dinoprost and Menorrhagia

Topics: Diagnosis, Differential; Dinoprost; Dysmenorrhea; Estrogens; Female; Hemorrhagic Disorders; Humans; Menorrhagia; Polycystic Ovary Syndrome; Prognosis; Uterine Diseases; Uterus; Vitamin B 6 Deficiency

Topics: Anovulation; Arachidonic Acid; Dinoprost; Dysmenorrhea; Endometriosis; Female; Humans; Intrauterine Devices; Menorrhagia; Menstruation Disturbances; Premenstrual Syndrome; Prostaglandin Antagonists; Prostaglandins; Uterine Contraction

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.

Topics: Blood Platelets; Dinoprost; Dinoprostone; Endometrium; Female; Fibrin; Fibrinolysis; Hemostasis; Heparin; Humans; Mast Cells; Menorrhagia; Menstruation; Prostaglandins E; Prostaglandins F

Despite a key role in the pathogenesis of menorrhagia, the factors controlling the uterine vascular bed are poorly understood. This study has assessed the effects of the potent vasoconstrictor endothelin (ET)-1 on prostaglandin (PG) release from human endometrial explants in short-term culture. There was no significant difference between the production of PGF2 alpha in proliferative and secretory tissue (1709 and 2434 pg/mg/h--median values, range 70,3745 and 219,6700 pg/mg/h). Less PGE was released than PGF2 alpha, and the amount did not vary with the phase of the menstrual cycle (308 and 296 pg/mg/h (range 65,387 and 105,429) for proliferative and secretory tissue). ET-1 (10 and 100 nM) and arachidonic acid (AA, 30 microM), stimulated PGF2 alpha release from proliferative, but not secretory endometrium, by 78%, 86% (P less than 0.01) and 80% respectively, compared with control tissue. No effect was seen on PGE release. ET-1 may play a role in the local control of the endometrial vascular bed either directly, or via the release of PGF2 alpha.

Topics: Adult; Culture Techniques; Dinoprost; Endometrium; Endothelins; Female; Humans; Menorrhagia; Menstrual Cycle

Dysfunctional uterine bleeding is defined as abnormal uterine bleeding in the absence of organic disease. It is the result of anovulation or the abnormal local production of prostaglandins, and in each case the primary fault is inappropriate hormone formation. There are two approaches to diagnosis. The traditional one is primarily concerned with the exclusion of cancer of the endometrium; this concern results in the frequent resort to uterine curettage. The second approach is to limit curettage to patients whose symptoms are not ameliorated by medical therapy. The aim of medical treatment is either to produce secretory change in the endometrium or to decrease the formation of uterine prostaglandins. Intermittent progesterone treatment is used to cause secretory changes in the endometrium. Decreased production of the prostaglandins is achieved indirectly by causing atrophy of the endometrium or directly through the use of prostaglandin synthetase inhibitors. Surgery in the form of dilatation and curettage has no long-term therapeutic effect; hysterectomy is definitive therapy.. Dysfunctional uterine bleeding is defined as abnormal uterine bleeding in the absence of organic disease. It is the result of anovulation or the abnormal local production of prostaglandins (PGs), and in each case, the primary fault is inappropriate hormone formation. There are 2 approaches to diagnosis. The traditional one is primarily concerned with the exclusion of cancer of the endometrium; this concern results in the frequent resort to uterine curettage. The 2nd approach is to limit curettage to patients whose symptoms are not ameliorated by medical therapy. The aim of the medical treatment is either to produce secretory change in the endometrium or to decrease the formation of uterine PGs. Intermittent progesterone treatment is used to cause secretory changes in the endometrium. Decreased production of the PGs is achieved indirectly by causing strophy of the endometrium or directly through the use of PG synthetase inhibitors. Surgery in the form of dilatation and curettage has no longterm therapeutic effect; hysterectomy is definitive therapy. (author's)

Topics: Adult; Contraceptives, Oral; Cyclooxygenase Inhibitors; Dilatation and Curettage; Dinoprost; Dinoprostone; Emergencies; Estrogens, Conjugated (USP); Female; Humans; Hysterectomy; Medroxyprogesterone; Medroxyprogesterone Acetate; Mefenamic Acid; Menorrhagia; Norethindrone; Progesterone; Prostaglandins E; Prostaglandins F

In this study we have obtained endometrium and myometrium from women whose menstrual blood loss had been measured objectively. Samples of tissue were snap frozen in liquid nitrogen for the estimation of PG content and tissue was homogenized and incubated with and without added arachidonic acid. PGE, PGF2 alpha and 6-oxo PGF1 alpha were measured by gas chromatography - mass spectometry. We confirm that the F2 alpha/E2 ratio in the snap frozen samples was significantly lower in women with a high blood loss although this was not reflected in the production by incubated homogenates. Incubation of endometrial tissue with myometrium from the same patient and with a pool of myometrium showed that the source of myometrium was not important. This suggests that previous observations of increased 6 oxo F1 alpha production in incubations of endometrium and homologous myometrium from women with high MBL, resulted from differences in endometrium. When prostaglandin E and F production by endometrium is studied there is a significant inverse correlation between the percentage difference in production with and without added arachidonic acid and menstrual blood loss which suggests that women with high MBL have relatively high levels of available arachidonic acid in their endometrium.

Topics: Arachidonic Acid; Arachidonic Acids; Dinoprost; Dinoprostone; Endometrium; Female; Humans; Menorrhagia; Menstruation; Myometrium; Prostaglandins; Prostaglandins E; Prostaglandins F

Menstrual fluid was collected in vaginal cups inserted for 2 h during the first 2 days of menstruation and menstrual serum concentrations of prostaglandins PGF2 alpha and PGE2 were measured by radioimmunoassay. In 16 women from whom menstrual fluid was collected on both days, PGF2 alpha and PGE2 concentrations were significantly higher on day 1 than on day 2. The highest concentrations of PGF2 alpha and PGE2 were found in dysmenorrhoeic women on day 1. In non-dysmenorrhoeic women, the amount of PGF2 alpha and PGE2 collected in 2 h correlated directly with total menstrual blood loss. There was no statistically significant difference in the amount of prostaglandins collected in 2 h in pain-free menorrhagic women and dysmenorrhoeic women with normal loss. There was also no significant 9-ketoreductase or 9-hydroxydehydrogenase activity present in menstrual fluid which could suggest PGE2 to PGF2 alpha interconversion.

Topics: Adult; Dinoprost; Dinoprostone; Dysmenorrhea; Female; Humans; Menorrhagia; Menstruation; Middle Aged; Prostaglandins E; Prostaglandins F

The pattern of prostaglandins (PGs) synthesized by persistent proliferative endometrium of women with excessive menstrual bleeding (greater than 50 ml) associated with anovulatory cycles was compared to endometrium collected from women with normal menstrual blood loss (less than 50 ml). Levels of PGF2 alpha in normal and persistent proliferative endometrium were lower than the levels of PGF2 alpha found in normal secretory endometrium (P less than 0.005 for both normal and persistent proliferative endometria). When incubated with exogenous [1-14C]arachidonic acid (9.1 nmol), normal secretory endometrium synthesized more PGF2 alpha and PGE2 than did normal proliferative endometrium, but the amounts of PGF2 alpha and PGE2 released by persistent proliferative endometrium were similar to those obtained by normal secretory endometrium. These findings suggest that persistent proliferative and normal secretory endometria have the same PG synthetase activity, and that the low endogenous concentrations of PGF2 alpha in the former arise from a lack of endogenous precursor. PGF2 alpha has predominantly vasoconstricting properties, and a reduced capacity to synthesize this PG by persistent proliferative endometrium may result in excessive menstrual bleeding, as was suggested by the inverse correlation between the ratio of the endogenous concentrations of PGF2 alpha and PGE and the menstrual blood loss (r = -0.7; P less than 0.005; n = 26).

Topics: Adult; Arachidonic Acid; Arachidonic Acids; Dinoprost; Endometrium; Female; Humans; Menorrhagia; Prostaglandins; Prostaglandins E; Prostaglandins F