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In 1922, Widal et al. were the first to describe intolerance reactions to acetylsalicylic acid (ASA, e.g. in aspirin) and to other nonsteroidal anti-inflammatory drugs (NSAIDs). The full clinical picture reveals a classic triad of symptoms (Samters Triad): aspirin induced bronchial asthma (with severe acute asthma attacks), aspirin-sensitivity and chronic rhinosinusitis with nasal polyps. In many cases, nasal polyps reveal as the first symptom of ASA sensitivity indicating that the upper airways are predominantly involved in the pathogenetic process. Therefor, emphasis of this article mainly focuses on the upper airways in ASA-intolerant patients. In the last decade, clear evidence has been pointed out that ASA-intolerance is related to the abnormal metabolism of arachidonic acid leading towards excessive leukotriene (LTs) production. The resulting dysbalance of the eicosanoids leukotrien and prostaglandine might be the crucial pathophysiologic keypoint of the disease. The incidence of aspirin hypersensitivity in the general population ranges from 0.6 % to 2.5% and in adult astmatics from 4,3 % to 11%. Besides the patients history, challenge tests with Lysin-aspirin are performed as the diagnostic tool of choice. Apart from surgical or pharmacological therapy, ASA desensitization therapy is the only specific treatment of choice. As first described by Stevensson et al. in the early 1984, oral administration by means of an initial desensitization with gradually ascending doses of aspirin is followed by a daily maintenance-dose. In the last years, many publications on various desensitization protocols and routes of administration have been worked out. Recently, the intravenous route for the inititial increment desensitization has been described which might offer new therapeutical possibilities in the treatment of ASA-intolerant patients.
 Vitamin D (VD) and its different analogues, besides their classic role as regulators of calcium and phosphor homeostasis, have emerged as a large family of antiproliferative agents. Such properties suggested VD potential as a therapy for chronic inflammatory diseases, including nasal polyposis (NP). NP growth involves both an inflammatory process and the proliferation of fibroblast as an important factor inducing aberrations in the phenotype of the epithelium. The aim of this study was to investigate the possible influence of 1α,25-dihydroxyvitamin D3 (calcitriol) and 1α,24(R)-dihydroxyvitamin D3 (tacalcitol) in monotherapy and in combination with budesonid R (BR) on NP fibroblast proliferation. Material and methods: The study involved 26 samples of NP. NP cells were cultured on 96-well plates beginning with a concentration of 5 × 103 cells per well with RPMI 1640 medium supplemented with antibiotics and 10% foetal bovine serum. After the fourth to sixth passage the medium was replaced with a nutrient medium with calcitriol or tacalcitol in a defined concentration (from 10-9 M to 10-3 M) alone or in combination with BR in 1:1, 1:3 or 3:1 ratios, each at concentrations from 10-5 M to 10-3 M. Results: Growth inhibition of nasal fibroblasts exposed to calcitriol or tacalcitol was noted. Significant antiproliferating activity was observed at calcitriol concentrations of 10-4 M and 10-3 M after 48 h, and at a concentration of 10-3 M after 72 h with the percentage of proliferating cells reduced to 30% compared to the control samples (P < 0.05). In cells treated with tacalcitol the maximal effect was seen at 10-4 M after 48 h and at 10-3 M after 72 h with a 60% inhibition with respect to the control (P < 0.05). The inhibition of fibroblast proliferation reached the maximal level when they were exposed to calcitriol: BR (1 : 1) or tacalcitol: BR (1 : 1), each at a concentration of 10-4 M, after 72 h (82% and 69%, respectively). Conclusions: The antiproliferative activity of calcitriol and tacalcitol in NP cultures was confirmed. Because of its lower toxicity and higher activity tacalcitol seems to be the more promising agent in NP therapy, both as a single medication and in treatment protocols with BR.
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