PURPOSE: To assess subjective symptoms and objective clinical signs of dry eye and investigate corneal sensitivity after high myopic LASIK. METHODS: Twenty eyes of 20 patients with a mean age of 34±7.5 years who had undergone high myopic LASIK 2 to 5 years previously and 10 eyes of 10 controls with a mean age of 39.8±10.4 years were enrolled in the study. Clinical signs of dry eye and subjective dry eye symptoms were determined. The corneal sensitivity was assessed using non-contact esthesiometer. RESULTS: The preoperative spherical equivalent refraction was -11.40±1.40 diopters (D) (range: -9.10 to -14.00 D) and the intended spherical equivalent refraction correction was -10.40±1.10 D (range: -8.30 to -12.50 D). Schirmer'stest score was 14.4+8.9 mm in patients and 9.0±4.2 mm in controls (P= .066). The break-up time was 15.9 ±11.2 seconds in patients and 14.0±10.0 seconds in controls (P=. 505). The mean corneal sensitivity was 73.5±29.6 mL/min in patients and 78.0±18.7 mL/min in controls (P=. 666). The majority (55%) of patients still reported dry eye symptoms. Ocular surface disease index indicating degree of dry eye symptoms was significantly higher in LASIK patients (18.6+13.4%) compared to controls (7.5±5.7%; P=.022). CONCLUSIONS: The majority of patients who received LASIK for high myopia reported ongoing dry eye symptoms, although objective clinical signs of tear insufficiency and hypoesthesia were not demonstrable. We assume that symptoms represent a form of corneal neuropathy rather than dry eye syndrome. [J Refract Surg. 2007;23:338-342.]
Both EMMPRIN and MMP-1 are upregulated in keratoconus, but MMP-1 may not be the only tissue destructive MMP upregulated by EMMPRIN as only EMMPRIN expression correlated topologically very well with corneal damage.
ABSTRACT.Purpose: To describe a patient with a long disease history who was finally diagnosed with neurosarcoidosis and to discuss the reasons behind the delayed diagnosis. Case Report: A 58-year-old man with sick sinus syndrome and bradycardia, which was treated with a pacemaker, developed first right and then left facial palsy. Subsequently, multiple cranial nerve palsies developed and later spontaneously resolved. Neurosarcoidosis was suspected at that stage, but excluded because the patient had no typical sarcoid lung changes, his serum and cerebrospinal fluid angiotensin converting enzyme activity levels were normal and a computed tomography scan disclosed no central nervous system changes. During follow-up, the patient developed extremely dry eyes and mouth, suggesting Sjo¨gren's syndrome. Rheumatology consultation did not reveal any autoimmune or visceral features typical of Sjo¨gren's syndrome and autoantibodies were negative. However, both labial salivary gland and conjunctival biopsies revealed non-caseating granulomas, and neurosarcoidosis was diagnosed. Conclusions: Neurosarcoidosis is a relatively rare disease with a somewhat poor longterm prognosis in one-third of cases, although the neurological manifestations often diminish or disappear in response to glucocorticoid treatment. Diagnosis is often a clinical challenge, especially in the absence of pulmonary changes or other features typical of sarcoidosis. The labial salivary gland and conjunctiva provide helpful biopsy sites for histopathological confirmation of the diagnosis.
Purpose The epithelial recurrent erosion dystrophy (ERED) is a rare autosomal dominant corneal disease. Recently, mutations in collagen type XVII, alpha 1 (COL17A1) gene have been identified as the cause of ERED. Here we report a Finnish family with recurrent erosions with dominant inheritance pattern. We performed COL17A1 candidate gene sequencing. Methods Five affected and five unaffected family members underwent standard ophthalmological examination, corneal topography, anterior segment optical coherence tomography and in vivo confocal microscopy. Next‐generation exome sequencing of peripheral blood was made in two of the affected individuals to identify mutations in the large COL17A1 gene. Sanger sequencing was used to verify the presence of the identified variant in the other family members. Results Affected patients reported recurrent corneal erosions beginning at the age of 4‐6 years. The frequency of erosions decreased in adult age. Corneal scarring and anterior stromal opacities were observed. The visual acuity slowly deteriorated. Exome‐sequencing revealed a synonymous splice‐altering variant c.3156C>T in COL17A1 in two affected patients. Sanger sequencing confirmed the presence of the same variant in four affected family members and its absence from two unaffected ones. The variant was not present in the Sequencing Initiative Suomi (SISu) database consisting of 10,490 Finns. Conclusions The variant c.3156C>T in COL17A1 is reported recently in five English, American, New Zealand, and Tasmanian families with ERED. Our finding of the same synonymous variant in yet another population strengthens the evidence this variant is a frequent cause of ERED.
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