Myasthenia gravis after botulinum toxin A for Meige syndrome.
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Biomedical subjects
Publications and source records attributed to G Borodic.
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PURPOSE: To report the clinicopathologic features of a newly recognized tumor, giant cell angiofibroma. DESIGN: Observational case series. MAIN OUTCOME MEASURES: Clinical and histopathologic features of giant cell angiofibroma. METHODS: Light and electron microscopy and immunohistochemistry of five cases of giant cell angiofibroma. RESULTS: A total of five patients (4 women and 1 man) are described: two presented with a painless mass in the eyelid, two with a mass in the orbit, and one presented with a conjunctival lesion. All lesions were well demarcated with no capsule and were composed of blood vessels, a patternless spindle-shaped cell proliferation with a solid and pseudovascular appearance, and multinucleated giant cells. Both spindle-shaped and giant tumor cells were intensely positive for CD34 and vimentin. CONCLUSION: Giant cell angiofibroma resembles solitary fibrous tumor and giant cell fibroblastoma and should be considered in the differential diagnosis of spindle-cell tumors in the eyelid, orbit, and conjunctiva.
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Botulinum toxin is a valuable technology for the treatment of regional movement disease. High-dose applications ( > 100 LD50 units per injection cycle) have been associated with sensitization that renders further therapeutic injections ineffective. The true incidence of sensitization is probably underestimated by the mouse bioassay. Other immunotypes of botulinum toxin have been effective in producing some therapeutic benefit; however, duration of action (botulinum toxin type F) and lower potencies may make these less attractive alternatives than botulinum type A. Increased specific activity botulinum toxin may be a method to reduce antigen exposure and mitigate against immunoresistance associated with dystonia therapy. Limiting the dose to < or = 100 LD50 units per injection cycle may limit this complication in the interim.
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The ophthalmic histopathology is detailed in a case of trisomy 18 (Edwards's syndrome). In addition to the ocular pathology already reported, previously unreported findings of iris stromal hypoplasia, abnormal lens shape, and decreased ganglion cells in the retina are noted. The ophthalmic histopathology associated with this syndrome and the relationship of several genetic disorders to their ocular manifestations are discussed.
Data based on the prospective study of Job et al. are reanalyzed while initial number of microaneurysms and duration of patient follow-up are controlled. The reported statistical difference in the rate of microaneurysm increase between the single- and the multiple-daily-injection groups may be due to a difference in a subgroup who had a larger number of microaneurysms initially and who were studied for a shorter period of time. No uniform difference was observed in the results of their treatment between the groups given a single injection and those given multiple injections. While this does not invalidate the conclusions of the study, it does point out the need for greater control in conducting future studies.