Corneal calcification typically progresses slowly but can occasionally advance rapidly. This report details severe stromal calcification following repeat Descemet\'s stripping automated endothelial keratoplasty (DSAEK) in a 75-year-old patient with diabetes, hypertension, and prior ocular surgeries, including cataract surgery, intraocular lens extraction with suturing, and trabeculectomy. Persistent epithelial defects after the surgery led to rapid central stromal calcification within four weeks, significantly reducing visual acuity. Management included switching from betamethasone sodium phosphate to fluorometholone, facilitating complete epithelial recovery within two months. However, persistent stromal opacity necessitated a subsequent penetrating keratoplasty. Infrared absorption spectrophotometry identified calcium phosphate as the primary component of the calcification. This case highlights the importance of vigilant monitoring and proactive management of epithelial defects to prevent rapid calcification following endothelial keratoplasty.

Familial lecithin:cholesterol acyltransferase (LCAT) deficiency (FLD) is an ultra-rare autosomal recessive disease characterized by very low HDL-C levels, corneal opacity, anemia, and progressive renal disease. The rate and severity of renal disease are variable across FLD patients and the biomarkers and risk factors for disease progression are poorly understood. Here we report a 30 year-long comparative analysis of the clinical and laboratory biomarkers in an FLD patient with accelerated renal decline, who underwent 2 kidney and one liver transplantations. Results show that elevated TG and non-HDL-C levels may promote the formation of LpX and accelerate renal function decline, whereas markers of anemia may be early predictors. Conversely, corneal opacity progresses at a steady rate and does not correlate with lipid, hematologic, or renal biomarkers. Our study suggests that monitoring of markers of anemia may aid the early detection and timely management of kidney disease with conservative therapies. Furthermore, it suggests that controlling hypercholesterolemia and hypertriglyceridemia may help improve renal disease prognosis.

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Childhood glaucoma is a rare disorder that occurs from birth until teenage years caused by an abnormality of aqueous humor pathways. About 50-70% of Peters\' anomaly is accompanied by secondary childhood glaucoma. The presence of glaucoma will affect the prognosis. We reported the evaluation and treatment of secondary childhood glaucoma due to Peters\' anomaly. A 5 months-old boy was presented with the complaint of a enlarged left eye since 3 months old. The complaint was accompanied by a watering eye and frequently closed upon light exposure. The left eye looked opaquer than contralateral. Examination under anesthesia showed that the intraocular pressure (IOP) was 35 mmHg in the left eye and the corneal diameter was 14 mm. Other findings were keratopathy, diffuse corneal edema, buphthalmos, shallow anterior chamber, anterior synechiae, and linear slit shaped pupils in the nasal region. Patient was treated with ophthalmic timolol maleate which was later followed by trabeculectomy. After 1 week post-surgery, IOP assessment by palpation suggested the right eye within normal range while the IOP of left eye was higger than normal. Blepharospasm, epiphora, photophobia, bleb on superior, subconjunctiva bleeding, buphthalmos, keratopathy, minimal corneal edema, anterior chamber with shallow image, and posterior synechia were found in left eye anterior segment. In conclusion, trabeculotomy and trabeculectomy are recommended if there is no reduction of IOP observed after receiving timolol maleate therapy. The choice of surgical management is dependent on the feasibility of the protocol.

Hypercupremia-induced corneal copper deposition secondary to monoclonal gammopathy is rare and shows a characteristic corneal opacity quite different from other causes of hypercupremia, such as Wilson\'s disease. This report describes a case of corneal copper deposition in a patient with monoclonal gammopathy associated with chronic lymphocytic leukemia. An 84-year-old man with slowly progressive corneal opacity was referred to our hospital. The corneal opacity was present at least five years ago. The patient\'s best-corrected visual acuity was 20/25 OU (in both eyes) at the initial visit to our hospital. Slit-lamp examination and anterior segment optical coherence tomography revealed bilateral brown-colored opacity localized to deep layers of the central cornea. In vivo confocal microscopy (IVCM) showed indistinct corneal stromal cells in the deep layer and endothelial cells. The possible differential diagnoses were corneal dystrophy and Wilson\'s disease, but the color, shape, or site of corneal opacity was inconsistent with the disease. As the patient had a history of chronic lymphocytic leukemia, which is often associated with monoclonal gammopathy, we suspected that the corneal opacity was copper deposition in association with the hematologic diseases. Laboratory examinations showed elevated serum copper and normal ceruloplasmin. Serum protein electrophoresis revealed significantly high IgG levels with depression of IgA, IgE, and IgM. These results supported our diagnosis. Followingly, we consulted the patient\'s attending hematologist, and the doctor initiated treatment for hypercupremia. In conclusion, hypercupremia secondary to monoclonal gammopathy should be considered a possible cause of central brown-colored corneal opacity.

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OBJECTIVE: To describe an approach using sequential excimer laser ablation of the stromal surface of the corneal flap with or without subsequent excimer ablation to the stromal bed to reduce presbyopic inlay-associated corneal haze.
METHODS: Twelve patients who underwent KAMRA inlay (Acufocus) explantation due to corneal haze were included. The mean interval between explantation and the primary surgery (phototherapeutic keratotomy [PTK] to corneal flap) was 16.2 ± 29.7 months (range = 1 to 83 months). The corneal flap was lifted and laid on an evisceration spoon and an excimer laser was used to ablate the flap stroma by 30 to 40 µm depth. Subsequently, an excimer laser was used to ablate and treat the stromal bed following a second flap lift according to the manifest refraction, leaving a minimal residual stromal bed thickness of greater than 300 µm. For both procedures, mitomycin C 0.02% was applied to the stromal bed before the flap was replaced and a bandage contact lens applied.
RESULTS: Reductions in corneal haze were observed, following PTK to the corneal flap with or without photorefractive keratectomy (PRK) to the stromal bed, both clinically and on imaging. No significant changes in uncorrected distance visual acuity (P = .442) and corrected distance visual acuity (P = .565) were observed. Improvements were observed for both spherical equivalent refractive errors (P = .036) and corneal light backscatter (P = .019). There were significant improvements in spherical aberrations (P = .014) but no changes in total lower and higher order aberrations.
CONCLUSIONS: PTK to the corneal flap with or without subsequent stromal bed PRK is an effective technique in treating corneal haze following presbyopic inlay explantation. [J Refract Surg. 2023;39(9):639-646.].

The purpose of this report is to provide a comprehensive account of an exceptional case involving the presentation of congenital rubella syndrome (CRS) in a newborn. Furthermore, it aims to document the successful regression of CRS through medical treatment alone. We present the case of a five-day-old infant who was referred to our facility as a CRS case. The patient presented with bilateral white corneal opacity, which was observed shortly after birth. The mother was diagnosed as rubella-positive during pregnancy. Upon the initial examination under anesthesia, both eyes exhibited central white corneal opacity accompanied by large intrastromal cysts. Although a few breaks in Descemet\'s membrane were observed in both eyes, there were no signs of vascularization or the presence of iridocorneal or lenticular-corneal adhesions. After undergoing medical treatment consisting of topical sodium chloride and steroids, the cysts in both eyes completely regressed. Subsequently, the patient underwent penetrating keratoplasty to further address the dense scar. This case enhances our comprehension of ophthalmological complications associated with CRS and provides valuable insights into alternative therapeutic approaches for corneal stromal cysts.

OBJECTIVE: The aim of this study was to elucidate a rare corneal association of the coronavirus disease 2019 (COVID-19) vaccine. Although cases of corneal involvement after vaccination have been reported, we present the first case of Thygeson superficial punctate keratitis (TSPK) linked to the COVID-19 vaccine.
METHODS: This study is a case report.
RESULTS: A 25-year-old woman was assessed in the ophthalmology clinic for recurrent ocular surface symptoms after receiving the COVID-19 vaccine. She was followed in clinic and was found to have a remitting and recurring pattern of bilateral intraepithelial corneal opacities with associated subepithelial haze primarily overlying the pupillary area. These corneal lesions responded well to topical corticosteroid ophthalmic drops. Based on the clinical appearance, the response to treatment, negative herpes simplex virus serology, and the temporal relationship between vaccination and ocular findings, a diagnosis of COVID-19 vaccine-induced TSPK was suspected.
CONCLUSIONS: Although the COVID-19 vaccine remains overwhelmingly safe, clinicians should be aware of possible corneal side effects, including TSPK. Prompt ophthalmic assessment in those presenting with ocular symptoms after vaccination is encouraged.

BACKGROUND: Corneal opacity can be caused by various disease. Generally, the opacity gradually increases as the disease progresses. Sudden corneal opacity is mainly caused by corneal trauma, toxic drugs entering the cornea, or acute edema of the keratoconus. However, sudden corneal opacity caused by diabetes has not been reported.
METHODS: A 60-year-old man reported blurred vision and the black eye became white in appearance in the left eye for 5 days. The patient had a history of diabetes which had not been treated.
METHODS: He underwent slit-lamp examination, anterior segment optical coherence tomography, ultrasound bio microscopy, B-mode ultrasound, corneal endothelial examination, random blood glucose testing, and other examinations. The diagnosis of Diabetic Keratopathy was made.
METHODS: Topical glucocorticoids and dilating eye drops were administered and undergo blood sugar control treatment.
RESULTS: The corneal of the patient was completely transparent in a few days, and the flocculent exudation in the anterior chamber disappeared.
CONCLUSIONS: Although diabetes generally causes chronic corneal edema, acute corneal edema may also occur when blood sugar is poorly controlled. Therefore, when we see sudden corneal opacity without obvious incentives, we must consider systemic diseases, especially diabetes.