1,720,994 research outputs found

    Gastroesophageal reflux disease and the presence of pepsin in the tears.

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    The nasolacrimal duct in association with the lacrimal puncta, lacrimal canaliculi and lacrimal sac functions to collect and drain the tear film into the nasal cavity at the inferior nasal meatus where a fold of nasal mucosa, the so-called valve of Hasner, prevents mucous from entering the nose. High-resolution computed tomography demonstrated air inside the sac and nasolacrimal duct in approximately 29.3% of healthy patients suggesting that the system is not completely competent and that air and secretions might reach the precorneal film. Gastroesophageal reflux disease may contribute to dacryostenosis and subsequent primary acquired nasolacrimal duct obstruction. However a cause-effect relationship is unclear and only presumptive unless the presence of pepsin in tears can be demonstrated. Gastroesophageal and extra-esophageal reflux could reach the tear film via the nasolacrimal duct in a retrograde fashion and the middle ear via the Eustachian tube. We postulated that the ascending products of gastroesophageal reflux could cause edema of the nasolacrimal duct mucosa, which might progress to fibrosis and chronic inflammation and, ultimately, complete obstruction of the duct with epiphora. The role of reflux in the initial phase of this pathophysiological mechanisms could be demonstrated indirectly by pepsin. By contrast, the development of dacryostenosis blocking the passage of the nasolacrimal duct and thereby preventing pepsin from reaching the lacrimal film failed to explain the influence of gastroesophageal reflux disease with certainty

    Un caso anomalo di sindrome di Posner – Schlossman

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    Gli autori hanno riportato un caso anomalo di Posner-Schlossman in una giovane paziente di 46 anni. Tale sindrome, come è noto, è caratterizzata da episodi acuti e recidivanti di ipertensione oculare, associata a segni modesti di flogosi uveale anteriore che colpisce essenzialmente soggetti giovani di età compresa tra 20 e 50 anni. Ciò che ha interessato particolarmente nello studio di questo caso clinico è la particolare insorgenza, la brevissima durata (qualche ora) e la monolateralità degli episodi ipertensivi affiancati da una negatività dell’esame obiettivo e di quelli diagnostici svolti

    Platelet-Rich Plasma (PRP) to promote corneal healing in firework-related ocular burn and total limbal stem cell deficiency (LSCD)

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    Purpose: To report the case of persistent corneal epithelial defect in total limbal stem cell deficiency (LSCD) after severe firework-related ocular burn treated with autologous Platelet-Rich Plasma (PRP). Case description: A young patient, victim of fireworks trauma, presented with a large persistent epithelial defect affecting the central cornea of his left eye and progressing to stromal melting, in the context of grade VI ocular surface burn with 12 h limbal involvement. Impression cytology to the cornea confirmed a complete LSCD. Assessment of corneal sensitivity by Cochet Bonnet esthesiometer revealed complete corneal anesthesia. Based on progressive clinical worsening under conventional therapy, the patient was started on very pure autologous PRP eye drops obtained using the Hy-Tissue PRP® technology. Six times a day eye drops administration for 30 days was scheduled in the affected eye. At the end of treatment, the epithelial defect had disappeared being replaced by advancing conjunctiva. Conclusion: Our findings provide information on management of ocular burns from fireworks, a subject of current interest and concern. Autologous PRP eye drops prepared using the Hy-Tissue PRP® system and administered in the presence of total LSCD and complete corneal anesthesia, prevented corneal stromal melting to progress and allowed the ocular surface epithelial coverage to re-establish. This paved the way for later successful restorative and reconstructive intervention. Also, first description of the Hy-tissue PRP procedure for ophthalmological use is reported

    Histological findings in a failed corneal riboflavin-UVA collagen cross-linking performed for progressive keratoconus

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    Purpose: To report the histological and immunohistochemical findings in a cornea removed from a patient who had undergone collagen cross-linking (CXL) with riboflavin and ultraviolet-A for progressive keratoconus. CXL was performed following the Siena protocol. Two years post-CXL, a visual acuity impairment in the treated eye secondary to corneal stromal opacity had occurred, together with corneal thinning and flattening. Methods: The excised cornea was formalin-fixed, paraffin-embedded, and examined microscopically. Deparaffinized 4-mu m sections were stained with hematoxylin-eosin and Masson trichrome. Further tissue sections were subjected to immunohistochemical evaluation of CD34 and Ki-67 antigens. Results: Histologically, there was no scar tissue in the failed cornea. The biomicroscopic stromal opacity corresponded microscopically to an acellular area, devoid of keratocytes, and to compaction of the lamellar collagen. Amorphous, weakly eosinophilic interlamellar deposits, extending from the anterior to the posterior two thirds of the stroma, were noted. Conclusions: CXL is a promising procedure for the treatment of progressive keratoconus with minimal reported side effects. In the present case, we speculate that the short corneal soaking time (15 minutes according to the Siena protocol) may have resulted in inefficient ultraviolet-A blocking, thermal injury, and deeper keratocyte death. Inadequate keratocyte stem cells reservoir could also play a role in individual cases

    Understanding vernal keratoconjunctivitis: beyond allergic mechanisms

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    Abstract: Vernal keratoconjunctivitis (VKC) is a chronic, recurrent, inflammatory disease of the cornea and conjunctiva mostly affecting boys in prepubertal age. VKC recurrence is characterized by intense symptoms of itching, redness, and photophobia associated with corneal damage, impairment of visual function, and quality of life. The pathogenesis of VKC has not yet been completely understood, and it is still controversial. In fact, VKC is considered an ocular allergic disease due to the involvement of immunoglobulin E, eosinophils, and mast cells, and of a lymphocyte T-helper type 2 reaction. However, approximately half of VKC patients have negative allergological history and testing, suggesting that other pathogenic mechanisms participate in VKC development and severity. Specifically, evidence suggests that genetic, endocrine, neuronal factors and an imbalance of innate immunity are involved in the pathogenesis of VKC. The purpose of this review is to summarize evidence on the pathogenic role of innate immunity, neuroimmune reaction, and hormonal changes in VKC. Increasing understanding of the pathogenic mechanisms behind VKC may lead to the identification of novel biomarkers for diagnosis and/or potential therapeutic targets in order to improve the management of this challenging condition
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