Sheppard B L
Clin Obstet Gynaecol. 1984 Apr;11(1):227-36.
The mechanism of dysfunctional uterine bleeding remains unknown. Recent studies suggest that the majority of cases of dysfunctional uterine bleeding are due to local endometrial, or myometrial, dysfunction. Changes in the pattern of production of prostaglandins PGE2, PGF2 alpha, prostacyclin and thromboxane and increased fibrinolytic activity in the endometrium have been implicated in this disorder. Successful treatment of excessive menstrual bleeding with the prostaglandin synthetase inhibitor mefenamic acid and the fibrinolytic inhibitors epsilon amino caproic acid and tranexamic acid further substantiates the role of prostaglandins and fibrinolysis in pathological menstruation. The relationship between uterine mast cells, heparin-like activity and menstrual bleeding still needs to be elucidated. Further studies are required to improve our understanding of the pathogenesis of dysfunctional uterine bleeding, so that advances can be made in a specific treatment to restore normal menstrual function.
功能失调性子宫出血的机制尚不清楚。最近的研究表明，大多数功能失调性子宫出血病例是由于局部子宫内膜或肌层功能障碍所致。前列腺素PGE2、PGF2α、前列环素和血栓素生成模式的改变以及子宫内膜中纤维蛋白溶解活性的增加与这种疾病有关。用前列腺素合成酶抑制剂甲芬那酸以及纤维蛋白溶解抑制剂ε-氨基己酸和氨甲环酸成功治疗月经过多进一步证实了前列腺素和纤维蛋白溶解在病理性月经中的作用。子宫肥大细胞、类肝素活性与月经出血之间的关系仍有待阐明。需要进一步研究以增进我们对功能失调性子宫出血发病机制的理解，从而在恢复正常月经功能的特异性治疗方面取得进展。
