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)

Clinical resistance of herpetic keratitis to antiviral agents constitutes one of the reasons for failure of treatment after their administration. A retrospective study of 42 cases of superficial herpetic keratitis resistant to IDU, IDU and IDC, and Ara-A demonstrated that in 2 out of 3 cases this resistance appeared in patients previously treated locally with antiviral compounds for anterior ocular lesions. Patients resistant to IDU were then treated with Ara-A, and those not responding to Ara-A, with TFT. Resistance may be observed following this new treatment during the subsequent relapses.
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PMID:[Clinical resistance of herpetic keratitis to antiviral agents (author's transl)]. 626 Aug 50

Only a few agents with antiviral activity are available for routine clinical use. Amantadine hydrochloride is effective in the prophylaxis of influenza A. In addition, accumulated evidence shows that amantadine has some therapeutic effect when used early in the course of an influenza A infection. Idoxuridine and adenine arabinoside have found application as topical agents in the treatment of herpes simplex keratitis. Adenine arabinoside has also been approved for the treatment of disseminated infections due to herpes zoster and herpes simplex. Acyclovir sodium has been approved as a topical agent in the treatment of limited mucocutaneous herpes simplex viral infections in immunosuppressed patients and of initial episodes of genital herpes simplex infections in patients with normal immunity. Ribavirin, an experimental agent with a wide spectrum of activity in vitro, has not fulfilled expectations in clinical trials. Because of the eradication of smallpox, methisazone has become obsolete as a prophylactic agent in smallpox.
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PMID:Antiviral agents. 633 31

The clinical value of five synthetic antiherpetic nucleosides is discussed: iododeoxyuridine (IDU), adenine-arabinoside (Ara-A), trifluorothymidine (TFT), acyclovir (ACV), and bromovinyldeoxyuridine (BVDU). Depending on the type of herpes simplex virus eye disease, either TFT or ACV are currently the drugs of choice. For BVDU, further controlled studies have to be awaited. For the special situation of superficial herpetic keratitis (dendritic keratitis), a combination therapy with either TFT or ACV plus interferon has proven to be significantly better than a monotherapy with only nucleosides.
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PMID:Use of nucleoside analogues in the treatment of herpes simplex virus eye diseases. 668 78

Arabinosyladenine (Ara-A) is an antiviral compound employed for ophthalmological lesions in the form of a 3 p. cent ointment. This purine nucleoside has been shown to possess antiviral activity against several ADN viruses, including herpes simplex virus, but it is ineffective against ARN viruses. Its action in superficial herpetic keratitis is comparable with that of idoxuridine, tolerance to the two compounds being almost identical. Ara-A is of value for treating superficial keratitis lesions not responding to idoxuridine. The weak intra-ocular penetration of Ara-A explains its lack of efficacy in stromal keratitis and herpetic kerato-uveitis, forms in which certain analogues of Ara-A could be beneficial.
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PMID:[Arabinosyladenine in ophthalmology (author's transl)]. 702 53

The relative efficacy of 5-methoxymethyldeoxyuridine (MMUdR), adenine arabinoside (Ara-A), 5-iododeoxyuridine (IUdR) and the combination of MMUdR and Ara-A in the treatment of experimental herpes simplex keratitis was investigated in rabbits. Treatment was initiated either at 4 or 24 h post virus inoculation. The parameter used to evaluate effectiveness was lesion size. Each eye was graded daily for the first 5 days and on alternate days thereafter to day 11. At concentrations of 2 or 5% both MMUdR and Ara-A were found to have potent antikeratitis activity. At 5% concentration, Ara-A provided essentially the same protection against herpes keratitis as 0.1% IUdR, while MMUdR was slightly less effective. The simultaneous application of 2% MMUdR and 2% Ara-A in combination was more effective than 5% MMUdR alone and was effective as 5% Ara-A or 0.1% IUdR in controlling the viral keratitis.
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PMID:Comparative efficacy of 5-methoxymethyl-2'-deoxyuridine, 9 beta-D-arabinofuranosyladenine and 5-iodo-2'-deoxyuridine in the treatment of experimental herpes simplex keratitis. 735 40

Infection with Herpes simplex virus type 1 (HSV-1) typically causes lesions of the mouth, face, skin, esophagus, or brain. Herpes simplex virus type 2 (HSV-2) usually causes infections of the genitals, rectum, skin, hands, or meninges. The herpes viruses are a major cause of blindness from keratitis. The usual drugs used for herpes are Vidarabine, Acyclovir, Penciclovir and Ganciclovir; they are associated with several complications. The aim of this study was to investigate if a formulation containing 2.5 mg melatonin and 100 mg SB-73 would help patients with herpes, and to compare the preparation with 200 mg Acyclovir. SB-73 is a mixture of magnesium, phosphate, fatty acids extracted from Aspergillus sp. which has anti-herpes virus properties. A single blind randomized study was performed in which 70 patients underwent treatment using the supplement cited above (group A) and 75 received treatment of 200 mg Acyclovir (group B). Sixty-seven patients of the group A (95.7%) reported a complete regression of symptoms after 7 days of treatment. By comparison, 64 subjects (85.3%) of the Acyclovir reported regression of symptoms in the same period. There was statiscally significant difference between the groups (P < 0.05).
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PMID:Regression of herpes viral infection symptoms using melatonin and SB-73: comparison with Acyclovir. 1841 May 85

Vidarabine was the first clinically approved antiviral drug, but due to safety and efficacy issues the drug is currently only used topically for herpes virus keratitis. Scientific interest in vidarabine has been recently renewed due to the fact that the compound exhibits beneficial effects in animal models of heart failure and cancer, replicating effects of the knockout of adenylyl cyclase 5 (AC5). Therefore, vidarabine has been suggested to mediate these effects via selective inhibition of AC5. Based on these results, clinical studies with vidarabine in humans for heart failure and cancer have been proposed. Here, evidence is presented that vidarabine is neither a potent nor a selective AC5 inhibitor. Greatest caution should be exerted when proposing new mechanisms of actions and clinical uses for vidarabine.
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PMID:Vidarabine is neither a potent nor a selective AC5 inhibitor. 2439 24


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