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Standard treatment emerges for N. fowleri
Mediated by interleukin-1 (IL-1), beta tumor necrosis factor (beta-TNF), histamine, prostacyclin (PGI2) and other cytokines, the inflammatory reaction causes tissue damage, necrosis and increased permeability of the surrounding vasculature. Severe toxicity can occur with amphotericin B, including in...
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Published in: | Infectious Disease News 2017-04, Vol.30 (4), p.15-15 |
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Main Authors: | , |
Format: | Article |
Language: | English |
Subjects: | |
Online Access: | Get full text |
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Summary: | Mediated by interleukin-1 (IL-1), beta tumor necrosis factor (beta-TNF), histamine, prostacyclin (PGI2) and other cytokines, the inflammatory reaction causes tissue damage, necrosis and increased permeability of the surrounding vasculature. Severe toxicity can occur with amphotericin B, including infusion reaction, nephrotoxicity, nausea, vomiting, changes in blood pressure, hypokalemia and hypomagnesemia. [...]new therapies have been further investigated, early identification, intracranial pressure management, and the combination of antifungals, azithromycin, steroids and miltefosine will continue to be recommended for patient survival. ? |
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ISSN: | 1056-9251 |