This experimental study suggests that I-CXL is a promising alternative methodology for riboflavin delivery in crosslinking treatments, preserving the epithelium.
BackgroundDupilumab is approved for use in moderate‐to‐severe atopic dermatitis (AD) and as an add‐on maintenance treatment in patients suffering from severe asthma with type 2 inflammation. Ocular adverse events (OAEs) have been reported with dupilumab almost exclusively in patients treated for AD.ObjectivesThe objectives of this study were to describe the incidence and nature of dupilumab‐induced OAEs and to assess the potential predisposing factors.Patients and methodsWe conducted a prospective, single‐centre, real‐life study in adult AD patients treated with dupilumab, who were systematically examined by an ophthalmologist before and during treatment.ResultsForty‐six patients were included prospectively with a median age of 41.1 years and a median initial SCOring Atopic Dermatitis of 46.0 (IQR: 34.5–55.5). OAEs concerned 34.8% of patients and were mostly of mild to moderate severity. Two patients had to discontinue treatment due to OAE. The majority of patients developed or aggravated dry eye disease, with superficial punctate keratitis (SPK). Six patients developed conjunctivitis. Dupilumab‐induced OAEs were associated with the following pre‐existing parameters: dry eye disease with SPK (Odds ratio (OR); 6.3 [95% confidence interval (CI): 1.3–31.6]), eyelid eczema (OR: 8.7 [95%CI: 1.8–40.6]), history of food allergy (OR 3.8 (95% CI: 1.002–14,070) and IgE serum level> 1000 kU/L (OR:10.6 [CI 95%: 1.2–91.3]).ConclusionAtopic dermatitis patients with eyelid eczema or dry eye disease symptoms may be referred to an ophthalmologist before starting dupilumab to consider initiating preventive eye hydration measures. Further multicentric and translational studies are warranted to better explain OAEs pathophysiology.
Background
Corneal intraepithelial dyskeratosis is an extremely rare condition. The classical form, affecting Native American Haliwa-Saponi tribe members, is called hereditary benign intraepithelial dyskeratosis (HBID). Herein, we present a new form of corneal intraepithelial dyskeratosis for which we identified the causative gene by using deep sequencing technology.
Methods and results
A seven member Caucasian French family with two corneal intraepithelial dyskeratosis affected individuals (6-year-old proband and his mother) was ascertained. The proband presented with bilateral complete corneal opacification and dyskeratosis. Palmoplantar hyperkeratosis and laryngeal dyskeratosis were associated with the phenotype. Histopathology studies of cornea and vocal cord biopsies showed dyskeratotic keratinisation. Quantitative PCR ruled out 4q35 duplication, classically described in HBID cases. Next generation sequencing with mean coverage of 50× using the Illumina Hi Seq and whole exome capture processing was performed. Sequence reads were aligned, and screened for single nucleotide variants and insertion/deletion calls. In-house pipeline filtering analyses and comparisons with available databases were performed. A novel missense mutation M77T was discovered for the gene NLRP1 which maps to chromosome 17p13.2. This was a de novo mutation in the proband’s mother, following segregation in the family, and not found in 738 control DNA samples. NLRP1 expression was determined in adult corneal epithelium. The amino acid change was found to destabilise significantly the protein structure.
Conclusions
We describe a new corneal intraepithelial dyskeratosis and how we identified its causative gene. The NLRP1 gene product is implicated in inflammation, autoimmune disorders, and caspase mediated apoptosis. NLRP1 polymorphisms are associated with various diseases.
Bone morphogenetic protein-1/mTLD and PCPE-1 are upregulated in corneal scars. Both proteins may therefore contribute to the process of corneal scarring.
At 1 year postoperatively, TG-CXL seems to be as safe as C-CXL with stronger flattening in Kmax and I index and better improvement in CDVA. TG-CXL induces a biological gradient between the cone and the surrounding area that facilitates nerve and cell recovery. [J Refract Surg. 2017;33(5):290-297.].
Purpose: To compare transepithelial (TE) photorefractive intrastromal corneal cross-linking (PiXL) and photorefractive keratectomy (PRK) in low myopia. Setting: Monocentric study conducted in France (Purpan Hospital, Toulouse) Design: Prospective, intraindividual ethics committee-approved, comparative nonrandomized study. Methods: Myopic patients with manifest refraction spherical equivalent (MRSE) of -1.00 to -2.50 diopters (D), and cylindrical component plano to -0.75 D were included. Dominant eye underwent PRK, and non-dominant eye TE-PiXL procedure with riboflavin (Paracel ® Part 1 & 2, Avedro Inc., Waltham, MS, USA), 30 mW/cm 2 pulsed UVA irradiation centered on pupil (Mosaic™ System,Avedro Inc., Waltham, MS, USA) for 16 minutes and 40 seconds and supplemental oxygen delivery mask. The primary outcome measure was the change in MRSE. Other outcome measures were uncorrected and corrected distance visual acuity (UDVA and CDVA), mean keratometry (Km), and endothelial cell count (ECC) with a 6month follow-up. Adverse events were also assessed. Results: Nineteen patients were included. At 6 months, mean MRSE decreased by 0.72 ± 0.42 D in TE-PiXL eyes and by 1.35 ± 0.46 D in PRK eyes (P <.001). The mean change in UDVA was -0.35 ± 0.21 LogMAR in TE-PiXL eyes and -0.66 ± 0.19 LogMAR in PRK eyes (P <.001). No complications were reported. ECC and CDVA were statistically unchanged. Conclusion: PRK provided better visual and refractive outcomes than TE-PiXL. TE-PiXL however demonstrated the potential refractive effect of corneal cross-linking but with a limited magnitude of myopic correction to this point.
The present findings suggest that the ICD 16.5 mini-scleral GP lens is an effective and safe alternative for managing challenging corneas in a therapeutic impasse.
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