Jonathan E. Moore

Purpose: Evaluate postoperative visual performance in patients with bilaterally implanted AT LARA or AT LARA/AT LISA tri (Carl Zeiss AG, Jena, Germany) intraocular lenses. Methods: Multicentered, comparative, open-label, retrospective/prospective study. Post-IOL implantation, patients were prospectively enrolled into this study; preoperative patient data were collected retrospectively. Follow-up was at 2–4 and 5–8 months post-surgery. The primary endpoint was binocular best corrected distance visual acuity (CDVA). The study was retrospectively registered on clinicaltrials.gov (#NCT05462067). Results: Seventy-one patients (142 eyes) were enrolled; 67 patients (134 eyes) have 5–8 months data. The mean binocular CDVA at 2–4 months was -0.10 ± 0.06 logMAR in the bilateral AT LARA group (“bilateral”) and -0.11 ± 0.09 logMAR in the combined implantation AT LARA/ AT LISA tri group (“combined implantation”); (P = 0.4856). At 5–8 months, mean binocular CDVA was -0.13 ± 0.06 logMAR in the bilateral group and -0.11 ± 0.09 in the combined implantation group (P = 0.4003). At 5–8 months, more eyes in the bilateral group attained 0.2 logMAR or better binocular uncorrected intermediate VA (UIVA; 67 cm) than those in the combined implantation group (100% vs. 94%, respectively). The bilateral group achieved a mean of 0.24 ± 0.11 logMAR in uncorrected near VA (UCNVA), compared to a mean of 0.16 ± 0.12 logMAR in the combined implantation group at 5–8 months (P = 0.0041). Conclusions: A combined implantation approach (AT LARA in the distance dominant eye/AT LISA tri in the non-dominant eye) produced similar CDVA outcomes but better UCNVA as bilateral implantation with the AT LARA. UIVA was comparable between groups. No new safety concerns were reported.

Corneal cross-linking is nowadays the most used strategy for the treatment of keratoconus and recently it has been exploited for an increasing number of different corneal pathologies, from other ectatic disorders to keratitis. The safety of this technique has been widely assessed, but clinical complications still occur. The potential effects of cross-linking treatment upon the limbus are incompletely understood; it is important therefore to investigate the effect of UV exposure upon the limbal niche, particularly as UV is known to be mutagenic to cellular DNA and the limbus is where ocular surface tumors can develop. The risk of early induction of ocular surface cancer is undoubtedly rare and has to date not been published other than in one case after cross-linking. Nevertheless it is important to further assess, understand, and reduce where possible any potential risk. The aim of this review is to summarize all the reported cases of a pathological consequence for the limbal cells, possibly induced by cross-linking UV exposure, the studies donein vitroorex vivo, the theoretical bases for the risks due to UV exposure, and which aspects of the clinical treatment may produce higher risk, along with what possible mechanisms could be utilized to protect the limbus and the delicate stem cells present within it.

PURPOSE: To evaluate outcomes of high myopic LASIK using the MEL 80 excimer laser (Carl Zeiss Meditec, Jena, Germany). METHODS: Retrospective analysis of 479 consecutive high myopic LASIK procedures (318 patients) using the MEL 80 excimer laser and VisuMax femtosecond laser (Carl Zeiss Meditec) in 77% of cases or zero compression Hansatome microkeratome (Bausch & Lomb, Rochester, NY) in 23% of cases. Inclusion criteria were preoperative spherical equivalent refraction (SEQ) of between −8.00 and −14.25 diopters (D) and corrected distance visual acuity (CDVA) of 20/20 or better. Patients were observed for a minimum of 1 year. Flap thickness was between 80 and 160 µ m and optical zone was between 5.75 and 6.50 mm. Standard outcomes analysis was performed. RESULTS: Mean attempted SEQ was −9.39 ± 1.22 D (range: −8.00 to −14.18 D) and mean cylinder was −1.03 ± 0.84 D (range: 0.00 to −4.50 D). Mean age was 37 ± 9 years (range: 21 to 60 years) with 54% female patients. Postoperative SEQ was ±0.50 D in 55% and ±1.00 D in 83% of eyes after primary treatment. After re-treatment, 69% of eyes were within ±0.50 D and 95% were within ±1.00 D. UDVA was 20/20 or better in 89% of eyes after final treatment. One line of CDVA was lost in 3% of eyes and no eyes lost two or more lines. Statistically significant increases ( P < .001) were measured in contrast sensitivity (CSV-1000) at 12 and 18 cycles per degree. CONCLUSIONS: The MEL 80 excimer laser was found to achieve high efficacy and safety for treatment of high myopia between −8.00 and −14.25 D and up to −4.50 D of cylinder. [ J Refract Surg. 2016;32(5):290–297.]

Meesmann epithelial corneal dystrophy (MECD) is a rare autosomal dominant disorder caused by dominant-negative mutations within the KRT3 or KRT12 genes, which encode the cytoskeletal protein keratins K3 and K12, respectively. To investigate the pathomechanism of this disease, we generated and phenotypically characterized a novel knock-in humanized mouse model carrying the severe, MECD-associated, K12-Leu132Pro mutation. Although no overt changes in corneal opacity were detected by slit-lamp examination, the corneas of homozygous mutant mice exhibited histological and ultrastructural epithelial cell fragility phenotypes. An altered keratin expression profile was observed in the cornea of mutant mice, confirmed by western blot, RNA-seq and quantitative real-time polymerase chain reaction. Mass spectrometry (MS) and immunohistochemistry demonstrated a similarly altered keratin profile in corneal tissue from a K12-Leu132Pro MECD patient. The K12-Leu132Pro mutation results in cytoplasmic keratin aggregates. RNA-seq analysis revealed increased chaperone gene expression, and apoptotic unfolded protein response (UPR) markers, CHOP and Caspase 12, were also increased in the MECD mice. Corneal epithelial cell apoptosis was increased 17-fold in the mutant cornea, compared with the wild-type (P < 0.001). This elevation of UPR marker expression was also observed in the human MECD cornea. This is the first reporting of a mouse model for MECD that recapitulates the human disease and is a valuable resource in understanding the pathomechanism of the disease. Although the most severe phenotype is observed in the homozygous mice, this model will still provide a test-bed for therapies not only for corneal dystrophies but also for other keratinopathies caused by similar mutations.

No author has a financial or proprietary interest in any material or method mentioned.