Concomitant Bandage Contact Lens, Oral Nicergoline, and Topical Autologous Serum for Severe Neurotrophic Keratitis.

BACKGROUND: To report the outcomes of using the combination of oral nicergoline, autologous serum, and contact lens to enhance corneal epithelization in neurotrophic keratitis and to discuss the clinical potential of this management. METHODS: This was a prospective consecutive case series study of eight patients treated for neurotrophic keratitis at the "Conde de Valenciana" Institute of Ophthalmology. Oral nicergoline, autologous serum, and bandage contact lens were initiated at the same time, immediately after stage 3 diagnosis keratitis was confirmed clinically, and until corneal epithelialization was achieved or eminent corneal perforation was seen. In patients where diabetes was a cause, glycosylate hemoglobin was measured to asses metabolic control. Corneal esthesiometry and corrected distance visual acuity were assessed before and after treatment. RESULTS: This study included eight eyes of eight patients (5 men [62.5%], average age 57±17.9 years). All patients completed at least 1 month of follow-up after nicergoline and contact lens suspension. Of the eight eyes, no one had positive culture growth and complete epithelial healing was achieved in all cases. Half of patients had diabetes and had a poor metabolic control. Corneal sensitivity improved in all eyes almost 2 centimeters in Cochet-Bonnet esthesiometry ( P= 0.01). In addition, final visual acuity gains were obtained ( P= 0.100). CONCLUSIONS: The combination of oral nicergoline, autologous serum, and bandage contact lens simultaneously could be an alternative in the management of stage 3 neurotrophic keratitis when conventional medical treatment has no improvement of corneal epithelization.

CHORIORETINAL ATROPHY IN VITREORETINAL LYMPHOMA: Risk Factors and Visual Outcomes.

PURPOSE: To investigate the frequency, risk factors, and functional prognosis of chorioretinal atrophy (CRA) in vitreoretinal lymphoma (VRL). METHODS: This was a retrospective cohort study of consecutive patients with vitreoretinal lymphoma. The demographic, clinical, and retinal features and the treatment modalities of each patient were collected. The charts and the multimodal imaging at each visit were reviewed. The risk factors associated with CRA were investigated with a mixed-model Cox regression. RESULTS: Of the 79 eyes of 40 patients included, 41 eyes (52%) had CRA; 27 and 14 eyes had focal and diffuse CRA, respectively. The rate of vitreoretinal lymphoma lesions in the macula was similar between focal and diffuse CRA (96% vs. 93%). The eyes with CRA had worse best-corrected visual acuity (P = 0.006) than eyes with no CRA; diffuse atrophy had the worst best-corrected visual acuity (P < 0.001). The presence of retinal infiltrates (hazard ratio = 3.75, 95% confidence interval [CI] 1.46-9.59, P = 0.006) and vertical hyperreflective lesions (hazard ratio= 4.13 95% CI 1.14-14.93, P = 0.03) on optical coherence tomography and macular involvement (hazard ratio = 6.59, 95% CI 1.41-30.53, P = 0.02) were associated with a higher risk of CRA. CONCLUSION: Vitreoretinal lymphoma presenting with retinal infiltrates and macular involvement carried a higher risk of CRA. Risk factors for CRA should be identified for the potential of severe visual loss. Prompt diagnosis of vitreoretinal lymphoma may allow better control of the disease.

DIFFUSE CHORIORETINAL ATROPHY IN CHINESE HIGH MYOPIA: The ZOC-BHVI High Myopia Cohort Study.

PURPOSE: To explore the associations between diffuse chorioretinal atrophy (DCA) and age, sex, axial length, spherical equivalent, and best-corrected visual acuity (BCVA) among highly myopic eyes. METHODS: This study included right eyes of 857 bilaterally highly myopic individuals from the ZOC-BHVI Cohort Study. Participants underwent examinations, including BCVA, ocular biometry, autorefraction, and color fundus photography. An Early Treatment Diabetic Retinopathy Study grid was applied on the fundus photographs to evaluate the location of DCA, which was graded into four categories (D0-D3). The characteristics and ocular biometry were compared between participants' eyes with and without DCA. RESULTS: Diffuse chorioretinal atrophy was found in 177 (20.6%) eyes. The proportion of participants with DCA in age groups of 7 to 11, 12 to 18, 19 to 39, and ≥ 40 years old was 20.9%, 9.2%, 23.1%, and 52.9%, respectively. The proportion of DCA significantly increased with longer axial length and worse myopic spherical equivalent. Eyes with DCA had poorer BCVA (Snellen visual acuity 20/36, logarithm of minimal angle of resolution 0.26 ± 0.25) than those without DCA (Snellen visual acuity 20/23, logarithm of minimal angle of resolution 0.06 ± 0.14) (P < 0.001). The BCVA gradually declined as the lesion got closer to the fovea (P for trend < 0.001). CONCLUSION: The proportion of DCA increased with older age, longer axial length, and more myopic spherical equivalent. Diffuse chorioretinal atrophy is a vision-threatening complication of high myopia where BCVA gradually worsens with foveal involvement.

Defect in phosphoinositide signalling through a homozygous variant in PLCB3 causes a new form of spondylometaphyseal dysplasia with corneal dystrophy.

BACKGROUND: Bone dysplasias are a large group of disorders affecting the growth and structure of the skeletal system. METHODS: In the present study, we report the clinical and molecular delineation of a new form of syndromic autosomal recessive spondylometaphyseal dysplasia (SMD) in two Emirati first cousins. They displayed postnatal growth deficiency causing profound limb shortening with proximal and distal segments involvement, narrow chest, radiological abnormalities involving the spine, pelvis and metaphyses, corneal clouding and intellectual disability. Whole genome homozygosity mapping localised the genetic cause to 11q12.1-q13.1, a region spanning 19.32 Mb with ~490 genes. Using whole exome sequencing, we identified four novel homozygous variants within the shared block of homozygosity. Pathogenic variants in genes involved in phospholipid metabolism, such as PLCB4 and PCYT1A, are known to cause bone dysplasia with or without eye anomalies, which led us to select PLCB3 as a strong candidate. This gene encodes phospholipase C ß 3, an enzyme that converts phosphatidylinositol 4,5 bisphosphate (PIP2) to inositol 1,4,5 triphosphate (IP3) and diacylglycerol. RESULTS: The identified variant (c.2632G>T) substitutes a serine for a highly conserved alanine within the Ha2' element of the proximal C-terminal domain. This disrupts binding of the Ha2' element to the catalytic core and destabilises PLCB3. Here we show that this hypomorphic variant leads to elevated levels of PIP2 in patient fibroblasts, causing disorganisation of the F-actin cytoskeleton. CONCLUSIONS: Our results connect a homozygous loss of function variant in PLCB3 with a new SMD associated with corneal dystrophy and developmental delay (SMDCD).

[Paraproteinemic Keratopathy as a Clinical Sign of Monoclonal Gammopathy]. / Paraproteinämische Keratopathie als klinisches Zeichen einer monoklonalen Gammopathie.

Patients with monoclonal gammopathy can show paraproteinemic keratopathy (PPK) with an indication to treatment. PPK has to be differentiated from corneal dystrophies, systemic metabolic disorders with corneal involvement, as well as from immunologic and inflammatory corneal diseases.

Salzmann's nodular degeneration of cornea associated with thyroid eye disease.

Salzmann's nodular degeneration (SND) typically occurs in patients who are female, 50-60 years old, and have a history of corneal inflammation and irritation. Multiple case reports have documented associations between SND and trachoma, viral infections, trauma, contact lens wear, corneal surgeries and corneal exposure. The authors describe a patient with bilateral SND confirmed by anterior segment optical coherence tomography (OCT) imaging in the context of thyroid eye disease (TED) and history of LASIK. Treatment involved propylthiouracil (PTU), artificial tear use, loteprednol etabonate ophthalmic gel, eyelid taping and selenium supplementation and prospective superficial keratectomy with diamond burr polish.

In vivo confocal microscopy of pre-Descemet corneal dystrophy associated with X-linked ichthyosis: a case report.

BACKGROUND: Pre-Descemet corneal dystrophy (PDCD) is characterized by the presence of numerous, tiny, polymorphic opacities immediately anterior to Descemet membrane, which is a rare form of corneal stromal dystrophy and hard to be diagnosed. In vivo confocal microscopy (IVCM) is a useful tool to examine the minimal lesions of the cornea at the cellular level. In this article, we report a rare case of PDCD associated with X-linked ichthyosis and evaluate IVCM findings. CASE PRESENTATION: We present a 34-year-old male Chinese patient with PDCD associated with X-linked ichthyosis. Slit-lamp biomicroscopy showed the presence of tiny and pleomorphic opacities in the posterior stroma immediately anterior to Descemet membrane bilaterally. IVCM revealed regular distributed hyperreflective particles inside the enlarged and activated keratocytes in the posterior stroma. Hyperreflective particles were also observed dispersedly outside the keratocytes in the anterior stroma. Dermatological examination revealed that the skin over the patient's entire body was dry and coarse, with thickening and scaling of the skin in the extensor side of the extremities. PCR results demonstrated that all ten exons and part flanking sequences of STS gene failed to produce any amplicons in the patient. CONCLUSIONS: IVCM is useful for analyzing the living corneal structural changes in rare corneal dystrophies. We first reported the IVCM characteristics of PDCD associated with X-linked ichthyosis, which was caused by a deletion of the steroid sulfatase (STS) gene, confirmed by gene analysis.

[Analysis of TGFBI gene mutation in a Chinese family affected with Reis-Bucklers corneal dystrophy].

OBJECTIVE: To analyze the clinical features and TGFBI gene mutation in a Chinese family affected with Reis-Bucklers corneal dystrophy. METHODS: Genomic DNA was extracted from 53 members including 9 patients from the family. The 17 exons and splice region of introns of the TGFBI gene were amplified by PCR and directly sequenced. All family members were subjected to ophthalmologic examination. RESULTS: A heterozygous mutation (R124L) was found in exon 4 of the TGFBI gene among all patients from the family. The same mutation was not found among unaffected family members. The inheritance pattern of the family was identified as autosomal dominant, and the Reis-Bucklers corneal dystrophy in the family was diagnosed as the geographic type. CONCLUSION: The R124L mutation of the TGFBI gene probably underlies the pathogenesis of Reis-Bucklers corneal dystrophy in this Chinese family. Molecular genetic approach is useful for the proper diagnosis of this type of corneal dystrophy.

Autophagy in granular corneal dystrophy type 2.

Autophagy is a lysosomal degradative process that is essential for cellular homeostasis and metabolic stress adaptation. Defective autophagy is involved in the pathogenesis of many diseases including granular corneal dystrophy type 2 (GCD2). GCD2 is an autosomal dominant disorder caused by substitution of histidine for arginine at codon 124 (R124H) in the transforming growth factor ß-induced gene (TGFBI) on chromosome 5q31. Transforming growth factor ß-induced protein (TGFBIp) is degraded by autophagy, but mutant-TGFBIp accumulates in autophagosomes and/or lysosomes, despite significant activation of basal autophagy, in GCD2 corneal fibroblasts. Furthermore, inhibition of autophagy induces cell death of GCD2 corneal fibroblasts through active caspase-3. As there is currently no pharmacological treatment for GCD2, development of novel therapies is required. A potential strategy for preventing cytoplasmic accumulation of mutant-TGFBIp in GCD2 corneal fibroblasts is to enhance mutant-TGFBIp degradation. This could be achieved by activation of the autophagic pathway. Here, we will consider the role and the potential therapeutic benefits of autophagy in GCD2, with focus on TGFBIp degradation, in light of the recently established role of autophagy in protein degradation.

Phototherapeutic keratectomy (PTK) for treatment of recurrent corneal erosion: Correlation between etiology and prognosis - prospective longitudinal study.

BACKGROUND: To evaluate and compare the efficacy of phototherapeutic keratectomy (PTK) for recurrent corneal erosion (RCE) caused by trauma, map-dot-fingerprint dystrophy (MDF) or instances without an established cause. METHODS: Single center prospective longitudinal study. Between January 2003 and November 2006 we treated 89 eyes of 82 patients with PTK. All patients presented with refractory RCE caused either by trauma, MDF or with no established cause. During follow-up (until May 2013), patients, treating ophthalmologists and/or family doctors were interviewed about the patients' state of health, recurrence of pain, the necessity of further treatments or the occurrence of complications. Five patients died or were lost during follow-up and were thus excluded from the analysis. Freedom of recurrence was estimated using logistic regression analysis using indicator variates for the following three etiologic groups: trauma (55 eyes), MDF (29 eyes) and idiopathic (no established cause; 5 eyes). RESULTS: Overall 89 eyes of 82 patients were followed-up. Average follow-up among failures and non-failures was 51.56 months (standard deviation (SD) 21.22, range 24 to 91) and 95.25 months (SD 15.99, range 35 to 137 months), respectively. Fifty-seven percent were female and the average age at first PTK was 45.3 years (range: 23 to 70 years). During follow-up, there were 25 recurrences and 15 of these patients received a re-PTK. Compared to patients with a traumatic cause of epithelial erosions, the likelihood of experiencing a recurrence was higher in patients with MDF [odds ratio (OR) 5.48; 95 % confidence interval (CI) 1.93 to 15.59; p = 0.001]; the OR was 8.81 (95 % CI 1.27 to 61.32; p = 0.028) for patients with an idiopathic cause. CONCLUSIONS: In view of the available evidence, we want to raise the awareness of those managing patients with MDF and idiopathic causes that, in order to control the disease, recurrent PTK treatments are expected to be necessary more often than in cases of traumatic RCE.

Late reactivation of herpes zoster keratitis results in band keratopathy.

PURPOSE: To report an unusual case of a late-stage reactivation of immune stromal keratitis associated with herpes zoster ophthalmicus (HZO), occurring without any apparent predisposing factors, more than 4 years after an acute zoster dermatomal rash. Significant corneal hypoesthesia and a central band keratopathy developed within 6 months of the late-stage reactivation. The clinical case management, issues associated with management, and management options are discussed, including the use of standardized, regulatory approved, antibacterial medical honey. CASE REPORT: An 83-year-old woman presented for routine review with a reactivation of right anterior stromal keratitis and mild anterior uveitis, occurring more than 4 years after an acute HZO dermatomal rash and an associated initial episode of anterior stromal keratitis. Corneal sensation became markedly impaired, and over the subsequent 6 months, a right central band keratopathy developed despite oral antiviral and topical steroid therapy. Visual acuity with pinhole was reduced to 20/100 in the affected eye and moderate irritation and epiphora were experienced. The patient declined the surgical intervention options of chelation, lamellar keratectomy, and phototherapeutic keratectomy to treat the band keratopathy. Longer-term management has involved preservative-free artificial tears, eyelid hygiene, standardized antibacterial medical honey, topical nonpreserved steroid, and UV-protective wraparound sunglasses. The clinical condition has improved over 14 months with this ocular surface management regimen, and visual acuity of 20/30 is currently achieved in a comfortable eye. CONCLUSIONS: The chronic and recurrent nature of HZO can be associated with significant corneal morbidity, even many years after the initial zoster episode. Long-term review and management of patients with a history of herpes zoster stromal keratitis are indicated following the initial corneal involvement. Standardized antibacterial medical honey can be considered in the management of the chronic ocular surface disease associated with HZO and warrants further evaluation in clinical trials.

[Lattice degeneration of the retina].

Lattice degeneration of the retina is a clinically important type of peripheral retinal dystrophies due to its participation in the pathogenesis of rhegmatogenous retinal detachment. In spite of extensive epidemiological, morphological, and clinical data, the question on causes of this particular type of retinal dystrophies currently remains debatable. Existing hypotheses on pathogenesis of retinal structural changes in lattice degeneration explain it to a certain extent. In clinical ophthalmology it is necessary to pay close attention to this kind of degenerations and distinguish between cases requiring preventive treatment and those requiring monitoring.

Unilateral Granular Type 2 Corneal Dystrophy With Exacerbation After LASIK.

PURPOSE: The aim of this study was to report a case of unilateral granular corneal dystrophy type 2 (GCD2) with exacerbation after bilateral laser in situ keratomileusis (LASIK). METHODS: Clinical evaluation, Scheimpflug imaging, anterior segment optical coherence tomography (AS-OCT), cytology, and genetic testing were used to confirm the diagnosis of unilateral GCD2 with exacerbation after bilateral LASIK. Detailed literature review for possible unilateral GCD2 presentations was performed. RESULTS: A 54-year-old White woman presented with blurred vision in her left eye and a history of bilateral LASIK performed 8 years before. Examination revealed dense opacities in the left cornea only, which were confirmed to be confined to the LASIK interface and adjacent corneal stromal tissue, as determined by AS-OCT. The patient underwent flap lift, interface debris removal, and stromal bed phototherapeutic keratectomy. Cytological analysis showed eosinophilic corneal stromal deposits that stained with trichrome stain and were congophilic on Congo red stain. Genetic testing was positive for heterozygous GCD2 transforming growth factor ß-induced gene ( TGFBI ), c.371G>A, p.R124H mutation. There were no opacities identifiable in the right eye on serial slit-lamp examination, Scheimpflug imaging, or OCT imaging at 4 or 8 years after bilateral LASIK. Literature review failed to identify any previous reports of unilateral GCD2. CONCLUSIONS: This is the first known reported case of unilateral granular corneal dystrophy type 2. LASIK is contraindicated in eyes with corneal stromal dystrophies related to mutations in TGFBI as both flap creation and laser ablation can exacerbate visually significant opacity formation. Scheimpflug and AS-OCT imaging are useful to identify opacities in GCD2.

Neurotrophic Keratopathy After Slow Coagulation Transscleral Cyclophotocoagulation.

PURPOSE: Decreased corneal sensation and subsequent neurotrophic keratopathy (NK) is an uncommon complication after transscleral cyclophotocoagulation (TSCPC). Post-TSCPC NK has been rarely reported in the literature, predominantly after traditional, "pop technique" continuous-wave TSCPC or micropulse CPC. The authors report the first case series of NK after slow-coagulation TSCPC (SC-TSCPC). METHODS: This was a respective chart review of patients who developed NK after SC-TSCPC. The collected data included demographic data, type of glaucoma, risk factors for corneal anesthesia in addition to the number of laser spots, and the extent of the treated area. RESULTS: Four eyes experienced NK after SC-TSCPC. The median time for the development of NK was 4 weeks. At the final visit, 2 patients had a resolution of NK, 1 had a persistent corneal ulcer, and 1 had worsening NK and corneal perforation. CONCLUSIONS: NK is a rare but a vision-threatening complication that can develop after SC-TSCPC in patients with risk factors for decreased corneal sensation. Early diagnosis and proper management are crucial to reducing the risk of vision loss and improving the prognosis of these cases.

Paraproteinemic Keratopathy in a Patient With Previous LASIK Procedure Mimicking Lattice Corneal Dystrophy.

PURPOSE: The aim of this study was to report a unique clinical presentation of paraproteinemic keratopathy after a myopic uneventful laser in situ keratomileusis (LASIK) procedure that led to the diagnosis of gammopathy of undetermined significance. METHODS: This was an interventional case report. A 55-year-old woman present with bilateral branching opacities limited to the optical zone of myopic LASIK. The patient's medical history was unremarkable. RESULTS: After ruling out a mutation in TGF-ß1 , a systemic workup was performed, revealing an IgG level of 12.8 mg/dL, lambda-free light chain of 12.8 mg/dL, and M-spike of 0.6 g/dL. Bone marrow aspiration was slightly hypercellular, without evidence of neoplastic infiltration by plasma cells. The patient underwent 3 cycles of systemic chemotherapy, with improvement in best-corrected visual acuity. CONCLUSIONS: Paraproteinemic keratopathy is a rare clinical presentation that may lead to a systemic diagnosis of hematologic malignancy. To the best of our knowledge, this is the first reported case of paraproteinemic keratopathy after LASIK.

Corneal Electrolysis for Granular Corneal Dystrophy Type 2 (Avellino Corneal Dystrophy) Exacerbation After LASIK.

PURPOSE: To report two cases in which exacerbation of granular corneal dystrophy type 2 (GCD2; Avellino corneal dystrophy) after laser in situ keratomileusis (LASIK) was successfully removed by corneal electrolysis. METHODS: This study involved a 66-year-old man and a 43-year-old man with GCD2 who had undergone bilateral LASIK for myopia 10 or more years prior to presentation. In both patients, GCD2 corneal opacity gradually developed postoperatively at the LASIK flap interface, thus resulting in a decrease of visual acuity. For treatment, the LASIK flaps in both patients were surgically lifted to directly remove the opacity. Corneal electrolysis was then applied to the back of each LASIK flap and stromal bed. RESULTS: Postoperatively, the ocular symptoms and corneal opacities related to GCD exacerbation disappeared, with improvement of corrected and uncorrected distance visual acuity and almost no change of refractive error. CONCLUSIONS: The findings reveal that corneal electrolysis is safe and effective for treating exacerbations of GCD2 following LASIK when applied to a surgically lifted flap, and that it successfully removes GCD2-related LASIK flap interface opacities with almost no change of refractive error postoperatively. [J Refract Surg. 2023;39(1):61-65.].

[Neurological manifestations of AGel amyloidosis (Meretoja's syndrome) in a German family]. / Neurologische Manifestationen der AGel-Amyloidose (Meretoja-Syndrom) bei einer deutschen Familie.

AGel amyloidosis is an autosomal dominantly inherited systemic amyloidosis which is most commonly observed in Finland. The clinical manifestation is characterised by lattice corneal dystrophy, bilateral facial palsy with myokymias, and cutis laxa. We report on a German family with an AGel amyloidosis due to a gelsolin p.Asp214Asn/D187N mutation encoded by exon 4 of the GSN gene on chromosome 9q34.

Exacerbation of Granular Corneal Dystrophy Type 2 After Small Incision Lenticule Extraction.

PURPOSE: To report the outcome of unilateral small incision lenticule extraction (SMILE) in a patient with granular corneal dystrophy type 2 (GCD2). METHODS: Slit-lamp photography and Fourier domain optical coherence tomography were used to document the clinical course and appearance of the corneas in a patient with genetically determined GCD2 who underwent unilateral SMILE in the right eye. RESULTS: Slit-lamp examination of a 23-year-old woman revealed 2 faint opacities at the surgical interface approximately 2 months after the SMILE procedure had been performed on her right eye. Nine and 3 typical GCD2 deposits located immediately beneath the Bowman layer were observed in the right and left corneas, respectively. Over time, the deposits at the interface increased in size, density, and number in the right eye. Fourier domain optical coherence tomography performed 33 months after the SMILE procedure revealed deposits at the SMILE interface that were distinct from those located immediately beneath the Bowman layer. The severity of disease exacerbation was less in this patient than what is typically observed in others who have undergone laser-assisted in situ keratomileusis or photorefractive keratectomy. CONCLUSIONS: SMILE is contraindicated in patients with GCD2, as are other corneal refractive surgical procedures. This case highlights the importance of genetic testing before the performance of refractive corneal procedures-especially for patients with corneal opacities on preoperative slit-lamp examination or a family history of corneal disease compatible with that of a corneal dystrophy.

Recurrence of Avellino Corneal Dystrophy Following Penetrating Keratoplasty: A Case Report.

Granular - lattice (Avellino) corneal dystrophy is inherited in an autosomal dominant fashion which affects stroma of the cornea with recurrent erosions and decreased vision due to clouding of cornea in later stage. We reported a case of 53-year old woman presented with pain and blurring of vision of left eye for 10 days with history of right eye deep anterior lamellar dystrophy and Left eye penetrating keratoplasty 5years back for Avellino dystrophy. On examination right eye graft was clear and left eye showed circular edges of irregular epithelium with patchy stains and epithelial defect suggestive of recurrence of dystrophy. A patient with recurrent corneal erosions and opacity in cornea has to be examined carefully so as not to overlook Avellino corneal dystrophy. Being a rare disorder this case has been reported to draw the attention of ophthalmologists about its recurrence following keratoplasty.

Ethylenediaminetetraacetic Acid Chelation in Herpes Zoster Ophthalmicus Is Associated With a High Rate of Corneal Melt and Perforation.

PURPOSE: To examine the rate and risk factors for band keratopathy after herpes zoster ophthalmicus (HZO) and the outcomes of ethylenediaminetetraacetic acid (EDTA) treatment. METHODS: This is a retrospective review of all subjects with HZO seen at Auckland District Health Board between January 2006 and December 2016. RESULTS: A total of 869 subjects with HZO were included in the study. Median follow-up was 6.3 years (total 5504.4 patient-years). Band keratopathy developed in 13 subjects (1.5%). On multivariate analysis, older age at onset [hazard ratio (HR), 1.092; P = 0.034], intraocular pressure ≥30 mm Hg at presentation (HR, 5.548; P = 0.013), and number of recurrences (HR, 1.849; P < 0.001) were associated with increased risk for band keratopathy. Corneal melt occurred in 22 subjects (2.5%) during the follow-up period. On multivariate analysis, uveitis (HR, 8.618; P = 0.004) and disodium EDTA chelation (HR, 8.666; P < 0.001) were associated with increased risk for corneal melt. EDTA chelation was performed in 8 subjects. Corneal melt occurred after EDTA chelation in 4 subjects, and corneal perforation occurred in 2 subjects. One subject was eviscerated due to severe endophthalmitis after repeated corneal perforation and another required enucleation for recurrent corneal melt and microbial keratitis. CONCLUSIONS: Band keratopathy is an uncommon complication of HZO. Treatment with EDTA chelation might be associated with a significant risk for severe complications in these eyes and should be approached with caution.