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道疾病和某些慢性特发性荨麻疹病例是服用阿司匹林后白三烯 (LT)E4 基线尿排泄量进一步增加的疾病。系统性肥大细胞增多症 (SM) 和肥大细胞活化综合征 (MCAS) 中前列腺素 D2、11β-前列腺素 (PG)F2α 和 (2,3-dinor)-11β-PGF2α 代谢物的尿液排泄增加。阿司匹林（环加氧酶 (COX)1 和 COX2 的抑制剂）可以预防因 PGD2 基线和/或间歇性释放增加而导致的症状。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 排泄量也相应增加，平均增加近 13-折叠。这种现象在 SM 中的普遍程度尚不清楚。然而，在解释阿司匹林治疗期间这些尿肥大细胞介导代谢物的变化时，需要考虑这种情况。