ABSTRACT
No abstract available.
Subject(s)
Aged , Humans , Male , Dacryocystorhinostomy/methods , Dry Eye Syndromes/metabolism , Eyelids/surgery , Lacrimal Apparatus/metabolism , Suture Techniques/instrumentation , Tears/metabolismABSTRACT
Recently, the association of Th-17 cells or IL-17 with ocular inflammatory diseases such as uveitis, scleritis and dry eye syndrome was discovered. We assessed whether interleukin (IL)-17 was present in the tears of various ocular surface inflammatory diseases and the tear IL-17 concentrations were clinically correlated with various ocular surface inflammatory diseases. We measured concentrations of IL-17 in tears of normal subjects (n = 28) and patients (n = 141) with meibomian gland dysfunction (MGD), dry eye syndrome (DES), Sjogren syndrome (SS), Stevens-Johnson syndrome (SJS), graft-versus-host disease (GVHD), filamentary keratitis, and autoimmune keratitis associated with rheumatoid arthritis or systemic lupus erythematosus. Clinical epitheliopathy scores were based on the surface area of corneal and conjunctival fluorescein staining. The mean concentrations of IL-17 in tears of patients with filamentary keratitis, GVHD, autoimmune keratitis, SS, DES, MGD, SJS were significantly higher in order than that in normal subjects. Tear IL-17 concentration was significantly correlated with clinical epitheilopathy scores in the patients with systemic inflammatory disease, while tear IL-17 was not correlated with clinical severity of the cornea and conjunctiva in the dry eye patients without any systemic inflammatory disease. Tear IL-17 is likely to correlate clinically with corneal disease severity only in the patients with systemic inflammatory disease.
Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Dry Eye Syndromes/metabolism , Eye Diseases/diagnosis , Eyelid Diseases/metabolism , Graft vs Host Disease/metabolism , Interleukin-17/analysis , Keratitis/metabolism , Meibomian Glands/physiopathology , Severity of Illness Index , Sjogren's Syndrome/metabolism , Stevens-Johnson Syndrome/metabolism , Tears/metabolismABSTRACT
El ojo seco es una compleja enfermedad multifactorial de la película lagrimal y de la superficie ocular caracterizada por síntomas de desconforto, alteraciones de la visión e inestabilidad del film lagrimal que puede provocar daño potencial sobre la superficie ocular. La inestabilidad del film producirá aumentos en la osmolaridad de la película lagrimal, lo que desencadena a su vez lesiones osmóticas epiteliales e inflamación. Al producirse estos cambios sobre la superficie ocular, los mecanismos neurofisiológicos de homeostasis se verán alterados lo que complicará aún más el proceso, con la aparición de circuitos viciosos fisiopatológicos.
Dry eye is a complex multifactorial disease of the tears and ocular surface that results in symptoms of discomfort, visual disturbance, and tear film instability with potential damage to the ocular surface. It is accompanied by increased osmolarity of the tear film and inflammation of the ocular surface. Inestability of the tear film may also cause an increased osmolarity of the tear film, thus triggering epithelial osmotic lesions and inflammation. The occurrence of such changes on the eye surface results in disturbances of homeostatic neurophysiologic mechanisms which further worsen the process and vicious pathophysiological cycles occur.
Subject(s)
Humans , Dry Eye Syndromes/metabolism , Tears/chemistry , Osmolar ConcentrationABSTRACT
Oxidative stress is caused by an imbalance between the production of reactive oxygen species and ability the biological systems' defense mechanisms necessary to eliminate the stress. It has been accepted that oxidative stress is involved in many acute and chronic diseases and even in normal aging. Recently, increased awareness of oxidative stress damage and its relation with ocular surface diseases incite researchers to discover possible mechanisms in the development of dry eye disease. This review focuses on the evaluation of the influence of oxidative stress on eye diseases emphasizing its relation with the pathogenesis of dry eye disease.
Estresse oxidativo é causado por um desequilíbrio entre a produção de espécies reativas do oxigênio e a habilidade dos mecanismos de defesa do sistema biológico necessários para eliminar este estresse. O estresse oxidativo tem sido aceito como um fator envolvido em várias doenças agudas, crônicas e até mesmo no envelhecimento fisiológico. Recentemente, o crescente conhecimento dos danos causados pelo estresse oxidativo e a sua relação com doenças da superfície ocular estimulou pesquisadores a descobrir possíveis mecanismos no desenvolvimento da doença do olho seco. Esta revisão tem como foco a avaliação da influência do estresse oxidativo nas doenças do olho e enfatiza a sua relação com a patogênese da doença do olho seco.
Subject(s)
Aged , Humans , Dry Eye Syndromes/etiology , Keratitis/etiology , Oxidative Stress/physiology , Aging/physiology , Dry Eye Syndromes/metabolism , Dry Eye Syndromes/pathology , Environment , Keratitis/metabolism , Keratitis/pathologyABSTRACT
Dry eye is a multifactorial condition that results in a dysfunctional lacrimal functional unit. Evidence suggests that inflammation is involved in the pathogenesis of the disease. Changes in tear composition including increased cytokines, chemokines, metalloproteinases and the number of T cells in the conjunctiva are found in dry eye patients and in animal models. This inflammation is responsible in part for the irritation symptoms, ocular surface epithelial disease, and altered corneal epithelial barrier function in dry eye. There are several anti-inflammatory therapies for dry eye that target one or more of the inflammatory mediators/pathways that have been identified and are discussed in detail.
Olho seco é uma doença multifatorial que resulta em disfunção da unidade lacrimal glandular. Evidências sugerem que inflamação está involvida na patogênese da doença. Mudanças na composição das lágrimas, incluindo aumento de citocinas, quimiocinas, metaloproteinases e o número de células T na conjuntiva são encontrados em pacientes com olho seco e em modelos animais. Esta inflamação é responsável em parte pelos sintomas de irritação, doença epitelial de surperfície ocular e função epitelial de barreira alterada em olho seco. Existem várias terapias antiinflamatórias que se direcionam para um ou mais mediadores/vias que foram identificados e são discutidos em detalhe.
Subject(s)
Humans , Anti-Inflammatory Agents/therapeutic use , Dry Eye Syndromes/drug therapy , Adrenal Cortex Hormones/therapeutic use , Cyclosporine/therapeutic use , Dry Eye Syndromes/metabolism , Tetracycline/therapeutic useABSTRACT
Diabetes mellitus and its clinical association with dry eye and ocular surface are becoming a frequent and sometimes complicate problem in Ophthalmology. Epidemiological data show that an increase in the number of patients with this association is expected following the trend to rise of the disease. The present work reviews the clinical and functional aspects of this problem. The observations indicate that metabolic, neuropathic and vascular tissue damages lead to an inflammatory process and functional degeneration. The physiopathological mechanism include hyperglycemia, advanced glycated end product accumulation, oxidative stress and inflammation mediated by NF-κB signaling pathways. Potential treatments enlightened by those findings would include antioxidant, anti-inflammatory, secretagogues and/or anabolic agents that would mimic insulin effects.
O diabetes mellitus e sua associação clínica com olho seco e doença da superfície ocular estão se tornando um problema freqüente e muitas vezes complicado em oftalmologia. Os dados epidemiológicos mostram que o número de casos deve crescer acompanhando a tendência de aumento da incidência da doença. Esse trabalho revê seus aspectos clínicos e funcionais. As observações indicam que as lesões metabólicas, neuropáticas e vasculares levam a um processo inflamatório e degeneração funcional. Os mecanismos fisiopatológicos incluem hiperglicemia, acúmulo de produtos finais de glicosilação avançada, estresse oxidativo e inflamação mediada pelas vias de sinalização do NF-kB. Os tratamentos potenciais sugeridos por essas observações incluiriam antioxidantes, antiinflamatórios, secretagogos e/ou agentes anabólicos com efeitos miméticos ao da insulina.