| Abstrakt: |
IN REPLY.— The letter from Dr Krause, regarding the report by Riccardi1 of decreased rate of neurofibroma growth observed during treatment with ketotifen, addresses the fundamental question of ketotifen therapeutic mechanisms in the treatment of neurofibromatosis. Specifically, Dr Krause raises concerns about the evidence that ketotifen can stabilize mast cells in vivo and, hence, the potential for mast-cell blockers to be important in the treatment of neurofibromatosis. Ketotifen has been shown to have several effects on mast cells in vitro. First, ketotifen has antihistamine activity as an H-1 receptor antagonist.2,3 Second, ketotifen can prevent mast-cell degranulation as determined by membrane-triggered histamine release.2,3 Third, ketotifen can prevent calcium flux across the cell membrane.4 Evidence that ketotifen can prevent mast-cell degranulation in vivo is presented in the report by Huston et al5 regarding three patients with physical urticarias.Dr Krause raises a concern regarding the observations of Huston and |
