In Vivo Confocal Microscopic Findings of Subepithelial Infiltrates Associated with Epidemic Keratoconjunctivitis

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Psödoeksfoliasyon Sendromu ve Konjonktivaşalazisli Olgularda Oküler Yüzey Parametrelerinin Deǧerlendirilmesi

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Glokom ve Oküler Hipertansiyon Hastalarında Humphrey Matriks Perimetrisi ve Standart Otomatik Perimetrinin SITA Stratejisi ile Elde Edilen Görme Alan Sonuçlarının Karşılaştırılması

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In Vivo Confocal Microscopic Findings in the Corneas of Patients with Topical Anesthetic Abuse Keratopathy

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The COVID-19 pandemic: Clinical information for ophthalmologists

[No abstract available

Myocilin Mt1 Promoter Polymorphism In Turkish Patients With Primary Open Angle Glaucoma

Purpose: To evaluate the association of the myocilin gene promoter variant -1000C>G (MYOC.mt1) with primary open angle glaucoma (POAG) and its possible role on the phenotype and the severity of glaucoma in Turkish patients. Methods: Eighty eight POAG patients and 123 healthy subjects were included in the study. All subjects were genotyped by PCR-RFLP. Allele and genotype frequencies between healthy subjects and glaucoma patients were compared by the chi(2) test. The age at diagnosis, the age at inclusion, the maximum IOP at diagnosis and the number of antiglaucomatous medications were compared between MYOC.mt1 carriers and non-carriers using the Student's t-test; C/D ratio, mean deviation (MD), and pattern standard deviation values were compared with the Mann-Whitney U-test. Statistical significance was defined as p0.05). No significant difference was found in the distribution of genotypes between different stages of glaucoma groups (p=0.93). Conclusions: Our results suggest that in our Turkish glaucoma patients, MYOC.mt1 is not a risk factor for the development of POAG and is not associated with the phenotype and severity of glaucoma.Wo

Clinical Impact Of Inflammation In Dry Eye Disease: Proceedings Of The Odissey Group Meeting

Dry eye disease (DED) is a common, multifactorial ocular condition with major impact on vision and quality of life. It is now well recognized that the pathophysiology of chronic DED can include a cycle of inflammation involving both innate and adaptive immune responses. Recently, in vitro/in vivo models have been used to obtain a better understanding of DED‐related inflammatory processes at molecular/cellular levels although they do not truly reproduce the complex and chronic hallmarks of human DED. In clinical DED research, advanced techniques such as impression cytology, conjunctival biopsy, in vivo confocal microscopy and multiplex tear analyses have allowed an improved assessment of inflammation in DED patients. This was supported by the identification of reliable inflammatory markers including matrix metalloproteinase‐9, human leucocyte antigen‐DR or intercellular adhesion molecule‐1 in tears and impression cytology samples. One of the current therapeutic strategies focuses on breaking the inflammatory cycle perpetuating the ocular surface disease, and preclinical/clinical research has led to the development of promising anti‐inflammatory compounds. For instance, cyclosporine, already approved in the United States, has recently been authorized in Europe to treat DED associated with severe keratitis. In addition, other agents such as corticosteroids, doxycycline and essential fatty acids, through their anti‐inflammatory properties, show encouraging results. We now have a clearer understanding of the inflammatory processes involved in DED, and there is hope that the still emerging preclinical/clinical findings will be translated into new and highly effective therapies for patients in the near future.PubMedWoSScopu