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Query: UMLS:C0033377 (prolapse)
 11,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endometrial tissue from uteri of 35 nonpregnant, premenopausal women was assayed for prostaglandin E2 and F2 alpha binding site content as a function of the phase of the menstrual cycle and the pathologic state. For all specimens, tritium-labeled prostaglandin F2 alpha, binding was very low (less than 8 fmol/mg of protein) or undetectable regardless of the phase of the menstrual cycle or pathologic state or in the presence or absence of 10 mumol/L of indomethacin, a prostaglandin synthetase inhibitor. However, tritium-labeled prostaglandin E2 binding was detected in every specimen and was independent of the presence or absence of indomethacin. Binding of tritium-labeled prostaglandin E2, as determined by Scatchard analyses, was biphasic (dissociation constant approximately 1 nmol/L; dissociation constant for low-affinity sites approximately 10 nmol/L) for both proliferative and secretory endometrial tissue. However, the total number of prostaglandin E2 binding sites, determined from Scatchard or single-point analyses, was significantly higher (p less than 0.01) in proliferative endometrium compared to secretory endometrium. In addition, for endometrium from the proliferative phase of the menstrual cycle, the diagnosis of abnormal uterine bleeding was associated with higher (p less than 0.01) tritium-labeled prostaglandin E2 binding than diagnosis of dysmenorrhea, stress urinary incontinence and uterine prolapse, or pelvic inflammatory disease. Endometrial specimens with the last four diagnoses did not differ significantly (p greater than 0.1) from each other.
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PMID:Human endometrial prostaglandin E2 binding sites and their profiles during the menstrual cycle and in pathologic states. 285 25

Circulating prostaglandin metabolites 13,14-dihydro-15-keto-prostaglandin F2 alpha and the bicyclo derivative of prostaglandin E2 were measured in maternal plasma by radioimmunoassay after transabdominal cervicoisthmic cerclage and after transvaginal cerclage (Shirodkar and McDonald procedures) performed in the first and second trimesters. Statistically significant elevations in prostaglandin E2 metabolite or 13,14-dihydro-15-keto-prostaglandin F2 alpha occurred after transabdominal cervicoisthmic and transvaginal cerclage; they returned to control levels within 6 to 24 hours after surgery and were associated with good fetal outcome. Increases in 13,14-dihydro-15-keto-prostaglandin F2 alpha were proportionately greater than in prostaglandin E2 metabolite. Mean basal levels and the rise in prostaglandin metabolites were not related to cerclage type, trimester of pregnancy, or cervical status (dilatation less than or equal to 3 cm; effacement less than or equal to 60%). Highest basal and postcerclage 13,14-dihydro-15-keto-prostaglandin F2 alpha and prostaglandin E2 metabolite levels were associated with advanced cervical changes, uterine irritability, membrane prolapse or rupture, and premature delivery. Routine administration of prostaglandin synthetase inhibitors is not indicated for transvaginal cerclage or transabdominal cervicoisthmic cerclage; plasma prostaglandin metabolite levels may identify patients not suitable for cerclage.
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PMID:Plasma concentrations of prostaglandin F2 alpha and prostaglandin E2 metabolites after transabdominal and transvaginal cervical cerclage. 347 37