Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022575 (keratoconjunctivitis sicca)
 772 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Feline herpesvirus-1 (FHV-1) infection is ubiquitous in the domestic cat population worldwide. The most common clinical ocular manifestations of infection with FHV-1 are conjunctivitis and keratitis. This paper reviews the pathogenesis of feline herpesvirus-1 and discusses the various clinical ocular manifestations, diagnostic techniques and treatment of FHV-1-induced diseases. Ocular manifestations include: conjunctivitis, keratitis, stromal keratitis, keratoconjunctivitis sicca, ophthalmia neonatorium, symblepharon, corneal sequestrum, eosinophilic keratitis and anterior uveitis. Diagnostic techniques discussed include: virus isolation, fluorescent antibody testing, serum neutralising titers, ELISA and polymerase chain reaction. Various therapies are also discussed.
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PMID:Ocular manifestations of feline herpesvirus. 1171 25

Chronic corneal epithelial defects (CCEDs; indolent corneal ulcerations) are the most common refractory ulcerations in veterinary medicine and are diagnosed by their classic appearance. CCEDs are superficial ulcerations without stromal involvement and have a nonadherent epithelial border (lip). Fluorescein stain adheres to the exposed stroma and extends below the epithelial border, outlining the epithelial lip. CCEDs occur secondary to adnexal disease, keratoconjunctivitis sicca, exposure keratitis, neurotrophic keratitis, and primary corneal disease. In cats, herpes keratitis is associated with the development of CCEDs. Bacterial infections are not responsible for the refractory nature of CCEDs. Because of the refractory nature of CCEDs, treatment can be frustrating for both owner and veterinarian. Current treatment recommendations consist of identifying and treating the underlying cause and performing procedures that stimulate epithelialization and adhesion of the corneal epithelium. Initial treatment of CCEDs includes ulcer debridement and grid keratotomy. Superficial keratectomy is indicated in refractory cases.
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PMID:Diagnosis and management of chronic corneal epithelial defects (indolent corneal ulcerations). 1460 91

Keratoconjunctivitis sicca (KCS), also known as dry eye syndrome, dry eye disease, chronic dry eye disease, or keratitis sicca, refers to disorders of the tear film caused by reduced tear production, poor tear quality, or excessive tear evaporation. These disorders are associated with such symptoms of ocular discomfort as irritation, foreign body sensation, or redness, and may cause disease of the ocular surface.
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PMID:Guidelines for the treatment of chronic dry eye disease. 1472 10

Connective tissue disorders have well-known ocular associations that may be presenting features of the disease or occur as complications during the course of the disorder. Keratoconjunctivitis sicca, keratitis, scleritis, uveitis, retinal vasculitis, choroidopathy, and their associations with rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, psoriatic arthritis, juvenile idiopathic arthritis, and polymyositis are reviewed.
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PMID:Ocular involvement in connective tissue disorders. 1596 77

Systemic lupus erythematosus (SLE) is a chronic, immunologically mediated inflammatory connective tissue disorder with manifestations including various body organs (joints, pleura, pericardium, kidneys, brain, skin), caused by accumulation of immune complexes. According to epidemiological data SLE affects 0.12% of the population worldwide, while in Poland the number of reported cases is c. 60 000 - 80 000. SLE may also involve the eye. Anterior segment findings include keratoconjunctivitis sicca, keratitis and scleritis. Retinal manifestations of SLE are cotton wool spots, hemorrhage and vasculitis. The ARA (American Rheumatism Association), criteria are used in establishing the diagnosis of SLE. Although the ocular symptoms are not included in the ARA criteria, they may be initial findings and precede other manifestations of SLE.
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PMID:[General and ocular symptoms in systemic lupus erythematosus (SLE)]. 1768 18

A 10-year-old female West Highland white terrier was presented with refractory hyperplastic keratitis of the left cornea of one month's duration. At this time, a vascularised and rough lesion 5 mm in diameter was observed on the left cornea. No other abnormality was recognised on the affected eye. The corneal neoplasm was surgically removed and histologically diagnosed as a squamous cell carcinoma. For two months after the surgery, 0.04 percent mitomycin C (MMC) eye drops were applied as adjuvant chemotherapy. Primary corneal squamous cell carcinoma with no history of keratoconjunctivitis sicca is rare in dogs. In the present report, surgical removal of the neoplasm was combined with the topical administration of the anticancer drug mitomycin C and a good prognosis was obtained. The result indicates that the combination treatment used in this case may be an appropriate therapeutic choice for corneal squamous cell carcinoma in dogs.
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PMID:Superficial keratectomy and topical mitomycin C as therapy for a corneal squamous cell carcinoma in a dog. 1772 85

A 12-year-old Pug presented with a 3-mm corneal mass OD. The dog was currently being treated for keratoconjunctivitis sicca (KCS) and pigmentary keratitis OU. A superficial keratectomy followed by cryotherapy was performed OD. A histopathologic diagnosis of epithelial dysplasia and suppurative keratitis was made and the lesion resolved. Two months later, a yellow/tan conjunctival mass, diffuse chemosis and conjunctival thickening was discovered OD. Necrotizing conjunctivitis with protozoal parasites was diagnosed with histopathology. Complete blood count and a serum biochemistry panel were normal. Neospora caninum and Toxoplasma gondii titers were negative. The conjunctivitis resolved after a 6-week course of oral clindamycin. Two months later, the patient presented with a similar conjunctival mass OS. Toxoplasma gondii was confirmed as the etiologic agent with immunohistochemical staining. Repeat T. gondii titers were negative. Oral clindamycin was re-instituted. The corneal biopsy was re-reviewed and protozoal organisms were discovered. Three months later, a recurrence was suspected and oral ponazuril was initiated for 28 days. There has been no evidence of recurrence since this treatment. Ocular toxoplasmosis is rare in the dog but reports have included episcleritis, scleritis, retinitis, anterior uveitis, ciliary epithelium hyperplasia, optic neuritis and polymyositis. To our knowledge, this is the first confirmed report of toxoplasmosis causing only corneal and conjunctival disease in the dog. We hypothesize that these localized lesions may be associated with topical immunomodulating therapy for KCS. Toxoplasmosis should be considered as a differential for canine conjunctivitis and corneal disease and has the potential to manifest in one or both eyes.
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PMID:Keratoconjunctivitis associated with Toxoplasma gondii in a dog. 1915

NF-kappaB is well established as a key component of the inflammatory response. However, the precise mechanisms through which NF-kappaB activation contributes to inflammatory disease states remain poorly defined. To test the role of NF-kappaB in inflammation, we created a knock-in mouse that expresses a constitutively active form of NF-kappaB p65 dimers. These mice are born at normal Mendelian ratios, but display a progressive, systemic hyperinflammatory condition that results in severe runting and, typically, death 8-20 d after birth. Examination of homozygous knock-in mice demonstrates significant increases in proinflammatory cytokines and chemokines. Remarkably, crossing this strain with mice lacking TNF receptor 1 (TNFR1) leads to a complete rescue of the hyperinflammatory phenotype. However, upon aging, these rescued mice begin to display chronic keratitis accompanied by increased corneal expression of TNFalpha, IL-1beta, and MMP-9, similar to that seen in human keratoconjunctivitis sicca (KCS) or "dry eyes." Therefore, our results show that, while constitutively active NF-kappaB can trigger systemic inflammation, it does so indirectly, through increased TNF production. However, certain inflammatory disease states, such as keratitis or KCS, a condition that is seen in Sjogren's syndrome, are dependent on NF-kappaB, but are independent of TNFR1 signaling.
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PMID:Constitutively active NF-kappaB triggers systemic TNFalpha-dependent inflammation and localized TNFalpha-independent inflammatory disease. 2071 16

The clinical presentation and progression (over 9 months to 13 years) of congenital keratoconjunctivitis sicca and ichthyosiform dermatosis (CKCSID) in the Cavalier King Charles spaniel dog are described for six new cases and six previously described cases. Cases presented with a congenitally abnormal (rough/curly) coat and signs of KCS from eyelid opening. Persistent scale along the dorsal spine and flanks with a harsh frizzy and alopecic coat was evident in the first few months of life. Ventral abdominal skin was hyperpigmented and hyperkeratinized in adulthood. Footpads were hyperkeratinized from young adulthood with nail growth abnormalities and intermittent sloughing. Long-term follow-up of cases (13/25) is described. Immunomodulatory/lacrimostimulant treatment had no statistically significant effect on Schirmer tear test results, although subjectively, this treatment reduced progression of the keratitis. Histopathological analysis of samples (skin/footpads/lacrimal glands/salivary glands) for three new cases was consistent with an ichthyosiform dermatosis, with no pathology of the salivary or lacrimal glands identified histologically. Pedigree analysis suggests the syndrome is inherited by an autosomal recessive mode.
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PMID:Congenital keratoconjunctivitis sicca and ichthyosiform dermatosis in 25 Cavalier King Charles spaniel dogs. Part I: clinical signs, histopathology, and inheritance. 2221 37

Toxic epidermal necrolysis (TEN) or Lyell's syndrome is an acute life-threatening disease often triggered by an adverse drug reaction and/or infection. It is characterized by an extensive epidermal loss and severe mucosal involvement. Its pathophysiology is unresolved, but several studies support the hypothesis of an immune mediation. The authors review the ocular involvement of ten drug-induced TEN cases observed in the last four years (eight females and two males; mean age=47). An epidermal loss ranging from 24 to 95% of body surface area was associated with ocular (10/10), oral (9/10), genital (6/10) and anal (4/10) involvement. Ocular findings in the acute phase were: bilateral mucopurulent conjunctivitis (9/10), with inflammatory membranes (3/10), punctate epithelial keratitis (6/10) and corneal ulcers (3/10). Skin palpebral detachment occurred in seven cases, all with extensive and severe systemic disease. In the chronic phase of the disease the authors observed keratoconjunctivitis sicca (4/7), symblepharon (3/7), entropion with trichiasis (2/7) and corneal neovascularization (2/7). HLA B44 (B12) was observed in four of eight studied patients. In conclusion, ocular involvement is frequent in TEN patients and, in those who survive, it significantly contributes to the morbidity of the disease.
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PMID:Ocular involvement in toxic epidermal necrolysis. 2282 11


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