Aspirin-exacerbated respiratory disease and some cases of chronic idiopathic urticaria are disorders in which increased baseline urinary excretion of leukotriene(LT)E4 further increases following aspirin administration. Increased urinary excretion of the metabolites of prostaglandin D2, 11β-prostaglandin(PG)F2α and (2,3-dinor)-11β-PGF2α, have been documented in systemic mastocytosis (SM) and in mast cell activation syndrome (MCAS). Symptoms due to increased baseline and/or episodic release of PGD2 can be prevented with aspirin, an inhibitor of cyclooxygenase (COX)1 and COX2. Here by retrospective chart review we discovered 8 of 10 patients with SM in whom normalization of an elevated urinary (2,3-dinor)-11β-PGF2α occurred with aspirin therapy also had a parallel increased excretion of LTE4 by an average of nearly 13-fold. How widespread this phenomenon occurs in SM is unknown; however, this occurrence needs to be considered when interpreting changes in these urinary mast cell mediator metabolites during aspirin therapy.

阿司匹林加重的呼吸系统疾病和一些慢性特发性荨麻疹病例是阿司匹林给药后白三烯 (LT)E4 基线尿排泄增加进一步增加的疾病。前列腺素 D2、11β-前列腺素 (PG)F2α 和 (2,3-dinor)-11β-PGF2α 代谢物的尿排泄增加已在全身性肥大细胞增多症 (SM) 和肥大细胞活化综合征 (MCAS) 中得到证实。使用阿司匹林（一种环氧合酶 (COX)1 和 COX2 的抑制剂）可以预防因基线增加和/或 PGD2 偶尔释放而引起的症状。在此，通过回顾性图表回顾，我们发现 10 名 SM 患者中有 8 名患者在接受阿司匹林治疗后尿 (2,3-dinor)-11β-PGF2α 升高正常化，同时 LTE4 的排泄量平均增加近 13-折叠。这种现象在 SM 中发生的广泛程度是未知的；然而，在解释阿司匹林治疗期间这些尿肥大细胞介质代谢物的变化时，需要考虑这种情况。