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)

Corneal damage of various origins initiates a series of processes which lead to repair but also tend to perpetuate the damage; healing thus depends on the prevalence of repair over progression processes. The plasminogen/plasmin system has an important impact on this process, particularly by degrading the extracellular matrix components with resulting interference of the repair processes. This paper presents the immunoblotting analysis of fibronectin, tissue and urokinase-type plasminogen activators and plasminogen/plasmin in the tear fluid of control subjects and patients affected by various ocular pathologies (corneal ulcers, thermal or chemical burns, herpetic keratitis). A significant modification was noted in the protein profiles of fibronectin, tissue and urokinase-type plasminogen activators and plasminogen/plasmin in the cases of corneal ulcers and thermal or chemical burns relative to the pattern observed in the control subjects, while in cases of herpetic keratitis, only plasminogen/plasmin showed slight variations. The altered protein patterns gradually normalized during therapeutic treatment and, at remission, coincided with those of the control subjects.
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PMID:Analysis of fibronectin, plasminogen activators and plasminogen in tear fluid as markers of corneal damage and repair. 183 37

A rapid (5- to 10-min), sensitive (detection limit 0.6 IU/L), and moderately specific fluorometric plasmin assay for small volume tear fluid samples was developed. Addition of albumin (up to 0.1% final concentration) to the assay buffer improved the sensitivity of the test so that plasmin activity in healthy controls could be detected. pH in the reaction buffer was 8.0, Michaelis-Menten constant for the substrate, H-D-Val-Leu-Lys.7-amido-4-methyl-coumarin (AMC), was 0.28 mM, and final substrate concentration in the reaction buffer was 1 mM. Intra- and interassay imprecisions were 1.6 and 4.4%, respectively at a plasmin level of 10 IU/L. Tear fluid flow was significantly higher in the patients than in the healthy controls, and this dilatory effect must be considered when using plasmin determination for diagnostic purposes. This effect was counteracted by correcting the plasmin activity values by tear fluid flow. Plasmin flux is plasmin activity (microIU) secreted in units of time (min). This parameter showed highly significant differences between the patients and controls. All patients with microbial keratitis, corrosive trauma, ocular trauma, herpetic infection, and other diseases showed highly significant elevation of plasmin flux compared with controls. The highest plasmin flux values (several hundredfold that of controls) were recorded in patients with severe corneal ulcers. Few patient samples showed some involvement of other proteases, which were not inhibited by aprotinin.
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PMID:A rapid fluorometric assay for tear fluid plasmin activity. 815 87

In an experimentally induced Aspergillus fumigatus fungal keratitis in 20 rabbits, aprotinin, an antiplasmin agent, was studied to find out its role as an adjuvant when given along with other established antifungal agents like natamycin and fluconazole. The 20 rabbits included in this study were randomly divided into four equal treatment groups. Once the ulcer was produced after intrastromal injection of 0.03 ml of A. fumigatus (5.5 x 10(4) spores/ml), different drugs/agents in combination were used in a randomized manner. These were natamycin (5%) + placebo, natamycin + aprotinin (40 IU/ml), fluconazole (0.3%) + placebo and fluconazole + aprotinin. The rabbits were followed up every day to note the signs of healing which included subsidence of corneal infiltration, disappearance of stromal abscess and subsidence of corneal oedema till complete healing. Results showed that the average healing time was 28.2, 28.4, 49.8 and 49.0 days for natamycin + placebo, natamycin + aprotinin, fluconazole + placebo and fluconazole + aprotinin, respectively. It suggests that aprotinin as an adjuvant has no definite role in the management of fungal keratitis. The plasminogen activator-plasmin system which is inhibited by aprotinin may not be the pathway through which filamentous fungi like A. fumigatus cause tissue destruction.
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PMID:Role of aprotinin in the management of experimental fungal keratitis. 1134 Apr 5