Morphological changes in the meibomian glands of patients with phlyctenular keratitis: a multicenter cross-sectional study

Summary of 13 patients with phlyctenular keratitis. (XLSX 11 kb

Increased Tear Fluid Production as a Compensatory Response to Meibomian Gland Loss A Multicenter Cross-sectional Study

PurposeTo compare tear film parameters as well as meibomian gland morphologic features and function among patients with meibomian gland dysfunction (MGD), those with non–Sjögren syndrome aqueous-deficient dry eye (non-SS ADDE), those with non-SS ADDE and MGD, and normal subjects.DesignMulticenter, cross-sectional, observational case series.ParticipantsForty-one eyes of 41 patients (all women; mean age ± standard deviation, 62.1±9.9 years) with non-SS ADDE, 70 eyes of 70 patients (all women; 66.0±8.7 years) with MGD, 17 eyes of 17 patients (all women; 72.4±7.8 years) with non-SS ADDE and MGD, and 70 eyes of 70 normal control subjects (all women; 65.0±7.1 years).MethodsOcular symptoms were scored from 0 to 14 and lid margin abnormalities from 0 to 4 according to their respective number. Meibomian gland changes were scored from 0 to 6 (meiboscore) on the basis of noncontact meibography findings, and meibum was graded from 0 to 3 depending on its volume and quality. Conjunctival and corneal epithelial damage were scored from 0 to 9 (fluorescein score). Tear film break-up time (TBUT) was measured as an index of tear film stability, and tear fluid production was evaluated with Schirmer's test.Main Outcome MeasuresOcular symptom score, lid margin abnormality score, meiboscore, meibum grade, fluorescein score, TBUT, and Schirmer's test value.ResultsThe ocular symptom score did not differ significantly between the MGD and non-SS ADDE groups (P = 0.762). The lid margin abnormality score, meiboscore, and meibum grade were significantly higher in the MGD group than in the non-SS ADDE group (P = 0.0012, P < 0.0001, and P < 0.0001, respectively). The fluorescein score, TBUT, and Schirmer's test value were significantly worse in the non-SS ADDE group than in the MGD group (P < 0.0001, P = 0.0061, and P < 0.0001, respectively). The meiboscore correlated significantly with Schirmer's test value only in the MGD group (ρ = 0.508, P = 8.3×10−6).ConclusionsAn increase in tear fluid production likely compensates for loss of meibomian glands in individuals with MGD

Herpes simplex virus type 1 ICP0 localizes in the stromal layer of infected rabbit corneas and resides predominantly in the cytoplasm and/or perinuclear region of rabbit keratocytes

Herpes stromal keratitis (HSK) results from the reactivation of herpes simplex virus type-1 (HSV-1) in the cornea. The subsequent corneal inflammation and neovascularization may lead to scarring and visual loss. The cellular and molecular mechanisms underlying HSK remain unknown. The presence of stromal HSV-1 viral proteins or antigens in the HSK cornea remains a subject of debate. It was recently reported that HSV-1 ICP0 rapidly diffuses out of infected rabbit corneas. To investigate further the presence of HSV-1 ICP0 in the infected cornea, particularly in the corneal stroma, ex vivo confocal microscopy was used to scan rabbit corneas infected with the virus ICP0–EYFP, an HSV-1 derivative (strain 17+) that expresses ICP0 fused to the enhanced yellow fluorescent protein (EYFP). These results demonstrate that ICP0 is expressed in the corneal epithelium and stromal cells (keratocytes) of infected rabbit corneas throughout acute infection. Furthermore, expression of ICP0–EYFP appears localized to punctate, granular deposits within stromal keratocytes, showing both a cytoplasmic and perinuclear localization. These findings provide new data demonstrating that anterior corneal keratocytes become infected and express ICP0 during acute HSV-1 infection

Congenital Hypoplastic Trigeminal Nerve Revealed by Manifestation of Corneal Disorders Likely Caused by Neural Factor Deficiency

Purpose: To report a case of hypoplastic trigeminal nerve associated with corneal epithelial disorders that were successfully treated with peptides derived from substance P and insulin-like growth factor-1 (IGF-1). Case Report: A 16-month-old boy was referred for treatment of a persistent corneal epithelial defect on his left eye. Magnetic resonance imaging revealed the apparent absence of the trigeminal nerve on the left side, and the patient was therefore diagnosed with neurotrophic keratopathy. Treatment with eye drops containing the tetrapeptides FGLM-NH2 and SSSR derived from the neuropeptide substance P and the growth factor IGF-1, respectively, resulted in resurfacing of the corneal epithelial defect. Discussion: The trigeminal nerve anomaly of the patient likely gave rise to neurotrophic keratopathy as a result of a deficiency of neural factors, emphasizing the importance of neural regulation in corneal epithelial homeostasis

Spontaneous Healing of Corneal Perforation after Temporary Discontinuation of Erlotinib Treatment

Purpose: To report a case of corneal perforation associated with oral administration of erlotinib and its spontaneous healing after temporary discontinuation of drug treatment. Case Report: A 65-year-old man with metastatic lung cancer was treated with erlotinib (150 mg/day), a specific tyrosine kinase inhibitor of the epidermal growth factor receptor. He was referred to our corneal service for the treatment of bilateral corneal disorders, diagnosed with mild aqueous-deficient dry eye, and treated by insertion of punctal plugs. His corneal epithelial disorders initially improved, but subsequently worsened, as manifested by the development of bilateral corneal ulceration with corneal perforation in the right eye. The oral administration of erlotinib was interrupted in preparation for tectonic keratoplasty, but 2 days later the corneal perforation of the right eye and the bilateral epithelial defects had healed spontaneously. Treatment with erlotinib was resumed at half the initial dose, and the cornea of both eyes has remained apparently healthy. Discussion: Erlotinib may be secreted into tear fluid and thereby adversely affect the corneal epithelium. The development of corneal epithelial disorders in patients receiving this drug may be reversed by reducing its dose

Persistence of Structural Changes at the Anterior Cornea in Bullous Keratopathy Patients after Endothelial Keratoplasty

<div><p>Subepithelial fibrosis (SEF) and the transdifferentiation of keratocytes into fibroblasts or myofibroblasts (Fbs/MFbs) have been detected in the cornea of individuals with bullous keratopathy. We examined the anterior cornea of bullous keratopathy patients for such changes after Descemet’s stripping automated endothelial keratoplasty (DSAEK). Twenty-two individuals who underwent unilateral DSAEK at Yamaguchi University Hospital were enrolled in the study. The subjects were divided into groups A (<i>n</i> = 10) and B (<i>n</i> = 12) with a preoperative duration of stromal edema of less than or at least 12 months, respectively. The structure of the anterior stroma was examined by in vivo laser confocal microscopy at various times after surgery. SEF was detected in 1 (10.0%) and 11 (91.7%) cases in groups A and B, respectively, before surgery as well as in 0 (0%) and 7 (58.3%) cases, respectively, at 6 months after DSAEK. Fb/MFb transdifferentiation was detected in 0 (0%) and 8 (66.7%) cases in groups A and B, respectively, before surgery as well as in 0 and 1 (8.3%) case, respectively, at 6 months postsurgery. Anterior stromal scattering (ASS) was detected in 10 (100%) and 12 (100%) cases in groups A and B, respectively, before surgery as well as in 0 (0%) and 6 (50.0%) cases, respectively, at 6 months after DSAEK. Changes in anterior stromal structure apparent before surgery were thus also detected in bullous keratopathy patients after DSAEK. SEF and ASS persisted for more than 6 months in a substantial proportion of individuals with a preoperative duration of stromal edema of at least 12 months.</p> </div

Prediction of cycloplegic refraction for noninvasive screening of children for refractive error.

Detection of refractive error in children is crucial to avoid amblyopia and its impact on quality of life. We here performed a retrospective study in order to develop prediction models for spherical and cylinder refraction in children. The enrolled 1221 eyes of 617 children were divided into three groups: the development group (710 eyes of 359 children), the validation group (385 eyes of 194 children), and the comparison group (126 eyes of 64 children). We determined noncycloplegic and cycloplegic refraction values by autorefractometry. In addition, several noncycloplegic parameters were assessed with the use of ocular biometry. On the basis of the information obtained from the development group, we developed prediction models for cycloplegic spherical and cylinder refraction in children with the use of stepwise multiple regression analysis. The prediction formulas were validated by their application to the validation group. The similarity of noncycloplegic and predicted refraction to cycloplegic refraction in individual eyes was evaluated in the comparison group. Application of the developed prediction models for spherical and cylinder refraction to the validation group revealed that predicted refraction was significantly correlated with measured values for cycloplegic spherical refraction (R = 0.961, P < 0.001) or cylinder refraction (R = 0.894, P < 0.001). Comparison of noncycloplegic, cycloplegic, and predicted refraction in the comparison group revealed that cycloplegic spherical refraction did not differ significantly from predicted refraction but was significantly different from noncycloplegic refraction, whereas cycloplegic cylinder refraction did not differ significantly from predicted or noncycloplegic values. Our prediction models based on ocular biometry provide estimates of refraction in children similar to measured cycloplegic spherical and cylinder refraction values without the application of cycloplegic eyedrops

Frequency of SEF in groups A and B before and after DSAEK.

<p>Frequency of SEF in groups A and B before and after DSAEK.</p