Placental prostanoid release in severe intra-uterine growth retardation

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Citations from the literature/International

Journal of Gynecology & Obstetrics 53 (19%) 205-214

Pf8eentd prontamid releese in severe intra-ateriw growth Sorem K.A.; Siler-Khodr T.M. USA PLACENTA 1995 16/6 (503-515) Our objective was to evaluate prostanoid release from the placentae of pregnancies complicated by severe intra-uterine growth retardation (IUGR) and without hypertension, compared with placentae from normal, uncomplicated term pregnancies.A perifusion systemwas utilized to study the releaseof prostanoids 6-keto-prostaglandin F(la) (bketo-PGF(la)), thromboxane B2(TxB2), prostaglandin E2 (PGE,) and prostaglandin F(h) (PGF(2o)) from human placentae from pregnanciescomplicated by normotensive severeIUGR (n = 9, five at term and four preterm) and normal control pregnancies (n = 6). For each placenta, triplicate chambers of tissue mere perifused at a rate of 6 ml/h, and samples were collected from hours 5- 10.Prostanoids were measuredusing specific and sensitive radioimmunoassays. In the IUGR group, the basal placental production of the vasoconstrictor thromboxane was not increased nor was the ratio of cumulative TxBz to 6-ketoPGF(la) elevated compared with normal term controls. In three term IUGR placentae, the ratio was significantly decreased compared with controls. The basal placental production of the vasoconstrictor PGF(2a) was likewise not increased compared with controls, nor was the ratio of PGF(2a) to PGE2 elevated. Two of the placentae in the term IUGR group demonstrated significant elevations of PGEz and 6-ketoPGF(la). Overall, the IUGR placentae releasednormal or low normal levels of the prostanoids studied. The pattern of placental prostanoid releaseover time was similar to that of the normal term placentae. The term and preterm placentae of pregnanciescomplicated by severeIUGR did not exhibit an excess production of vasoconstrictor prostanoids. Therefore, strategiesdesignedto reducethromboxane production in severe IUGR without hypertension may be unjustified. llta pheeatd cmticotropbibreknsing bormow-adrenocortic~ W-d Challis J.R.G.; Matthews S.G.; Van Meir C.; Ramirez M.M. CAN PLACENTA 1995 16/6 (481-502) In this review the factors regulating production of corticotrophin-releasing hormone (CRH) in intra-uterine tissuesare discussedand interactions of placental CRH with placental pro-opiomelanocortin (PGMC~adrenocorticotrophin (ACT’H) and prostaglandins (PG) are examined. Discrepant results concerning localization of immunoreactive (IR-) CRH and its binding protein (CRH-BP) and their mRNAs in intrauterine tissues are described, and these issues require further resolution. It is suggestedthat the CRH-ACTH-PG axis in the placenta and choriodecidua may be important in relation to paracrine/autocrine regulation of uterop!acental blood flow, and in term and preterm labour. During the initial stages of preterm labour in the sewing of infection, intrauterine cytokines and other factors may stimulate CRH output, implying a role for the immune-neuroendccrine axes in this process. With loss of chronic trophoblasts in advanced infection leading

to preterm labour, a major intra-uterine site of CRH production may be lost and the influence of this pathway becomes minimal. At this time increasedintra-uterine prostaglandin synthesis,together with loss of prostaglandin dehydrogenaseactivity in the fetal membranes, may become the primary route leading to myometrial activity and delivery.

ONCOLOGY Breast and ovdaa eaaeer incidenceafter infertility end in vitro fertib.ation Venn A.; Watson L.; Lumley J.; Giles G.; Ring C.; Healy D. AUS

LANCET 1995346/8981(995-1800) Concern has been expressedthat exposure to fertility drugs might be associated with a risk of ovarian cancer. We have examined the incidence of breast and ovarian cancer in a cohort of 10358 women referred for in-vitro fertilization (IVF) treatment in Victoria, Australia, between 1978and 1992.The ‘exposed’ group (n = 5564)had had ovarian stimulation to induce multiple folliculogenesis and the ‘unexposed’ group (n = 4794) had been referred for IVF but were untreated or had had ‘natural cycle’ treatment without ovarian stimulation. Duration of follow-up ranged from 1 to 15 years. Cases of cancer were determined by record linkage with data from population-based cancer registries. Thirty-six casesof invasive breast cancer and 6 of invasive ovarian cancer were observed. A comparison with the expected numbers, derived by applying age-standardized general population rates to the cohort gave standardized incidence ratios (SIR) for breast cancer of 0.89 (95% C.I. 0.55-1.46) in the exposed group and 0.98 (0.62-1.56) in the unexposed group, and for ovarian cancer SIRS were 1.70 (0.55-5.27) and 1.62 (0.52-5.02), respectively. Rates of all cancerswere not significantly different from general population rates. The relative risk (RR) of cancer, adjusted for age and infertility type, was, in the treated group compared with the untreated group, 1.11(95% C.I. 0.56-2.20) for breast cancer and 1.45(0.28-7.55) for ovarian cancer. The risk of body of uterus cancer was increased in the exposed and unexposed groups combined (SIR 2.84 (1.18-6.81)). Women with unexplained infertility, independent of IVF exposure, had significantly increasedrisks of ovarian cancer (RR = 19.19(2.23-165.0)) and body of uterus cancer (RR = 6.34 (1.06-38.0)) compared with women with known causesof infertility. This relatively shortterm follow-up suggeststhat ovarian stimulation with IVF is not associated with an increased risk of breast cancer. Although there was no significantly increased risk of ovarian cancer after ovarian stimulation with IVF, the small number of cases limits the conclusions that can be drawn. Longer-term follow-up of large cohorts of women who have been in IVF programs will be necessary. andysis of l-integrins in cervical cancer Immuoohiat~ Valea F.A.; Haskill S.; Moore D.H.; Fowler WC. Jr. USA AM J OBSTET GYNECOL 1995 173/3I (808-813) Objective: The purpose of this study was to determine and