Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022568 (keratitis)
 5,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

X-linked anhidrotic/hypohidrotic ectodermal dysplasia (EDA) is caused by mutations in the (EDA) gene, which is required for the morphogenesis of ectoderm-derived tissues. Although EDA function in skin appendage development has been studied in Eda mutant "Tabby" mice, we have recently identified characteristic abnormalities in the ocular surface, an ectoderm-derived tissue. Histology of eyes of Tabby males revealed that 1) as previously reported, mice lacked meibomian glands; 2) >80% developed corneal lesions such as neovascularization, keratitis, ulceration, and keratinization identifiable from 9 weeks of age; and 3) > 80% showed ocular surface inflammation (blepharitis and conjunctivitis) when housed in a standard environment. Strikingly, both corneal defects and inflammation were prevented in Tabby mice bearing a transgene for the Eda-A1 isoform, but meibomian glands were restored little if at all. These findings suggest that intact ocular surface health is EDA dependent and that Tabby corneal abnormalities are not solely dependent on meibomian gland lipid secretion. Alternatively, susceptibility to inflammation and other phenotypes could result from failure of the usual EDA receptor to activate nuclear factor-kappaB transcription factors. This can be further tested in Tabby and Tabby-EDA transgenic mice, which provide unique models of severe ocular surface disease.
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PMID:X-linked anhidrotic ectodermal dysplasia disruption yields a mouse model for ocular surface disease and resultant blindness. 1597 55

Although the risk of developing contact lens associated microbial keratitis is small, the potential consequences of this condition, such as vision loss, are serious. This paper presents an analysis of the risk factors that have been identified for contact lens induced microbial keratitis, which include extended wear, hypoxia, non-compliance, blepharitis, diabetes mellitus, epithelial trauma, steroid use, therapeutic lens use, tobacco use, and possibly travel to warm climates. By remaining mindful of these risk factors, practitioners can take action and offer advice to patients so as to optimize the safety of contact lens wear.
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PMID:Risk factors for contact lens associated microbial keratitis. 1630 75

The purpose of this study was to investigate spontaneous eye disease in New Zealand White (NZW) rabbits, which are commonly used for toxicity tests, and to provide reference materials for pharmaceutical companies and research centers. A total of 586 NZW rabbits were randomly chosen without sex preference and were examined using ocular equipment, including a direct ophthalmoscope, an indirect ophthalmoscope, a slit-lamp biomicroscope, a focal illuminator, and a fundus camera. This study showed that the incidence rate of temporary cataracts, regarded as a change within normal variation, was 0.5% in the NZW rabbits. Regarding abnormal ophthalmic disease, blepharitis was the most commonly observed ocular disease. Other findings included cataract, conjunctivitis, choroidal hypoplasia, keratitis, corneal scarring, eyelid laceration, posterior synechiae, uveitis, dacryocystitis, and persistent pupillary membrane. In total, the incidence rate of ophthalmic diseases was 9.6%. Based on sex and age distributions, females had more ocular diseases than males, and rabbits were less susceptible to eye diseases as they got older. In this study, photographs were taken to document findings, such as normal fundus, normal variations, ophthalmic disease, and histopathologic examination.
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PMID:Spontaneous ophthalmic diseases in 586 New Zealand white rabbits. 1636 16

A 26-year-old Japanese woman was referred to our hospital with generalized hyperkeratosis associated with keratitis and a hearing defect. The patient was born from nonconsanguineous parents. Her skin was moderately hyperkeratotic at birth. During childhood, the thickness of the skin increased progressively. Bilateral sensorineural deafness was recognized at the age of 3 years. Visual disturbance was noted in later childhood, and corneal transplantations to the right eye were performed twice at the age of 16 and 25 years, but did not improve her visual acuity. There was no family history of similar disease. On physical examination, the patient showed erythematous, keratotic, scaly plaques on the cheeks, auricles, and perioral area (Fig. 1a). A grainy, spiculated, hyperkeratotic papillomatosis was particularly marked on the palms and the edge of the feet (Fig. 1b,c). The nails were slight hypertrophic, but not dystrophic. Ophthalmologic examination revealed the loss of eyebrows and eyelashes and hyperkeratotic lesions of the eyelids (Fig. 1d). Corneal opacification was observed in the right eye. Conjunctivitis and blepharitis with photophobia were also observed in both eyes (Fig. 1d,e). A skin biopsy specimen from the right lower thigh showed basket-wave hyperkeratosis and papillomatosis of the epidermis. Hyperkeratotic plugs were not observed (Fig. 1f). Laboratory data, including complete blood cell count, sedimentation rate, immunoglobulins and transaminases, urea, cholesterol, and triglycerides were normal. With informed consent, genomic DNA was extracted from blood samples. The complete open reading frame of the GJB2 gene was polymerase chain reaction amplified and sequenced. A transition mutation (148G --> A) was detected, resulting in a putative amino acid change from aspartic acid to asparagine at codon 50 (Fig. 2). The mutation was not present in her parents or two siblings. These clinical, pathologic, and genetic data supported the diagnosis of keratitis-ichthyosis-deafness syndrome.
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PMID:A case of keratitis-ichthyosis-deafness (KID) syndrome. 1744 83

A novel antiviral protein was purified from an extract of Grifola frondosa fruiting bodies using a procedure that included 40% ammonium sulfate precipitation and DEAE-cellulose ion exchange chromatography, and designated GFAHP. This protein inhibited herpes simplex virus type 1 (HSV-1) replication in vitro with an IC(50) value of 4.1 microg/ml and a therapeutic index >29.3. Higher concentrations of GFAHP (125 and 500 microg/ml) also significantly reduced the severity of HSV-1 induced blepharitis, neovascularization, and stromal keratitis in a murine model. Topical administration of GFAHP to the mouse cornea resulted in a significant decrease in virus production (mean virus yields: 3.4log10PFU in the treated group and 4.19log10PFU in the control group). We proved that GFAHP directly inactivates HSV-1 while simultaneously inhibiting HSV-1 penetration into Vero cells. Gel electrophoresis showed that GFAHP had a molecular weight of 29.5 kDa. GFAHP was tryptic digested and analyzed from the PMF of matrix assisted desorption ionization-time of flight mass spectrometry (MALDI-TOF-MS) and nanoelectrospray ionization tandem mass spectrometry. The N-terminal sequence of GFAHP consisted of an 11 amino acid peptide, NH(2)-REQDNAPCGLN-COOH that did not match any known amino acid sequences, indicating that GFAHP is likely to be a novel antivirus protein. To our knowledge, this is the first report that characterizes an anti-HSV protein from G. frondosa.
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PMID:Isolation, identification and function of a novel anti-HSV-1 protein from Grifola frondosa. 1747 44

Ocular infection with HSV-1 continues to be a serious clinical problem despite the availability of effective antivirals. Primary infection with HSV-1 can involve ocular and adenaxial sites and can manifest as blepharitis, conjunctivitis, or corneal epithelial keratitis. After initial ocular infection, HSV-1 can establish latent infection in the trigeminal ganglia for the lifetime of the host. During latency, the viral genome is retained in the neuron without producing viral proteins. However, abundant transcription occurs at the region encoding the latency-associated transcript, which may play significant roles in the maintenance of latency as well as neuronal reactivation. Many host and viral factors are involved in HSV-1 reactivation from latency. HSV-1 DNA is shed into tears and saliva of most adults, but in most cases this does not result in lesions. Recurrent disease occurs as HSV-1 is carried by anterograde transport to the original site of infection, or any other site innervated by the latently infected ganglia, and can reinfect the ocular tissues. Recurrent corneal disease can lead to corneal scarring, thinning, stromal opacity and neovascularization and, eventually, blindness. In spite of intensive antiviral and anti-inflammatory therapy, a significant percentage of patients do not respond to chemotherapy for herpetic necrotizing stromal keratitis. Therefore, the development of therapies that would reduce asymptomatic viral shedding and lower the risks of recurrent disease and transmission of the virus is key to decreasing the morbidity of ocular herpetic disease. This review will highlight basic HSV-1 virology, and will compare the animal models of latency, reactivation, and recurrent ocular disease to the current clinical data.
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PMID:Ocular HSV-1 latency, reactivation and recurrent disease. 1858 63

The role that interferon-gamma (IFNgamma) plays during herpetic stromal keratitis (HSK) has not been definitively determined. In primary HSK most reports suggest that IFNgamma may help control viral replication and contribute to corneal pathology. However, its role in recurrent HSK has not been directly addressed. The present study addresses its role in recurrent HSK by comparing HSK in latently infected normal and IFNgamma gene knockout (GKO) on the C57BL/6 background. We initially evaluated HSK following primary infection and observed that GKO mice had higher tear film virus titers, but virtually identical ocular disease as normal mice. In contrast, following reactivation of latent virus, GKO mice had a greater incidence and severity of opacity, neovascularization, and blepharitis. Interestingly, the incidence of reactivation after UV-B exposure was equivalent in GKO and normal mice, but virus shedding was increased in the GKO groups. We also observed diminished delayed-type hypersensitivity responses in GKO mice, as expected. These data indicate that IFNgamma is important for the control of virus replication in both primary and recurrent ocular HSV infection in C57BL/6 mice. The enhanced recurrent disease seen in GKO mice may be the result of increased viral titers and persistence in these mice which act to prolong the stimulation of an inflammatory response.
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PMID:Interferon gamma is not required for recurrent herpetic stromal keratitis. 1875 90

Ocular mucous membrane pemphigoid presents some of the most challenging dilemmas in anterior segment management. Diagnosis is made difficult by the insensitivity of immunopathological investigations and the differential diagnosis of other scarring conjunctival disorders. The management of the associated ocular surface disease involves control of blepharitis, dry eye, filamentary keratitis, keratinization, lid malposition, and persistent epithelial defect, as well as the identification and avoidance of toxicity. Inflammation associated with the underlying disorder demands the use of systemic immunosuppressive therapy in many patients. New biological immunotherapies have been used when conventional immunosuppressive therapies fail. Ophthalmic plastic surgery is essential for the management of lid malposition and corneal exposure. Improving vision may require the use of specialized contact lenses, cataract surgery, and corneal and ocular surface reconstructive surgery. All surgery must be integrated with ocular surface treatment and immunosuppressive treatment to avoid disease exacerbations.
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PMID:Ocular mucous membrane pemphigoid: diagnosis and management strategies. 1878 Dec 59

The diagnosis of allergic conjunctivis begins by a meticulous questioning emphasizing the existence of ocular itching, the way of evolution of the signs and allergic preceeding. The examination searchs after follicles and papillae of the conjunctiva who usually go with serous discharges, blepharitis and keratitis. So four clinical forms may be described the chronic conjunctivitis, the vernal kerato-conjunctivitis, the atopic conjunctivitis and the giganto-papillar conjunctivitis. For the treatment, all non specific signs of allergy must be eliminated, the focal infections also and allergic substance isolated. If evolution is worse, an antiallergic eye drop is given until the disappearance of all the physical signs. In the same time, steroids and anti H1 drugs must be avoided. In case of failure, the specialist in allergy will be helpful to exam the patient.
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PMID:[A systemic approach to the diagnosis and treatment of allergic conjunctivitis]. 1910 85

The aim of this study was to prepare bioadhesive sulfacetamide sodium (SA) microspheres to increase their residence time on the ocular surface and to enhance their treatment efficacy on ocular keratitis. Microspheres were fabricated by spray drying method using mixture of polymers such as pectin, polycarbophil and hydroxypropylmethyl cellulose (HPMC) at different ratios. The particle size and distribution, morphological characteristics, thermal behavior, encapsulation efficiency, mucoadhesion and in vitro drug release studies on formulations have been investigated. After optimisation studies, SA-loaded polycarbophil microsphere formulation with polymer:drug ratio of 2:1 was found to be the most suitable for ocular application and used in in vivo studies. In vivo studies were carried out on New Zealand male rabbit eyes with keratitis caused by Pseudomonas aeruginosa and Staphylococcus aureus. Sterile microsphere suspension in light mineral oil was applied to infected eyes twice a day. Plain SA suspension was used as a positive control. On 3rd and 6th days of the antimicrobial therapy, the eyes were examined in respect to clinical signs of infection (blepharitis, conjunctivitis, iritis, corneal oedema and corneal infiltrates) which are the main symptoms of bacterial keratitis and then cornea samples were counted microbiologically. The rabbit eyes treated with microspheres demonstrated significantly lower clinical scores than those treated with SA alone. A significant decrease in the number of viable bacteria in eyes treated with microspheres was observed in both infection models when compared to those treated with SA alone. In conclusion, in vitro and in vivo studies showed that SA-loaded microspheres were proven to be highly effective in the treatment of ocular keratitis.
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PMID:Bioadhesive sulfacetamide sodium microspheres: evaluation of their effectiveness in the treatment of bacterial keratitis caused by Staphylococcus aureus and Pseudomonas aeruginosa in a rabbit model. 1922 14


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