker than in pretreatment, but returned to the baseline level at the subsequent measurement points. The lens opacity index in the rapid glycemic control group increased significantly (P <.01, paired t test) 4 months after the glycemic control, which persisted throughout the 1-year study period. The lens thickness and opacity in the slow glycemic control group did not change significantly. CONCLUSION: It was suggested that rapid glycemic control can induce an irreversible increase in lens opacification.

Anterior capsular contraction after cataract surgery in vitrectomized eyes.

PURPOSE: To assess the contraction of continuous curvilinear capsulorhexis after cataract surgery in eyes with past pars plana vitrectomy. METHODS: In a prospective study, 16 eyes of 16 patients underwent phacoemulsification and implantation of a foldable acrylic intraocular lens after pars plana vitrectomy. Eyes after intensive or repeated vitrectomy were not included. Twenty eyes of 19 patients served as age-matched controls. Aqueous flare intensity was measured using the laser flare-cell meter 1 year after surgery. The area of anterior capsular opening (ACO) was determined by diaphanoscopy using the anterior eye segment analysis system EAS-1000 at 1 day and 1 year postoperatively. RESULTS: There was no significant difference in the mean ACO area between the vitrectomy and control groups both at 1 day and 1 year postoperatively. Aqueous flare intensity 1 year after surgery was slightly higher in the vitrectomy group, but the difference was not statistically significant. CONCLUSION: Eyes after simple vitrectomy are not at a higher risk of ACO contraction following cataract surgery.

Comparison of corneal wavefront aberrations after photorefractive keratectomy and laser in situ keratomileusis.

PURPOSE: To compare changes in the corneal wavefront aberrations after photorefractive keratectomy and laser in situ keratomileusis. METHODS: In a prospective randomized study, 22 patients with bilateral myopia received photorefractive keratectomy on one eye and laser in situ keratomileusis on the other eye. The procedure assigned to each eye and the sequence of surgery for each patient were randomized. Corneal topography measurements were performed preoperatively, 2 and 6 weeks, 3, 6, and 12 months after surgery. The data were used to calculate the wavefront aberrations of the cornea for both small (3-mm) and large (7-mm) pupils. RESULTS: Both photorefractive keratectomy and laser in situ keratomileusis significantly increased the total wavefront aberrations for 3- and 7-mm pupils, and values did not return to the preoperative level throughout the 12-month follow-up period. For a 3-mm pupil, there was no statistically significant difference between photorefractive keratectomy and laser in situ keratomileusis at any postoperative point. For a 7-mm pupil, the post-laser in situ keratomileusis eyes exhibited significantly larger total aberrations than the post-photorefractive keratectomy eyes, where a significant intergroup difference was observed for spherical-like aberration, but not for coma-like aberration. This discrepancy seemed to be attributable to the smaller transition zone of the laser ablation in the laser in situ keratomileusis procedure. Before surgery, simulated pupillary dilation from 3 to 7 mm caused a five- to six-fold increase in the total aberrations. After surgery, the same dilation resulted in a 25- to 32-fold increase in the photorefractive keratectomy group and a 28- to 46-fold increase in the laser in situ keratomileusis group. For a 3-mm pupil, the proportion of coma-like aberration increased after both photorefractive keratectomy and laser in situ keratomileusis. For a 7-mm pupil, coma-like aberration was dominant before surgery, but spherical-like aberration became dominant postoperatively. CONCLUSIONS: Both photorefractive keratectomy and laser in situ keratomileusis increase the wavefront aberrations of the cornea and change the relative contribution of coma- and spherical-like aberrations. For a large pupil, laser in situ keratomileusis induces more spherical aberrations than photorefractive keratectomy. This finding could be attributable to the smaller transition zone of the laser ablation in the laser in situ keratomileusis procedure.