Corneal sensitivity may decrease in adenoviral epidemic keratoconjunctivitis--a confocal microscopic study.

OBJECTIVES: To report a new clinical finding, decreased corneal sensitivity, in epidemic keratoconjunctivitis and to evaluate this sign with corneal confocal microscopy. METHODS: Forty-one eyes of 28 patients who developed corneal infiltrates after an outbreak of epidemic keratoconjunctivitis were included in the study. Clinical and confocal microscopic findings are described. RESULTS: In this outbreak of 72 patients, 28 (38.9%) developed corneal infiltrates. The corneal involvement was unilateral in 15 patients (53.6%) and bilateral in 13 patients (46.4%). Corneal sensitivities were measured in 35 eyes of 24 patients and found to be decreased in 26 eyes (74.3%). Decreased corneal sensation was a feature of mainly stage 2 (7 eyes) and stage 3 (11 eyes) keratitis. Corneal sensitivity returned to normal levels in all eyes in a mean of 8.5 days. The main confocal microscopic features during the period of decreased corneal sensitivity were morphologic changes in the infected epithelial cells, extracellular bright microdeposits, infiltration with round inflammatory cells and dendritic cells, increased brightness in the extracellular matrix and the stroma surrounding the corneal nerves, and increased keratocyte activity. The intensity of the inflammatory reaction in the extracellular space and corneal stroma and the reflectivity of the corneal nerves had subsided by the second confocal measurements. CONCLUSION: There may be a transient decrease in the corneal sensitivity during the course of epidemic keratoconjunctivitis. Confocal microscopy can help to evaluate the changes in the cornea during this period. Future studies are needed to understand the nature of this clinical finding.

NEUROTROPHIC KERATOPATHY AFTER RETINAL DETACHMENT SURGERY COMBINED WITH ENDOLASER PHOTOCOAGULATION.

PURPOSE: To report neurotrophic keratopathy after vitreoretinal surgery combined with aggressive photocoagulation. METHODS: We report a series of three cases with neurotrophic keratopathy after pars plana vitrectomy combined with endolaser photocoagulation. RESULTS: Three patients who had pars plana vitrectomy with different indications were identified. On follow-up, all patients were diagnosed with neurotrophic keratopathy. Two of the patients underwent amniotic membrane transplantation for the treatment of resistant neurotrophic corneal ulcers. CONCLUSION: Neurotrophic keratopathy may occur after pars plana vitrectomy. The possible mechanism is long ciliary nerve damage related to the extensive endolaser photocoagulation.

Unsuccessful probing and nasolacrimal canal agenesis in congenital epiphora.

PURPOSE: To present 3 cases with nasolacrimal canal agenesis who underwent repetitive unsuccessful probing for treatment of congenital epiphora. MATERIALS AND METHODS: Three patients who had undergone topical antibiotic therapy, lacrimal sac massage and repetitive probing in Ondokuz Mayis University, Medical School, Ophthalmology Department between June 2006 and March 2007 were included in the study. Thin-section computerized tomography (CT) scan was performed in all cases since nasolacrimal duct could not be detected during repetitive probing. RESULTS: Among the patients 2 were males and 1 was a female. They were within the age range 5-7. Since it was not possible to cannulate the nasolacrimal canal during probing, CT scans were performed and nasolacrimal duct agenesis was detected in 3 patients. One of the patients had additional upper punctum agenesis, who also had no right frontal sinus and left sphenoid sinus. All tomographic images revealed a rudimentary upper nasolacrimal canal ending blindly and a lower canal leading into the maxillary sinus, which was very typical for the duct agenesis. In all patients, lacrimal fossas were shallow and irregular. CONCLUSION: Nasolacrimal duct agenesis should be considered in patients with congenital nasolacrimal duct obstruction and unsuccessful repetitive probing, especially if it is difficult to cannulate nasolacrimal canal during probing. Although assessing whether dacryocystorhinostomy is in favor of the patient, the lacrimal sac and fossa should be examined with imaging in details.

Regression of severe corneal stromal neovascularization with topical cyclosporine 0.05% after penetrating keratoplasty for fungal corneal ulcer.

PURPOSE: To report regression of corneal stromal neovascularizations with the use of topical cyclosporine 0.05% in a corneal transplant patient performed for fungal corneal ulcer. DESIGN: Case report. METHODS: A 14-year-old boy treated for fungal corneal ulceration developed 360 degrees corneal stromal neovascularization peroperatively. Topical cyclosporine 0.05% was used to decrease the risk of rejection. RESULTS: The neovascularizations regressed totally within 2 months and no signs of graft rejection were present at 6 months follow up. CONCLUSION: Topical cyclosporine 0.05% may result in regression of stromal corneal neovascularizations and help to reduce the risk of graft rejection in selected cases.

Orbital drainage of different sizes of colloids in rabbits: a dynamic scintigraphic study.

PURPOSE: To investigate the drainage patterns of radiolabeled colloids of different sizes injected into the orbital cavity in an animal model. METHODS: Twenty-one orbits of 11 rabbits were included in the study. In group 1, human serum macroaggregates with particle sizes of 10 to 100 microm, labeled with 10 mL of 1480 MBq (40 mCi) technetium pertechnetate Tc 99m (99mTc), were used. In group 2, human serum albumin colloidal particles with particle sizes of 50 to 80 nm, labeled with 5 mL of 740 MBq (20 mCi) 99mTc, were used. In group 3, colloidal tin with particle sizes of 300 to 600 nm, labeled with 9 mL of 1665 MBq (45 mCi) 99mTc, were used. The dynamic acquisition of liver for 10 minutes (120 frames for 5 seconds) in a 128 x 128 matrix was acquired immediately after intraorbital injection and at the end of the second hour. RESULTS: The liver in groups 2 and 3 and the lung in group 1 were visualized in 10 seconds or less in six, five, and four rabbits, respectively. The injected activity persisted in the orbits in varying percentages in all rabbits at the end of acquisition. CONCLUSIONS: Intraorbital injections have a great potential for systemic absorption and should not be considered as local pharmaceutical administration.

A novel variant of combined granular-lattice corneal dystrophy associated with the Met619Lys mutation in the TGFBI gene.

OBJECTIVE: To report a novel mutation in TGFBI (GenBank NM_000358), p.Met619Lys, associated with a variant of combined granular-lattice corneal dystrophy. METHODS: Slitlamp examination and DNA collection from the proband and affected and unaffected relatives. All 17 exons of TGFBI were amplified and sequenced in the proband. Exon 14 was amplified and sequenced in the proband's family members and in 100 controls. Histopathologic examination of the excised corneal buttons from the proband and 3 family members was also performed. RESULTS: Affected individuals demonstrated an age-dependent phenotype, with the progression from central subepithelial needlelike deposits in younger individuals to polymorphic anterior stromal opacities in older family members. Screening of TGFBI in the proband demonstrated a novel mutation, p.Met619Lys, which was also present in all affected family members. Histopathologic examination revealed stromal deposits that stained with the Congo red and Masson trichrome stains as well as an antibody to the protein product of TGFBI. CONCLUSIONS: We present a unique corneal dystrophy phenotype associated with the novel p.Met619Lys mutation in TGFBI. Clinical Relevance The atypical and variable phenotype and the demonstration of both hyaline and amyloid stromal deposits indicate that neither clinical nor histopathologic features may be relied on to accurately diagnose and classify the corneal dystrophies.

Jellyfish sting injury to the cornea.

A 25-year-old woman presented to the emergency room 2 hours after a jellyfish sting to the left eye. Centrally located linear epithelial defects were observed on slit-lamp evaluation. The epithelial defects improved but did not heal totally after meticulous patching with antibiotic ointment and cycloplegic drops. Small, subepithelial negative staining areas within the epithelial defects were observed on day 3. Confocal microscopy was performed and revealed thread-like hyperreflective structures, mainly located at the basal epithelial layer. Following debridement of the traumatized areas, the corneal epithelium healed completely in 24 hours, resulting in increased visual acuity and decreased foreign body sensation. Jellyfish stings to the eye may involve the intrusion of the nematocysts, thread-like venomous structures, into the cornea. Debridement of these foreign bodies can be helpful in the treatment of resistant cases.

Identification of mutations in UBIAD1 following exclusion of coding mutations in the chromosome 1p36 locus for Schnyder crystalline corneal dystrophy.

PURPOSE: To identify the genetic basis of Schnyder crystalline corneal dystrophy (SCCD) through screening positional candidate genes and UBIAD1, in which mutations have been associated with SCCD, in affected families. METHODS: The coding region of each of the 16 positional candidate genes for which mutation screening has not been previously reported was screened with polymerase chain reaction (PCR) amplification and automated sequencing in four affected individuals from two families with SCCD. In addition, the coding region of UBIAD1, located just outside of the originally described SCCD candidate interval on chromosome 1p36, was directly sequenced in affected and unaffected individuals from three families with SCCD. RESULTS: Eighteen novel and 15 previously reported sequence variants were identified in 10 of the 16 positional candidate genes. Only two of the sequence variants segregated with the affected phenotype in either of the families screened. Both were novel single nucleotide polymorphisms (SNPs) predicted to result in synonymous amino acid substitutions in different predicted genes. However, one of these SNPs was also identified in control individuals, and the other SNP was not predicted to alter splicing. Screening of UBIAD1 revealed a different missense mutation in each of the three unrelated probands that was screened: p.Asn102Ser, p.Arg119Gly, and p.Leu121Val. Screening of the affected and unaffected relatives of the probands in whom the p.Asn102Ser and p.Leu121Val mutations were identified demonstrated that each mutation segregated with the affected phenotype. None of the three missense mutations was identified in 110 control individuals. CONCLUSIONS: No presumed pathogenic coding region mutations were identified in the genes mapped to the candidate region for SCCD. However, missense mutations in UBIAD1, located just outside of the originally described SCCD fine mapped region, were identified in each of the three families with SCCD, confirming that mutations in UBIAD1 are associated with SCCD.

Elucidating the molecular genetic basis of the corneal dystrophies: are we there yet?

The identification of the genetic basis of approximately half of the corneal dystrophies in the past decade has resulted in significant advances in our understanding of the genetic control of corneal clarity and has provided clinicians with a definitive means to confirm or refute presumptive clinical diagnoses. This article serves as a guide to understanding the genetic basis of the corneal dystrophies and provides a revised anatomically based classification system that is intended for the clinician, who must possess a working knowledge of the molecular genetic basis of the corneal dystrophies to accurately diagnose, counsel, and manage the disease in affected patients.

Central toxic keratopathy: description of a syndrome in laser refractive surgery.

PURPOSE: To describe the clinical spectrum of a syndrome in laser refractive surgery, which we call central toxic keratopathy, and to present cases that illustrate the range of this syndrome. DESIGN: Retrospective observational case series. METHODS: Eyes with noninflammatory central corneal opacification in the immediate postoperative period after photorefractive keratectomy (PRK) or laser in situ keratomileusis (LASIK) were identified, and the charts abstracted. RESULTS: Twenty-three eyes of 14 patients were identified who developed central corneal opacification three to nine days after laser refractive surgery. Nineteen of these eyes had LASIK and four had PRK. All eyes had central corneal opacification in the area of laser treatment that extended posteriorly from the interface into the stromal bed (in the case of LASIK eyes). The opacification persisted a minimum of two months to a maximum of 18 months before clearing. Nine eyes developed postoperative hyperopia of greater than 2 diopters. Pre- and postoperative best-spectacle corrected acuity was available on 19 eyes; one of these eyes lost two lines of corrected acuity, and two other eyes lost one line. Eighteen of 19 LASIK eyes had diffuse lamellar keratitis preceding the onset of corneal opacification. CONCLUSIONS: Central toxic keratopathy is characterized by noninflammatory central corneal opacification with a significant hyperopic shift. The opacification gradually clears over a period of months, leaving the eye hyperopic. Enhancement is indicated to treat residual hyperopia and remove residual striae. Topical or oral corticosteroid treatment is not indicated. The cause of central toxic keratopathy is unknown.

Identification of scanning slit-beam topographic parameters important in distinguishing normal from keratoconic corneal morphologic features.

PURPOSE: To identify morphologic parameters obtained using scanning slit-beam topography that help distinguish normal from keratoconic corneal morphologic features. DESIGN: Observational, retrospective, cross-sectional study. METHODS: This retrospective review examined 207 normal eyes of patients undergoing an initial consultation for primary refractive surgery and 42 eyes with clinical keratoconus (KCN). The following parameters were examined and compared between the two groups: astigmatism, central corneal power, irregularity indices at 3 mm (II3) and 5 mm (II5), maximal posterior elevation (MPE) magnitude and location, thinnest optical pachymetry (TOP) magnitude and location, anterior elevation best-fit sphere (ABFS), posterior elevation best-fit sphere (PBFS), the ratio of ABFS to PBFS, the difference between average inferior and average superior K values at 3 mm and 5 mm in both keratometric (I-S K3 and I-S K5) and tangential (I-S T3 and I-S T5) topographic maps, and skewed radial axis at 3 mm (SRAX3) and 5 mm (SRAX5) of the keratometric topography map. RESULTS: The II3, II5, MPE magnitude, TOP magnitude, ABFS, PBFS, ABFS-to-PBFS ratio, I-S K at both 3 mm and 5 mm, I-S T at both 3 and 5 mm, and SRAX at 3 mm and 5 mm values were significantly different among the two groups (P < .001). The least-correlated parameters were SRAX3, TOP magnitude, and II3 in the KCN group and I-S K3, amount of astigmatism and MPE magnitude in the normal group. CONCLUSIONS: Parameters obtained using scanning slit-beam topography may allow improved differentiation of keratoconic from normal corneal shapes, especially when the poorly correlated intragroup parameters are used.

A clinical and histopathologic examination of accelerated TGFBIp deposition after LASIK in combined granular-lattice corneal dystrophy.

PURPOSE: To report the clinical and histopathologic features of accelerated TGFBI protein (TGFBIp) deposition after lamellar keratorefractive surgery in a patient with combined granular-lattice corneal dystrophy (CGLCD) who underwent bilateral corneal transplantation. DESIGN: Interventional case report. METHODS: A 28-year-old woman with a presumed TGFBI corneal dystrophy, but who retained best corrected visual acuity of 20/20 in each eye, underwent myopic laser-assisted in-situ keratomileusis (LASIK) both eyes (OU). For definitive diagnosis of the corneal dystrophy, buccal epithelial cells were collected as a source of genomic DNA and screening of TGFBI exons 4 and 12 was performed. RESULTS: Four months after the performance of an uncomplicated LASIK procedure, the patient's uncorrected visual acuity was 20/15 OU. Over the following two years, the appearance of confluent white stromal deposits at the LASIK flap interface resulted in disabling glare and a reduced best-corrected visual acuity of 20/40 OU. Corneal transplantation was performed in each eye, and histopathologic examination of the excised corneal buttons was performed. Eosinophilic material that stained positively with the Masson trichrome stain was present in the LASIK flap interface, as well as in the stroma of the flap and the anterior portion of the stromal bed. No amyloid deposits were identified with the Congo red stain. Screening of TGFBI exons 4 and 12 revealed the Arg124His mutation associated with CGLCD. CONCLUSIONS: Accelerated deposition of TGFBIp may occur after lamellar corneal surgery in patients with CGLCD. Therefore, LASIK surgery should be avoided in patients with any of the TGFBI dystrophies, and surgeons should be aware of the potential for rapid interface TGFBIp deposition after lamellar corneal surgery.

An unusual presentation of macular corneal dystrophy associated with uniparental isodisomy and a novel Leu173Pro mutation.

PURPOSE: To report an unusual phenotype of macular corneal dystrophy (MCDC1) associated with a novel CHST6 mutation transmitted via maternal isodisomy. METHODS: Slit lamp examination of the patient and his parents was performed. DNA was collected from each individual for amplification and sequencing of the CHST6 coding region, as well as exons 4 and 12 of TGFBI. Serum antigenic keratan sulfate (AgKS) levels were measured for confirmation of the diagnosis and subtyping of MCDC1. Quantitative real-time PCR (qPCR) was performed to differentiate between homozygous and hemizygous sequence variants. Genotyping at 12 single nucleotide polymorphisms (SNPs) within and surrounding CHST6 was performed to determine the pattern of inheritance of mutations identified in CHST6. RESULTS: Examination of the proband revealed bilateral, discrete, axially distributed, gray-white deposits at the level of Bowman's layer, with diffuse fine corneal stromal haze. Screening of TGFBI exons 4 and 12 in the proband did not reveal any allelic variants. However, screening of CHST6 in the proband demonstrated a novel homozygous missense mutation involving a highly conserved amino acid (c.518T > C; Leu173Pro) and undetectable serum AgKS levels in the proband confirmed the diagnosis of type I MCDC1. Quantitative PCR confirmed that both copies of CHST6 were present in the patient, excluding the possibility that the mutation was present in the hemizygous state. The results of genotyping were consistent with maternal isodisomy, as the patient was homozygous for an allele possessed by his mother at each SNP, two of which were informative and demonstrated nonpaternal inheritance. CONCLUSION: A phenotypically unusual variant of MCDC1 was found to be associated with the novel Leu173Pro mutation in CHST6, transmitted via uniparental isodisomy, a previously unreported pattern of inheritance in the corneal dystrophies.

Autosomal dominant cornea plana is not associated with pathogenic mutations in DCN, DSPG3, FOXC1, KERA, LUM, or PITX2.

PURPOSE: To determine the genetic basis of autosomal dominant cornea plana (CNA1) through the performance of a genome-wide linkage analysis and screening of the decorin (DCN), dermatan sulfate proteoglycan 3 (DSPG3), forkhead box C1 (FOXC1), keratocan (KERA), lumican (LUM,) and paired-like homeodomain transcription factor 2 (PITX2) genes in members of an affected multigenerational family. METHODS: Cycloplegic refraction, slit lamp biomicroscopy, corneal pachymetry, and corneal topography were performed to determine each patient's affected status. DNA was obtained from affected and unaffected subjects for the performance of a genome-wide linkage analysis as well as PCR amplification and sequencing of DCN, DSPG3, FOXC1, KERA, LUM, and PITX2. RESULTS: Five affected and three unaffected individuals were examined and provided a peripheral blood sample for DNA isolation. All affected individuals demonstrated an average corneal dioptric power less than 39 D, as well as one or more of the following anomalies: high hyperopia, strabismus, microcornea, posterior embryotoxon, iridocorneal adhesions, iris atrophy, and pupillary irregularities. A genome-wide linkage analysis did not indicate or exclude linkage to the region on chromosome 12 to which CNA1 has been previously mapped, and did not provide a single or multipoint LOD score greater than 2.0 for any of the 400 microsatellite markers. Screening of DCN, DSPG3, FOXC1, KERA, LUM, and PITX2 revealed 12 previously described single nucleotide polymorphisms, 2 previously described duplications, and 1 previously described insertion. None of the mutations previously associated with autosomal recessive cornea plana (CNA2) were identified. Seven novel sequence variants were described, including 5 single nucleotide substitutions, 1 insertion and 1 deletion. None of the identified sequence variants demonstrated complete segregation with the affected phenotype in the pedigree. CONCLUSION: Although missense and nonsense mutations in KERA are associated with CNA2, we did not identify any of the previously described mutations or novel mutations that segregated with the disease phenotype in a family with CNA1. In addition, no pathogenic sequence variations were found in DCN, DSPG3, LUM, PITX2 and FOXC1, which have also been implicated in corneal and anterior segment dysgenesis.

Amniotic membrane transplantation with anterior stromal micropuncture for treatment of painful bullous keratopathy in eyes with poor visual potential.

PURPOSE: To report the use of anterior stromal micropuncture and amniotic membrane transplantation in the management of painful bullous keratopathy in patients with poor visual potential. METHODS: Interventional case series. A retrospective review was performed to identify all patients who were treated by one of us (A.J.A.) between January 1, 2003, and June 30, 2005. RESULTS: Five eyes of 5 patients were identified. Conjunctival scarring secondary to glaucoma and retinal surgeries prevented mobilization of the conjunctiva in each of the patients identified. Each eye showed an intact, smooth corneal epithelial surface 1 month after the procedure, and no patients developed recurrent bullae formation during the follow-up period (average follow-up, 21 months; range, 11-34 months). CONCLUSIONS: Anterior stromal micropuncture and amniotic membrane transplantation is an effective technique for the management of bullous keratopathy in patients with poor visual potential. The success rate of this combined procedure may exceed that of either procedure performed alone.

Keratoconus is not associated with mutations in COL8A1 and COL8A2.

PURPOSE: To evaluate the suggested role of the COL8A1 and COL8A2 genes in the pathogenesis of the corneal ectatic disorders keratoconus and keratoglobus through mutation screening in affected patients. METHODS: DNA extraction, polymerase chain reaction amplification, and sequencing of COL8A1 and COL8A2 were performed in 50 unrelated keratoconus and 2 unrelated keratoglobus patients. RESULTS: No sequence variations were identified in COL8A1 and COL8A2 in the 2 patients with keratoglobus. Screening of COL8A1 in keratoconus patients revealed a previously identified single nucleotide polymorphism (SNP; c.1850C>T; Pro535Pro), in 1 patient. Screening of COL8A2 in keratoconus patients revealed 7 previously described SNPs: c.14G>A (Gly3Arg); c.112G>A (Ala35Ala); c.1012C>G (Leu335Leu); c.1308G>A (Arg434His); c.1492G>A (Gly495Gly); c.1512C>T (Thr502Met); and c.1765C>T (Pro586Pro). Four novel sequence variants were also identified, each in 1 affected patient: c.38_40dupCTG (Leu11dup), also identified in an unaffected relative of the affected proband, c.667G>A (Gly220Gly), c.1588G>A (Pro527Pro), and c.2026C>T (Val673Val). None of the 3 novel synonymous substitutions identified in COL8A2 was predicted to produce a splice acceptor site. CONCLUSIONS: The absence of pathogenic mutations in COL8A1 and COL8A2 in patients with keratoconus indicates that other genetic factors are involved in the pathogenesis of this corneal ectatic disorder.

No pathogenic mutations identified in the COL8A1 and COL8A2 genes in familial Fuchs corneal dystrophy.

PURPOSE: To investigate the genetic basis of late-onset, familial Fuchs endothelial corneal dystrophy (FECD) through screening of the COL8A1 and COL8A2 genes, in which mutations have been associated with both early and late-onset, familial and sporadic FECD. METHODS: DNA extraction, PCR amplification, and direct sequencing of the COL8A1 and COL8A2 genes was performed in affected and unaffected members of 15 unrelated families with two or more members with late-onset FECD. RESULTS: Screening of the COL8A1 gene did not reveal sequence variants in any affected individuals from the 15 FECD families. In the COL8A2 gene, the previously identified mutations presumed to play a pathogenic role in cases of familial FECD (Arg155Gln, Leu450Trp, and Gln455Lys) were not discovered in any of the affected patients. A mutation previously considered causative of FECD (Arg434His) was shown not to segregate with the disease in the one family in which it was identified. Two previously identified single-nucleotide polymorphisms (SNPs), Pro575Leu and Pro586Pro, were identified in a single affected individual and three affected individuals (two families), respectively. CONCLUSIONS: The Arg434His mutation in the COL8A2 gene, previously associated with FECD, has been shown not to segregate with the disease phenotype, and thus may not be considered a disease-causing mutation. The absence of pathogenic mutations identified in the COL8A1 or COL8A2 genes in affected members of 15 pedigrees with familial FECD indicates that other genetic factors are involved in the development of this autosomal dominant corneal dystrophy.

Effect of glycemic control on refractive changes in diabetic patients with hyperglycemia.

PURPOSE: To investigate the effect of intensive glycemic control on hyperglycemia- induced changes in refraction, corneal topography, lenticular and corneal thickness in diabetic patients. METHODS: Eighteen diabetic patients with plasma glucose >300 mg/dl were enrolled in the study consecutively. Autorefraction, C-Scan corneal topography, Javal keratometry, corneal pachymetry and ultrasonic biometric measurements were carried out at presentation and after metabolic control of blood sugar (plasma glucose profile <200 mg/dl). One eye of each patient was selected randomly for statistical analysis. RESULTS: Mean plasma glucose levels were 356.00 mg/dl before and 133.78 mg/dl after treatment. The median values of the autorefractometric measurements were - 0.125 D on admission and + 0.375 D at the second examination. The difference in the refraction was statistically significant (P = 0.022). Nine of 18 patients became hyperopic, 2 became myopic and 7 showed no change after treatment. There was a significant change in the corneal topographic keratometric measurements at the flattest corneal meridian after treatment (P = 0.037). After treatment no statistically significant changes were observed in the pachymetric corneal thickness, anterior chamber depth, biometric dioptric lens calculations and Javal keratometric data. CONCLUSIONS: Hyperglycemia is the major cause of the transient refractive changes in diabetic patients. Following intensive medical treatment, a considerable number of patients tend to become more hyperopic compared with the hyperglycemic state. During the treatment period, changes in the corneal topographic parameters might be a potential source of error for keratorefractive and cataract surgery.

Comparison of normal and keratoconic corneas by Galilei Dual-Scheimpflug Analyzer.

BACKGROUND AND OBJECTIVE: To determine the efficacy of different Galilei Scheimpflug-Analyzer (GSA) parameters in discriminating between keratoconic and myopic eyes. PATIENTS AND METHODS: GSA measurements were obtained for 67 patients (67 eyes) with keratoconus and 151 patients (151 eyes) with myopia or myopic astigmatism. Several parameters, provided by the software or derived from the elevation maps, were evaluated and compared for the two groups. RESULTS: Between the two groups, statistically significant differences were observed for all corneal parameters obtained by GSA (P<0.001) except for the anterior chamber depth (P=0.149). ROC analysis determined that posterior corneal elevation was the best predictive parameter (area under the curve: 0.99). The posterior corneal elevation, at a cut-off value of 18.5µm, had 98.5% sensitivity and 98.3% specificity in discriminating keratoconus from myopic eyes. CONCLUSION: Elevation, pachymetric and keratometric parameters measured by the GSA, as well as the specific predictive GSA software parameters can effectively distinguish advanced keratoconus from myopic corneas. Also, keratoconus that is easily diagnosed by other means can be diagnosed easily by GSA software parameters.