J Gosepath1, D Schäfer, W J Mann. 1. Universitäts-HNO-Klinik Mainz, Germany. gosepath@hno.klinik.uni-mainz.de
Abstract
BACKGROUND: The full clinical picture of aspirin intolerance, Sampter's triad, is associated with nasal polyposis, clinical sensitivity to most non steroidal antiinflammatory drugs (NSAID) and intrinsic bronchial asthma. But the triad can be incomplete and nasal polyposis can be the first clinical symptom of aspirin sensitivity. Although the exact mechanisms of aspirin intolerance as well as those of desensitization remain obscure, an in vitro assay on eicosanoid metabolism has been proven to be helpful in diagnosis and treatment as it correlates well to the individual severity of clinical symptoms. METHODS: For this investigation 30 patients, who were undergoing adaptive desensitization for aspirin intolerance, were followed-up between 1 and 3 years. They received a maintenance dose of oral aspirin of only 100 mg a day after an initial application of higher doses. Their clinical course as well as their in vitro parameters of eicosanoid release were monitored throughout the individual observation period. RESULTS: Desensitization was successful in 25 of the 30 patients regarding the recurrence rate of nasal polyps, severity of bronchial asthma and sense of smell. There was a clear positive correlation between clinical and in vitro parameters. Discontinuing of aspirin therapy lead to worsening of clinical symptoms, regardless of the prior duration of treatment. CONCLUSIONS: This article reviews the role of the in vitro assay and presents a desensitization protocol that can be maintained as a long term treatment without adverse side effects. Results suggest that the recurrence rate of nasal polyps after surgical therapy can be reduced using this protocol, however, only long term treatment can secure a beneficial outcome over time.
BACKGROUND: The full clinical picture of aspirin intolerance, Sampter's triad, is associated with nasal polyposis, clinical sensitivity to most non steroidal antiinflammatory drugs (NSAID) and intrinsic bronchial asthma. But the triad can be incomplete and nasal polyposis can be the first clinical symptom of aspirin sensitivity. Although the exact mechanisms of aspirin intolerance as well as those of desensitization remain obscure, an in vitro assay on eicosanoid metabolism has been proven to be helpful in diagnosis and treatment as it correlates well to the individual severity of clinical symptoms. METHODS: For this investigation 30 patients, who were undergoing adaptive desensitization for aspirin intolerance, were followed-up between 1 and 3 years. They received a maintenance dose of oral aspirin of only 100 mg a day after an initial application of higher doses. Their clinical course as well as their in vitro parameters of eicosanoid release were monitored throughout the individual observation period. RESULTS: Desensitization was successful in 25 of the 30 patients regarding the recurrence rate of nasal polyps, severity of bronchial asthma and sense of smell. There was a clear positive correlation between clinical and in vitro parameters. Discontinuing of aspirin therapy lead to worsening of clinical symptoms, regardless of the prior duration of treatment. CONCLUSIONS: This article reviews the role of the in vitro assay and presents a desensitization protocol that can be maintained as a long term treatment without adverse side effects. Results suggest that the recurrence rate of nasal polyps after surgical therapy can be reduced using this protocol, however, only long term treatment can secure a beneficial outcome over time.