The pathology of dysfunctional uterine bleeding.
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.
D001792:Blood Platelets / Q000378:metabolism; D015237:Dinoprost; D015232:Dinoprostone; D004717:Endometrium / Q000473:pathology / Q000503:physiopathology; D005260:Female; D005337:Fibrin / Q000378:metabolism; D005342:Fibrinolysis; D006487:Hemostasis; D006493:Heparin / Q000502:physiology; D006801:Humans; D008407:Mast Cells / Q000378:metabolism / Q000473:pathology; D008595:Menorrhagia / Q000473:pathology; D008598:Menstruation; D011458:Prostaglandins E / Q000502:physiology; D011460:Prostaglandins F / Q000502:physiology
D011458:Prostaglandins E; D011460:Prostaglandins F; D005337:Fibrin; D006493:Heparin; D015237:Dinoprost; D015232:Dinoprostone