Incidence of Glaucoma-Related Adverse Events in the First 5 Years After Pediatric Lensectomy.

Importance: Glaucoma can develop following cataract removal in children. Objective: To assess the cumulative incidence of glaucoma-related adverse events (defined as glaucoma or glaucoma suspect) and factors associated with risk of these adverse events in the first 5 years after lensectomy prior to 13 years of age. Design, Setting, and Participants: This cohort study used longitudinal registry data collected at enrollment and annually for 5 years from 45 institutional and 16 community sites. Participants were children aged 12 years or younger with at least 1 office visit after lensectomy from June 2012 to July 2015. Data were analyzed from February through December 2022. Exposures: Usual clinical care after lensectomy. Main Outcomes and Measures: The main outcomes were cumulative incidence of glaucoma-related adverse events and baseline factors associated with risk of these adverse events. Results: The study included 810 children (1049 eyes); 443 eyes of 321 children (55% female; mean [SD] age, 0.89 [1.97] years) were aphakic after lensectomy, and 606 eyes of 489 children (53% male; mean [SD] age, 5.65 [3.32] years) were pseudophakic. The 5-year cumulative incidence of glaucoma-related adverse events was 29% (95% CI, 25%-34%) in 443 eyes with aphakia and 7% (95% CI, 5%-9%) in 606 eyes with pseudophakia; 7% (95% CI, 5%-10%) of aphakic eyes and 3% (95% CI, 2%-5%) of pseudophakic eyes were diagnosed as glaucoma suspect. Among aphakic eyes, a higher risk for glaucoma-related adverse events was associated with 4 of 8 factors, including age less than 3 months (vs ≥3 months: adjusted hazard ratio [aHR], 2.88; 99% CI, 1.57-5.23), abnormal anterior segment (vs normal: aHR, 2.88; 99% CI, 1.56-5.30), intraoperative complications at time of lensectomy (vs none; aHR, 2.25; 99% CI, 1.04-4.87), and bilaterality (vs unilaterality: aHR, 1.88; 99% CI, 1.02-3.48). Neither of the 2 factors evaluated for pseudophakic eyes, laterality and anterior vitrectomy, were associated with risk of glaucoma-related adverse events. Conclusions and Relevance: In this cohort study, glaucoma-related adverse events were common after cataract surgery in children; age less than 3 months at surgery was associated with elevated risk of the adverse events in aphakic eyes. Children with pseudophakia, who were older at surgery, less frequently developed a glaucoma-related adverse event within 5 years of lensectomy. The findings suggest that ongoing monitoring for the development of glaucoma is needed after lensectomy at any age.

Reactive infectious mucocutaneous eruption - repeat etanercept after intravenous immunoglobulin: A case report.

Reactive infectious mucocutaneous eruption is a recently distinguished mucosal-predominant blistering eruption triggered by respiratory infections. We describe a previously healthy 11-year-old Black female with rapidly progressive mucocutaneous blistering after prodromal respiratory infection symptoms. Reactive infectious mucocutaneous eruption was suspected and treated with systemic corticosteroids followed by etanercept. Twenty-four hours after etanercept, the diagnosis of multisystem inflammatory syndrome in children was raised and intravenous immunoglobulin was given. Rapidly worsening mucocutaneous disease ensued but was controlled by a second dose of etanercept. Our case highlights the following: (1) the novel observation of possible interaction/neutralization of etanercept by intravenous immunoglobulin, (2) the challenging differential diagnosis of multisystem inflammatory syndrome in children for reactive infectious mucocutaneous eruption patients in the Coronavirus disease 2019 (COVID-19) pandemic, and (3) the role of early treatment to prevent dyspigmentation.

G protein-coupled receptor kinase 5 regulates thrombin signaling in platelets via PAR-1.

The interindividual variation in the functional response of platelets to activation by agonists is heritable. Genome-wide association studies (GWASs) of quantitative measures of platelet function have identified fewer than 20 distinctly associated variants, some with unknown mechanisms. Here, we report GWASs of pathway-specific functional responses to agonism by adenosine 5'-diphosphate, a glycoprotein VI-specific collagen mimetic, and thrombin receptor-agonist peptides, each specific to 1 of the G protein-coupled receptors PAR-1 and PAR-4, in subsets of 1562 individuals. We identified an association (P = 2.75 × 10-40) between a common intronic variant, rs10886430, in the G protein-coupled receptor kinase 5 gene (GRK5) and the sensitivity of platelets to activate through PAR-1. The variant resides in a megakaryocyte-specific enhancer that is bound by the transcription factors GATA1 and MEIS1. The minor allele (G) is associated with fewer GRK5 transcripts in platelets and the greater sensitivity of platelets to activate through PAR-1. We show that thrombin-mediated activation of human platelets causes binding of GRK5 to PAR-1 and that deletion of the mouse homolog Grk5 enhances thrombin-induced platelet activation sensitivity and increases platelet accumulation at the site of vascular injury. This corroborates evidence that the human G allele of rs10886430 is associated with a greater risk for cardiovascular disease. In summary, by combining the results of pathway-specific GWASs and expression quantitative trait locus studies in humans with the results from platelet function studies in Grk5-/- mice, we obtain evidence that GRK5 regulates the human platelet response to thrombin via the PAR-1 pathway.

Familial pseudohyperkalemia induces significantly higher levels of extracellular potassium in early storage of red cell concentrates without affecting other standard measures of quality: A case control and allele frequency study.

BACKGROUND: Familial pseudohyperkalemia (FP) is characterized by an increased rate of potassium leakage in refrigerated red cells and is associated with the minor allele of the single nucleotide polymorphism rs148211042 (R723Q) in the ABCB6 gene. The study aims were to obtain the minor allele frequencies of ABCB6 variants and to measure supernatant potassium accumulation, and other red cell storage parameters, in red cell concentrates (RCC) from carriers of variant rs148211042 under standard blood bank conditions. STUDY DESIGN: Whole blood units were collected from 6 FP individuals and 11 controls and processed into RCC in additive solution. RCC were sampled and tested over cold storage for full blood count, extracellular potassium, glucose, lactate, microvesicle release, deformability, hemolysis, pH, adenosine triphosphate, and 2,3-diphosphoglycerate. RESULTS: Screening of genotyped cohorts identified that variant rs148211042 is present in 1 in 394 British citizens of European ancestry. FP RCC had significantly higher supernatant potassium at all time points from day 3 onwards (p < .001) and higher mean cell volume (p = .032) than controls. The initial rate of potassium release was higher in FP RCC; supernatant potassium reached 46.0 (23.8-57.6) mmol/L (mean [range]) by day 5, increasing to 68.9 (58.8-73.7) mmol/L by day 35. Other quality parameters were not significantly different between FP RCC and controls. CONCLUSION: These data suggest that if a blood donor has FP, reducing the RCC shelf-life to 5 days may be insufficient to reduce the risk of hyperkalemia in clinical scenarios such as neonatal large volume transfusion.

A genome-wide meta-analysis yields 46 new loci associating with biomarkers of iron homeostasis.

Iron is essential for many biological functions and iron deficiency and overload have major health implications. We performed a meta-analysis of three genome-wide association studies from Iceland, the UK and Denmark of blood levels of ferritin (N = 246,139), total iron binding capacity (N = 135,430), iron (N = 163,511) and transferrin saturation (N = 131,471). We found 62 independent sequence variants associating with iron homeostasis parameters at 56 loci, including 46 novel loci. Variants at DUOX2, F5, SLC11A2 and TMPRSS6 associate with iron deficiency anemia, while variants at TF, HFE, TFR2 and TMPRSS6 associate with iron overload. A HBS1L-MYB intergenic region variant associates both with increased risk of iron overload and reduced risk of iron deficiency anemia. The DUOX2 missense variant is present in 14% of the population, associates with all iron homeostasis biomarkers, and increases the risk of iron deficiency anemia by 29%. The associations implicate proteins contributing to the main physiological processes involved in iron homeostasis: iron sensing and storage, inflammation, absorption of iron from the gut, iron recycling, erythropoiesis and bleeding/menstruation.

Novel manifestations of immune dysregulation and granule defects in gray platelet syndrome.

Gray platelet syndrome (GPS) is a rare recessive disorder caused by biallelic variants in NBEAL2 and characterized by bleeding symptoms, the absence of platelet α-granules, splenomegaly, and bone marrow (BM) fibrosis. Due to the rarity of GPS, it has been difficult to fully understand the pathogenic processes that lead to these clinical sequelae. To discern the spectrum of pathologic features, we performed a detailed clinical genotypic and phenotypic study of 47 patients with GPS and identified 32 new etiologic variants in NBEAL2. The GPS patient cohort exhibited known phenotypes, including macrothrombocytopenia, BM fibrosis, megakaryocyte emperipolesis of neutrophils, splenomegaly, and elevated serum vitamin B12 levels. Novel clinical phenotypes were also observed, including reduced leukocyte counts and increased presence of autoimmune disease and positive autoantibodies. There were widespread differences in the transcriptome and proteome of GPS platelets, neutrophils, monocytes, and CD4 lymphocytes. Proteins less abundant in these cells were enriched for constituents of granules, supporting a role for Nbeal2 in the function of these organelles across a wide range of blood cells. Proteomic analysis of GPS plasma showed increased levels of proteins associated with inflammation and immune response. One-quarter of plasma proteins increased in GPS are known to be synthesized outside of hematopoietic cells, predominantly in the liver. In summary, our data show that, in addition to the well-described platelet defects in GPS, there are immune defects. The abnormal immune cells may be the drivers of systemic abnormalities such as autoimmune disease.

Whole-genome sequencing of patients with rare diseases in a national health system.

Most patients with rare diseases do not receive a molecular diagnosis and the aetiological variants and causative genes for more than half such disorders remain to be discovered1. Here we used whole-genome sequencing (WGS) in a national health system to streamline diagnosis and to discover unknown aetiological variants in the coding and non-coding regions of the genome. We generated WGS data for 13,037 participants, of whom 9,802 had a rare disease, and provided a genetic diagnosis to 1,138 of the 7,065 extensively phenotyped participants. We identified 95 Mendelian associations between genes and rare diseases, of which 11 have been discovered since 2015 and at least 79 are confirmed to be aetiological. By generating WGS data of UK Biobank participants2, we found that rare alleles can explain the presence of some individuals in the tails of a quantitative trait for red blood cells. Finally, we identified four novel non-coding variants that cause disease through the disruption of transcription of ARPC1B, GATA1, LRBA and MPL. Our study demonstrates a synergy by using WGS for diagnosis and aetiological discovery in routine healthcare.

Genome-wide association study of eosinophilic granulomatosis with polyangiitis reveals genomic loci stratified by ANCA status.

Eosinophilic granulomatosis with polyangiitis (EGPA) is a rare inflammatory disease of unknown cause. 30% of patients have anti-neutrophil cytoplasmic antibodies (ANCA) specific for myeloperoxidase (MPO). Here, we describe a genome-wide association study in 676 EGPA cases and 6809 controls, that identifies 4 EGPA-associated loci through conventional case-control analysis, and 4 additional associations through a conditional false discovery rate approach. Many variants are also associated with asthma and six are associated with eosinophil count in the general population. Through Mendelian randomisation, we show that a primary tendency to eosinophilia contributes to EGPA susceptibility. Stratification by ANCA reveals that EGPA comprises two genetically and clinically distinct syndromes. MPO+ ANCA EGPA is an eosinophilic autoimmune disease sharing certain clinical features and an HLA-DQ association with MPO+ ANCA-associated vasculitis, while ANCA-negative EGPA may instead have a mucosal/barrier dysfunction origin. Four candidate genes are targets of therapies in development, supporting their exploration in EGPA.

Risk thresholds for alcohol consumption: combined analysis of individual-participant data for 599 912 current drinkers in 83 prospective studies.

BACKGROUND: Low-risk limits recommended for alcohol consumption vary substantially across different national guidelines. To define thresholds associated with lowest risk for all-cause mortality and cardiovascular disease, we studied individual-participant data from 599 912 current drinkers without previous cardiovascular disease. METHODS: We did a combined analysis of individual-participant data from three large-scale data sources in 19 high-income countries (the Emerging Risk Factors Collaboration, EPIC-CVD, and the UK Biobank). We characterised dose-response associations and calculated hazard ratios (HRs) per 100 g per week of alcohol (12·5 units per week) across 83 prospective studies, adjusting at least for study or centre, age, sex, smoking, and diabetes. To be eligible for the analysis, participants had to have information recorded about their alcohol consumption amount and status (ie, non-drinker vs current drinker), plus age, sex, history of diabetes and smoking status, at least 1 year of follow-up after baseline, and no baseline history of cardiovascular disease. The main analyses focused on current drinkers, whose baseline alcohol consumption was categorised into eight predefined groups according to the amount in grams consumed per week. We assessed alcohol consumption in relation to all-cause mortality, total cardiovascular disease, and several cardiovascular disease subtypes. We corrected HRs for estimated long-term variability in alcohol consumption using 152 640 serial alcohol assessments obtained some years apart (median interval 5·6 years [5th-95th percentile 1·04-13·5]) from 71 011 participants from 37 studies. FINDINGS: In the 599 912 current drinkers included in the analysis, we recorded 40 310 deaths and 39 018 incident cardiovascular disease events during 5·4 million person-years of follow-up. For all-cause mortality, we recorded a positive and curvilinear association with the level of alcohol consumption, with the minimum mortality risk around or below 100 g per week. Alcohol consumption was roughly linearly associated with a higher risk of stroke (HR per 100 g per week higher consumption 1·14, 95% CI, 1·10-1·17), coronary disease excluding myocardial infarction (1·06, 1·00-1·11), heart failure (1·09, 1·03-1·15), fatal hypertensive disease (1·24, 1·15-1·33); and fatal aortic aneurysm (1·15, 1·03-1·28). By contrast, increased alcohol consumption was log-linearly associated with a lower risk of myocardial infarction (HR 0·94, 0·91-0·97). In comparison to those who reported drinking >0-≤100 g per week, those who reported drinking >100-≤200 g per week, >200-≤350 g per week, or >350 g per week had lower life expectancy at age 40 years of approximately 6 months, 1-2 years, or 4-5 years, respectively. INTERPRETATION: In current drinkers of alcohol in high-income countries, the threshold for lowest risk of all-cause mortality was about 100 g/week. For cardiovascular disease subtypes other than myocardial infarction, there were no clear risk thresholds below which lower alcohol consumption stopped being associated with lower disease risk. These data support limits for alcohol consumption that are lower than those recommended in most current guidelines. FUNDING: UK Medical Research Council, British Heart Foundation, National Institute for Health Research, European Union Framework 7, and European Research Council.

Incidental neuroblastoma with bilateral retinoblastoma: what are the chances?

A child with bilateral familial retinoblastoma underwent staging MRI brain and orbit which identified subtle leptomeningeal enhancement, thus prompting an MRI whole body, which revealed a retroperitoneal mass, confirmed on laparoscopic biopsy to be neuroblastoma. This is the first reported case of these two rare embryonal non-central nervous system tumors occurring concurrently. The cause of this concurrence is unknown despite their pathogenic similarities with a chance of 4 cases per 10 billion children aged 1-4 years. Incidental neuroblastomas in infants can regress spontaneously but this child underwent systemic chemotherapy for his retinoblastoma that may have caused regression of the neuroblastoma.

SNP in human ARHGEF3 promoter is associated with DNase hypersensitivity, transcript level and platelet function, and Arhgef3 KO mice have increased mean platelet volume.

Genome-wide association studies have identified a genetic variant at 3p14.3 (SNP rs1354034) that strongly associates with platelet number and mean platelet volume in humans. While originally proposed to be intronic, analysis of mRNA expression in primary human hematopoietic subpopulations reveals that this SNP is located directly upstream of the predominantly expressed ARHGEF3 isoform in megakaryocytes (MK). We found that ARHGEF3, which encodes a Rho guanine exchange factor, is dramatically upregulated during both human and murine MK maturation. We show that the SNP (rs1354034) is located in a DNase I hypersensitive region in human MKs and is an expression quantitative locus (eQTL) associated with ARHGEF3 expression level in human platelets, suggesting that it may be the causal SNP that accounts for the variations observed in human platelet traits and ARHGEF3 expression. In vitro human platelet activation assays revealed that rs1354034 is highly correlated with human platelet activation by ADP. In order to test whether ARHGEF3 plays a role in MK development and/or platelet function, we developed an Arhgef3 KO/LacZ reporter mouse model. Reflecting changes in gene expression, LacZ expression increases during MK maturation in these mice. Although Arhgef3 KO mice have significantly larger platelets, loss of Arhgef3 does not affect baseline MK or platelets nor does it affect platelet function or platelet recovery in response to antibody-mediated platelet depletion compared to littermate controls. In summary, our data suggest that modulation of ARHGEF3 gene expression in humans with a promoter-localized SNP plays a role in human MKs and human platelet function-a finding resulting from the biological follow-up of human genetic studies. Arhgef3 KO mice partially recapitulate the human phenotype.

Mutations in tropomyosin 4 underlie a rare form of human macrothrombocytopenia.

Platelets are anuclear cells that are essential for blood clotting. They are produced by large polyploid precursor cells called megakaryocytes. Previous genome-wide association studies in nearly 70,000 individuals indicated that single nucleotide variants (SNVs) in the gene encoding the actin cytoskeletal regulator tropomyosin 4 (TPM4) exert an effect on the count and volume of platelets. Platelet number and volume are independent risk factors for heart attack and stroke. Here, we have identified 2 unrelated families in the BRIDGE Bleeding and Platelet Disorders (BPD) collection who carry a TPM4 variant that causes truncation of the TPM4 protein and segregates with macrothrombocytopenia, a disorder characterized by low platelet count. N-Ethyl-N-nitrosourea-induced (ENU-induced) missense mutations in Tpm4 or targeted inactivation of the Tpm4 locus led to gene dosage-dependent macrothrombocytopenia in mice. All other blood cell counts in Tpm4-deficient mice were normal. Insufficient TPM4 expression in human and mouse megakaryocytes resulted in a defect in the terminal stages of platelet production and had a mild effect on platelet function. Together, our findings demonstrate a nonredundant role for TPM4 in platelet biogenesis in humans and mice and reveal that truncating variants in TPM4 cause a previously undescribed dominant Mendelian platelet disorder.

The Allelic Landscape of Human Blood Cell Trait Variation and Links to Common Complex Disease.

Many common variants have been associated with hematological traits, but identification of causal genes and pathways has proven challenging. We performed a genome-wide association analysis in the UK Biobank and INTERVAL studies, testing 29.5 million genetic variants for association with 36 red cell, white cell, and platelet properties in 173,480 European-ancestry participants. This effort yielded hundreds of low frequency (<5%) and rare (<1%) variants with a strong impact on blood cell phenotypes. Our data highlight general properties of the allelic architecture of complex traits, including the proportion of the heritable component of each blood trait explained by the polygenic signal across different genome regulatory domains. Finally, through Mendelian randomization, we provide evidence of shared genetic pathways linking blood cell indices with complex pathologies, including autoimmune diseases, schizophrenia, and coronary heart disease and evidence suggesting previously reported population associations between blood cell indices and cardiovascular disease may be non-causal.

A workforce in crisis: a case study to expand allied ophthalmic personnel.

OBJECTIVE: To examine how the development of allied ophthalmic personnel training programs affects human resource capacity. DESIGN: Using a qualitative case study method conducted at a single Ontario institution, this article describes 6 years of establishing a 2-tiered allied ophthalmic personnel training program. PARTICIPANTS: The Kingston Ophthalmic Training Centre participated in the study with 8 leadership and program graduate interviews. METHODS: To assess regional eye health workforce needs, a case study and iterative process used triangulations of the literature, case study, and qualitative interviews with stakeholders. This research was used to develop a model for establishing allied ophthalmic personnel training programs that would result in expanding human resource capacity. RESULTS: Current human resource capacity development and deployment is inadequate to provide the needed eye care services in Canada. A competency-based curriculum and accreditation model as the platform to develop formal academic training programs is essential. Access to quality eye care and patient services can be met by task-shifting from ophthalmologists to appropriately trained allied ophthalmic personnel. CONCLUSION: Establishing formal training programs is one important strategy to supplying a well-skilled, trained, and qualified ophthalmic workforce. This initiative meets the criteria required for quality, relevance, equity, and cost-effectiveness to meet the future demands for ophthalmic patient care.

Transcriptional diversity during lineage commitment of human blood progenitors.

Blood cells derive from hematopoietic stem cells through stepwise fating events. To characterize gene expression programs driving lineage choice, we sequenced RNA from eight primary human hematopoietic progenitor populations representing the major myeloid commitment stages and the main lymphoid stage. We identified extensive cell type-specific expression changes: 6711 genes and 10,724 transcripts, enriched in non-protein-coding elements at early stages of differentiation. In addition, we found 7881 novel splice junctions and 2301 differentially used alternative splicing events, enriched in genes involved in regulatory processes. We demonstrated experimentally cell-specific isoform usage, identifying nuclear factor I/B (NFIB) as a regulator of megakaryocyte maturation-the platelet precursor. Our data highlight the complexity of fating events in closely related progenitor populations, the understanding of which is essential for the advancement of transplantation and regenerative medicine.

Postoperative glaucoma following infantile cataract surgery: an individual patient data meta-analysis.

IMPORTANCE: Infantile cataract surgery bears a significant risk for postoperative glaucoma, and no consensus exists on factors that may reduce this risk. OBJECTIVE: To assess the effect of primary intraocular lens implantation and timing of surgery on the incidence of postoperative glaucoma. DATA SOURCES: We searched multiple databases to July 14, 2013, to identify studies with eligible patients, including PubMed, MEDLINE, EMBASE, ISI Web of Science, Scopus, Central, Google Scholar, Intute, and Tripdata. We also searched abstracts of ophthalmology society meetings. STUDY SELECTION: We included studies reporting on postoperative glaucoma in infants undergoing cataract surgery with regular follow-up for at least 1 year. Infants with concurrent ocular anomalies were excluded. DATA EXTRACTION AND SYNTHESIS: Authors of eligible studies were invited to contribute individual patient data on infants who met the inclusion criteria. We also performed an aggregate data meta-analysis of published studies that did not contribute to the individual patient data. Data were pooled using a random-effects model. MAIN OUTCOMES AND MEASURES: Time to glaucoma with the effect of primary implantation, additional postoperative intraocular procedures, and age at surgery. RESULTS: Seven centers contributed individual patient data on 470 infants with a median age at surgery of 3.0 months and median follow-up of 6.0 years. Eighty patients (17.0%) developed glaucoma at a median follow-up of 4.3 years. Only 2 of these patients had a pseudophakic eye. The risk for postoperative glaucoma appeared to be lower after primary implantation (hazard ratio [HR], 0.10 [95% CI, 0.01-0.70]; P = .02; I(2) = 34%), higher after surgery at 4 weeks or younger (HR, 2.10 [95% CI, 1.14-3.84]; P = .02; I(2) = 0%), and higher after additional procedures (HR, 2.52 [95% CI, 1.11-5.72]; P = .03; I(2) = 32%). In multivariable analysis, additional procedures independently increased the risk for glaucoma (HR, 2.25 [95% CI, 1.20-4.21]; P = .01), and primary implantation independently reduced it (HR, 0.10 [95% CI, 0.01-0.76]; P = .03). Results were similar in the aggregate data meta-analysis that included data from 10 published articles. CONCLUSIONS AND RELEVANCE: Although confounding factors such as size of the eye and surgeon experience are not accounted for in this meta-analysis, the risk for postoperative glaucoma after infantile cataract surgery appears to be influenced by the timing of surgery, primary implantation, and additional intraocular surgery.

Survey on allied health personnel in Canadian ophthalmology: the scalpel for change.

OBJECTIVE: To determine the recruiting and training needs for ophthalmic medical personnel (OMP), assess the value of their certification, and compare the ophthalmic practice productivity and performance of non-certified and certified OMP, as rated by both ophthalmologists and OMP. DESIGN: Comparative analysis. PARTICIPANTS: One hundred and sixteen Canadian ophthalmologists and 98 OMP. METHODS: An invitation to complete an online survey on OMP recruitment, training, certification, and productivity performance in a clinical setting was sent to 1081 ophthalmologists and OMP. RESULTS: Fifteen percent of ophthalmologists and 31% of OMP completed the survey. Ophthalmologists (61%) reported difficulty hiring OMP; employee referrals was the best method (40%). Awareness of formal OMP training programs was high and 50% of respondents supported developing additional training programs; 55% of OMP were encouraged by their employers to obtain certification. Personal challenge and achievement (79%) and improved skills (71%) were the main reasons for OMP to obtain certification. The majority of OMP and ophthalmologists felt that certified OMP enhanced most practice productivity measures. Higher wages associated with certification were reported by 73% of respondents. CONCLUSIONS: Training of qualified OMP was identified as a need by ophthalmologists. Ophthalmic practices can increase their overall productivity by adding certified OMP to their staff.

Laser-assisted subepithelial keratectomy and photorefractive keratectomy for post-penetrating keratoplasty myopia and astigmatism in adults.

PURPOSE: To evaluate whether laser-assisted subepithelial keratectomy (LASEK) and photorefractive keratectomy (PRK) achieve effective targeted correction and the extent of post-treatment corneal haze after corneal transplantation. SETTING: Nonhospital surgical facility, Calgary, Alberta, Canada. DESIGN: Evidence-based manuscript. METHODS: This study evaluated visual acuity, refractive error correction, and potential complications after LASEK or PRK to eliminate refractive error differences after penetrating keratoplasty in adults. A Nidek EC-5000 or Technolas 217 excimer laser was used in all treatments. RESULTS: At last follow-up (mean 20.50 months post laser), the mean spherical equivalent (SE) decreased from -2.71 diopters (D) ± 4.17 (SD) to -0.54 ± 3.28 D in the LASEK group and from -4.87 ± 3.90 D to -1.82 ± 3.34 D in the PRK group. The mean preoperative uncorrected distance visual acuity (UDVA) was 1.63 ± 0.53 and 1.45 ± 0.64, respectively, and the mean postoperative UDVA, 0.83 ± 0.54 and 0.90 ± 0.55, respectively. The improvement in SE and UDVA was statistically significant in both groups (P < .01). The mean haze (0 to 3 scale) at the last follow-up was 0.46 ± 0.708 in the LASEK group and 0.58 ± 0.776 in the PRK group. CONCLUSIONS: The UDVA improved and refractive errors were effectively reduced after LASEK or PRK in eyes with previous PKP. There was no significant difference in the change in SE, UDVA, or corrected distance visual acuity between LASEK and PRK. Some patients had evidence of corneal haze, although the difference between the groups was not significant.

Laser-assisted subepithelial keratectomy for bilateral hyperopia and hyperopic anisometropic amblyopia in children: one-year outcomes.

PURPOSE: To assess the refractive, visual acuity, and binocular results of laser-assisted subepithelial keratectomy (LASEK) in children with bilateral hyperopia or hyperopic anisometropic amblyopia. SETTING: Nonhospital surgical facility and hospital clinic, Calgary, Alberta, Canada. METHODS: This retrospective review comprised children with bilateral hyperopia or hyperopic anisometropic amblyopia who had LASEK. Refractive status, visual acuity, and binocular vision were assessed and recorded 2 months and 1 year postoperatively. RESULTS: The mean spherical equivalent (SE) in all 72 hyperopic eyes (47 patients) was +3.42 diopters (D) (range 0.00 to +12.50 D) preoperatively and +0.59 D (range -1.25 to +2.00 D) 1 year postoperatively. After LASIK, 41.7% of eyes had improved corrected distance visual acuity (CDVA). No patient had reduced CDVA or loss of fusional ability; there was a 25.0% improvement in stereopsis at 1 year. The mean anisometropic difference in the hyperopic anisometropic amblyopia subgroup (18 eyes, 10 patients) was 4.39 D (range +1.75 to +7.75 D) preoperatively and +0.51 D (range 0 to +0.875 D) at 1 year. One year postoperatively, 83% of anisometropic eyes were within +/-1.00 D of the fellow eye and 94.0% were within +/-3.00 D. Postoperatively, 64.7% of eyes had improved CDVA with no reduced CDVA or loss of fusional ability; there was a 22% improvement in stereopsis at 1 year. CONCLUSION: Laser-assisted subepithelial keratectomy improved visual acuity in pediatric hyperopia with or without associated hyperopic anisometropic amblyopia.