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)

The nonophthalmic physician confronted by a patient with a red eye should be able to distinguish common microbial or allergic conjunctivitis from potentially blinding disorders, such as acute angle closure glaucoma, uveitis, or herpes simplex keratitis, and should remain alert for an associated systemic disease, such as rheumatoid arthritis, polycythemia, or carotid cavernous fistula. The physician should approach the red eye systematically: take a careful history, including type of pain; measure visual acuity; observe the pattern of redness, the type of discharge, the shape of the pupil, and the opacities of the media; and measure the intraocular pressure.
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PMID:The red eye. 30 93

Three days after herpes simplex virus inoculation, an increased amount of DNA and RNA was observed in the superficial epithelium cells of rabbit cornea. Histochemical staining demonstrated the development of acid mucopolysaccharides and the destruction of reticulin. In the early stages, on rare occasions, giant polykaryocytes with multiple micronuclei were seen. From 1 week after infection, more and more cells became rounded and shrunken. Cytoplasm of these cells might contain DNA diffusely interspersed with RNA. This DNA is probably viral in nature. The nuclei of these cells varied in shape, size, and staining intensity. Nuclear fragments were often observed in the cytoplasm. Stainings for acid mucopolysaccharides were strongly positive in the rounded cells. These cells fused to form syncytia Variable-sized pseudopodialike processes containing DNA and RNA extend from some of the rounded and liquefied cells toward other cells. In the later stages, development of ghost cells was seen. Histochemical methods demonstrated the deposition of acid mucopolysaccharides on their cell membranes. Necrosis was more often present in the late stages. Nuclear debris and deformed cells were encountered in such areas. On the healing of the keratitis, 3 months after inoculation, the cell cytology and staining reactions reverted to normal.
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PMID:Histopathology and histochemistry of the superficial corneal epithelium in experimental herpes simplex keratitis. 31

Since the cornea responds to various toxic stimuli by swelling and ulcerating, these changes may assume a dendriform pattern. A case of herpes simplex dendritic keratitis is presented along with its treatment. In addition, several other etiologic sources of an arborescent keratitis are discussed as to their differentiation and management implication.
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PMID:Dendriform keratitis. 31 14

A review of 231 penetrating keratoplasties performed for corneal disease due to herpes simplex keratitis shows that clear grafts may be obtained in 75% and satisfactory visual results in about 70% during a long-term follow-up. Over a three-year follow-up period, recurrence of the herpetic disease in the graft was observed in 12%. Over a longer period of follow-up, up to 15 years, the rate of recurrence increased to 47%. About half of the corneas with recurrence achieved clear grafts with treatment. Recurrence did not appear to be less frequent in those cases which circumscribed scars as compared with those in which there was diffuse scarring. The state of activity of the disease preoperatively could not be demonstrated to influence greatly the results of the keratoplasty.
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PMID:Penetrating keratoplasty in herpes simplex keratitis. Recurrence in grafts. 32 50

In 20 cases of herpes simplex keratitis the efficacy of Vidarabin ointment has been tested, in 19 cases after corneal abrasion. The eyes were treated once a day and padded until the epithelial defects had closed. Thereafter the ointment was applied 4 times per day for about one week more. On the average epithelial closure had been achieved after 2.4 days, complete normalization of the epithelium after a total of 3.6 days. This therapy results in a considerable shortening of the healing process as compared to the topical use of anti-viral medication alone. From this aspect Vidarabin ointment has proved to be a valuable adjuvant.
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PMID:[Treatment of herpes simplex keratitis with Vidarabin ointment (author's transl)]. 34 60

104 renal transplant recipients have been examined regarding ocular complications. A high incidence of posterior subcapsular cataracts has been found, increasing with time after operation. Only 2 cases of open angle glaucoma were found, indicating a seemingly small risk for developing a corticosteroid-induced glaucoma in such patients. A high frequency of treatment-resistant herpes simplex keratitis, probably due to reduced corneal resistance, was found.
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PMID:Ocular complications in recipients of kidney transplants. 35 9

A double controlled clinical study comparing idoxuridine (IDU) and vidarabine (ara-A) in the treatment of uncomplicated herpes simplex keratitis was carried out with 10 patients. No statistically significant differences occurred in the healing time between IDU (6.8 days) and ara-A (8.0 days). Two moderately adverse reactions to IDU were observed, but no demonstrable ocular toxicity was noted with ara-A.
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PMID:Treatment of herpes simplex keratitis with idoxuridine and vidarabine: a double-blind study. 36 39

A 69-year-old male with chronic herpes simplex keratitis underwent penetrating keratoplasty, using cryopreserved tissue. Seven weeks postoperatively the patient developed cephalosporium endophthalmitis. Intensive medical and surgical therapy was unsuccessful and the eye had to be enucleated within three weeks. Cephalosporium species are isolated more often in intraocular infection than from corneal ulceration. Although favorable response to Amphotericin-B and Primaricin has been reported, the final outcome has been unfavorable in most of these cases.
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PMID:Cephalosporium endophthalmitis following penetrating keratoplasty. 37 Jul 8

The limulus endotoxin assay has been previously demonstrated to be the most sensitive method available for detection of bacterial endotoxin. A commercially available form of limulus amoebocyte lysate was used in this study for detection of Gram-negative corneal infections in both experimental animals and in a group of nine patients. The limulus assay enabled rapid detection of Gram-negative infections in both the experimentally induced ulcers in rabbits and in the patients studied. False-positive reactions did not occur in corneal infections due to either Gram-positive bacteria, fungi, or herpes simplex keratitis. The limulus test proved to be more sensitive than examination of Gram-stained smears of corneal scrapings and became positive earlier than bacterial cultures. The limulus test was helpful in the diagnosis of partially antibiotic-treated corneal infections but could not be used to assess the response to antimicrobial therapy, since endotoxin persisted in the corneal scrapings for some time after initiation of therapy.
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PMID:Limulus lysate assay for early detection of certain Gram-negative corneal infections. 37 85

Laboratory studies show that systemic immunity protects the corneal epithelium against herpes simplex virus (HSV) infection, this protection probably being humoral in origin. It can be shown that hyperimmune gammaglobulin (HGG) has a similar protective action when instilled up to 2 hours after the induction of the ulcerative disease. Topical steroids enhance proliferation of HSV in epithelial disease, but at low dilutions there is some evidence that resistance is enhanced. Human studies of systemic immunity show that there is a response in cell-mediated immunity (CMI) after primary and recurrent ulcerative disease. Certain patients with severe stromal keratitis have evidence of CMI deficiency compared to controls or to patients with epithelial disease. To prevent virus spread into the stroma, early use of antiviral therapy is essential. Stromal disease does not only represent a hypersensitivity phenomenon, but is probably associated with virus proliferation in the keratocytes. Potent steroid medication will theoretically deplete immuno-protective responses, and promote further virus proliferation. Therefore the lowest possible concentrations achieving a clinical response should be employed.
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PMID:Mechanisms of resistance and hypersensitivity in herpes simplex keratitis. 39


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