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)

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

Based on a review of 20 well-documented cases reported in the English literature between 1968 and 2008, herpes zoster ophthalmicus (HZO) may rarely be associated with complete unilateral ophthalmoplegia, defined here as impaired ocular ductions in all 4 directions within 3 months of onset of manifestations of HZO. Ophthalmoplegia occurred equally in immune-competent and immune-incompetent individuals. HZO preceded ophthalmoplegia in 75% by a mean interval of 9.5 days and a range of 2 to 60 days, occurred simultaneously with ophthalmoplegia in 20%, and followed by 2 days the onset of ophthalmoplegia in only 5%. Concurrent conjunctival inflammation, keratitis, or anterior uveitis was present in 90%. Lumbar puncture showed features of aseptic meningitis in 88%, slightly more than the 40%-50% found in patients with HZO without ophthalmoplegia. On orbit/brain imaging, abnormal enlargement of the extraocular muscles was present in 33%, and orbital soft tissue swelling was present in 17%. Enhancement of ocular motor cranial nerves was not reported. Complete or near-complete resolution of ophthalmoplegia occurred in 65% within a range of 2 weeks to 1.5 years (mean 4.4 months). A single autopsy report described granulomatous angiitis of the meninges and large vessels in the anterior cerebral circulation, as well as periaxial infarction in the optic nerve, pons, and medulla but without viral inclusion bodies or antigen. Unsettled issues are whether the pathogenesis is direct viral invasion or an immune reaction to the virus, whether the impaired ocular ductions are based on myopathic or neuropathic injury, whether there are predisposing factors to the combination of HZO and complete ophthalmoplegia, and whether treatment is effective.
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PMID:Complete unilateral ophthalmoplegia in herpes zoster ophthalmicus. 1995 8