The Combined Effect of Tropicamide and Phenylephrine on Corneal Astigmatism Axis.

PURPOSE: To analyze astigmatism axis changes after tropicamide and phenylephrine combined instillation. METHOD: One hundred and thirty-one eyes from 66 patients enrolled this cross-sectional study. An extensive ocular examination was carried out prior to tropicamide and phenylephrine instillation. Power and axis value from flat, steep, and mean keratometry were calculated using an Auto Kerato-Refractometer (AKR). Later, topography and tomography maps were evaluated with Pentacam HR® (Oculus, Wetzlar, Germany). Subsequently, a single drop of tropicamide 1% and phenylephrine hydrochloride 10% were instilled twice, with a five-minute gap between each instillation. After 30 minutes, the AKR and Pentacam HR® tests were repeated. RESULTS: Incyclotorsion was found in 59 eyes (45.1%) and mean absolute incyclotorsion change was 3.91 ± 3.62 degrees (0.10 to 14.20). Excyclotorsion was found in 72 eyes (54.9%) and mean excyclotorsion change was 4.99 ± 5.94 degrees (0.20 to 36.20). We observed that 74.6% and 68.1% of eyes experienced incyclotorsion and excyclotorsion within 0 to 5 degrees, respectively. Fewer patients experienced incyclotorsion and excyclotorsion changes within 5 to 10 degrees, precisely 11.8% and 19.4%, respectively. Eyes that experienced over 10 degrees of incyclotorsion and excyclotorsion were 13.6% and 12.5%, respectively. CONCLUSION: Astigmatism axis could change after combined tropicamide and phenylephrine instillation. Reference axis marking in astigmatism correction surgery should be performed under the same circumstances as the astigmatism axis has been measured.

Intraocular lens power calculation formula accuracy: Comparison of 12 formulas for a trifocal hydrophilic intraocular lens.

PURPOSE: To evaluate the accuracy of 12 intraocular lens (IOL) power formulas; Barrett Universal II, Emmetropia Verifying Optical (EVO), Haigis, Hill-Radial Basis Function (RBF), Hoffer Q, Holladay I, Kane, Ladas Super Formula, Olsen Lenstar, Panacea, Pearl-DGS, Sanders-Retzlaff-Kraff/theoretical (SRK/T). In addition, an analysis of the efficacy as a function of the axial length was performed. METHODS: About 171 from 93 patients: 68 male eyes and 103 female eyes. Twelve IOL power formula calculations were studied with one IOL platform (trifocal hydrophilic IOL, FineVision Micro F), one biometer (Lenstar LS 900), one topographer (CSO Sirius Topographer), one surgeon, and one optometrist. Optimization were determined to be zeroed mean refractive prediction error. Mean error (ME), mean absolute error (MAE), median absolute error (MedAE) and refractive accuracy within ±1.00 D was calculated. Axial length was split in short and medium eyes. RESULTS: One hundred and seventy eyes were included. Formulas were ranked by percentage within ±0.50 diopters and MAE (D). Among all eyes, Olsen 86.55% (0.273 D) and Barrett Universal II 86.55% (0.285D). For short eyes (<22.5 mm), Olsen 90.70% (0.273 D) and Kane 90.70% (0.225 D). For medium eyes, Barrett 89.34% (0.237 D) and Pearl 86.89% (0.263 D). CONCLUSION: Olsen and Barrett formula obtained excellent accuracy for overall eyes. Kane and Olsen formula obtained the best results in short eyes. For medium axial length Barrett formula achieved the best accuracy results.

Riboflavin and ultraviolet light a therapy as an adjuvant treatment for medically refractive Acanthamoeba keratitis: report of 3 cases.

PURPOSE: To present the first 3 cases of Acanthamoeba keratitis (AK), unresponsive to medical treatment, that were successfully treated with a novel adjunctive therapy using ultraviolet light A (UVA) and riboflavin (B2). DESIGN: Interventional case series. PARTICIPANTS: Two patients with confirmed AK and 1 patient with presumptive AK, which were all refractive to multidrug conventional therapy. INTERVENTION: Two treatment sessions involving topical application of 0.1% B2 solution to the ocular surface combined with 30 minutes of UVA irradiation focused on the corneal ulcer. MAIN OUTCOME MEASURES: Clinical examination by slit lamp, confocal microscopy, and histopathology, when available. RESULTS: All patients in these series showed a rapid reduction in their symptoms and decreased ulcer size after the first treatment session. The progress of the clinical improvement began to slow after 1 to 3 weeks of the first application and was then renewed after the second application. All ancillary signs of inflammation mostly resolved after the second treatment session. The ulcers in all patients continued to decrease and were closed within 3 to 7 weeks of the first application. Two patients developed dense central corneal scars, and penetrating keratoplasty was performed for visual rehabilitation. Histopathologic examination of the excised tissue revealed no Acanthamoeba organisms. The remaining patient had no symptoms or signs of infection, both clinically and by confocal microscopy, and was left with a semitransparent eccentric scar that did not affect visual acuity. CONCLUSIONS: The adjunctive use of UVA and B2 therapy seems to be a possible alternative for selected cases of medication-resistant AK.

Primary congenital glaucoma and Rieger's anomaly: extended haplotypes reveal founder effects for eight distinct CYP1B1 mutations.

PURPOSE: Mutations in the cytochrome P450 1B1 (CYP1B1) gene are a frequent cause of primary congenital glaucoma (PCG) in different ethnic groups. Cytochrome P450 proteins are monooxygenases, which catalyze many reactions involved in the metabolism of drugs as well as steroids and other lipids. The repeated occurence of several mutations in various ethnic groups raises the question if founder effects or mutation-prone sites in CYP1B1 are the cause for this observation. METHODS: A total of 30 individuals (26 PCG patients, three Rieger's anomaly patients, and one variant carrier), presenting 17 variants in CYP1B1 (15 mutations and two variations) were included in our study. We sequenced the entire genomic region of CYP1B1 and analyzed microsatellites flanking the gene in all individuals and constructed haplotypes for all variations using a combination of single nucleotide polymorphisms and microsatellites. RESULTS: For the CYP1B1 genomic region, we identified five extended haplotypes associated with 17 variations. These haplotypes were complemented with microsatellite information from the region surrounding this gene. A total of eight CYP1B1 mutations were found more than once, each of them presenting one identical haplotype in different individuals. Six mutations were represented in different ethnic groups. CONCLUSIONS: Our results confirm founder effects for most of CYP1B1 mutations. Most of these mutations must have occurred as unique events in the past.

Primary congenital glaucoma: a novel single-nucleotide deletion and varying phenotypic expression for the 1,546-1,555dup mutation in the GLC3A (CYP1B1) gene in 2 families of different ethnic origin.

PURPOSE: To present new molecular genetic data on primary congenital glaucoma from 2 families, 1 isolated case and 3 familial cases due to mutations in the cytochrome P-450 1B1 (CYP1B1) gene. METHODS: All diagnoses were made by slit-lamp biomicroscopy, gonioscopy, cornea and optic disk measurements, ultrasound-biometry, and automated static threshold perimetry where possible. Mutation screening was performed by direct sequence analysis of DNA extracted from peripheral blood of the patients and their relatives. RESULTS: For the isolated case, a child of 4 years, a homozygous nucleotide deletion within a tetrad of cytosines (nt622-625, 622delC) was found leading to a predicted nonsense codon 93 truncating the protein by 450 amino acids. For the familial cases, the 3 affected members showed a homozygous mutation 1,546-1,555dupTCATGCCACC for which 9 healthy relatives proved to be heterozygous. The phenotypic expression of these 3 patients varied widely. CONCLUSION: Our results confirm the crucial role of CYP1B1 mutations for congenital glaucoma.