Гемостатические, эндотелиальные и липопротеиновые параметры и кровяное давление выравниваются в женщинах с историей преэклампсии, страница 14

TI: [Tumor necrosis factor and pre-eclampsia]

[ Фактор некроза Опухоли и преэклампсия]

AU: Zhan-C; You-S; Li-S

SO: Chung-Hua-Fu-Chan-Ko-Tsa-Chih. 1997 Jan; 32(1): 52-4

CP: CHINA

MESH: Pre-Eclampsia-etiology; PregnancyMESH: *Pre-Eclampsia-metabolism; *Tumor-Necrosis-Factor-metabolism

TI: Cushing's syndrome in pregnancy secondary to adrenal adenoma. A case report and literature review.

: Синдром Кушинга в беременности, вторичной к надпочечной аденоме. История болезни и литературный обзор.

AU: Lo-KW; Lau-TK

AD: Department of Obstetrics and Gynaecology, Chinese University of Hong Kong, Prince of Wales Hospital, Shatin. wklo@cuhk.edu.hk

SO: Gynecol-Obstet-Invest. 1998; 45(3): 209-12

CP: SWITZERLAND

AB: We describe a case of Cushing's syndrome complicating pregnancy presented with acute heart failure, hypertension and glucose intolerance. A left adrenal adenoma was removed at 24 weeks of gestation. The pregnancy was ended with an emergency lower-segment Caesarean section at 31 weeks of gestation because of severe pre-eclampsia and HELLP syndrome. The case is reported not only because of its rarity but also to induce the discussion of surgical treatment during pregnancy.

: Мы описываем случай синдрома Кушинга, усложняющего беременность, представленную(доставленную,обеспеченную) острой сердечной недостаточностью, артериальной гипертензией и отсутствием толерантности глюкозы. Левая надпочечная аденома была удалена в 24 недели беременности. Беременность завершалась с чрезвычайной секцией Монархиста более низкого сегмента в 31 неделю беременности из-за тяжелой преэклампсии и hellp синдрома. Случай сообщен не только из-за его редкости но также и стимулировать обсуждение хирургической обработки(лечения) в течение беременности.

TI: Oxygen and placental villous development: origins of fetal hypoxia. : Кислород и плацентарное ворсинчатое развитие: происхождение эмбриональной гипоксии.

AU: Kingdom-JC; Kaufmann-P

AD: Department of Obstetrics and Gynaecology, University College London Medical School, UK.

SO: Placenta. 1997 Nov; 18(8): 613-21; discussion 623-6

CP: ENGLAND

AB: The increasing practice of preterm delivery in the fetal interest for conditions such as pre-eclampsia or intrauterine growth restriction (IUGR) has provided an opportunity to study placental structure in pregnancies with prenatal evidence of fetal compromise. These data suggest that the origin of fetal hypoxia in IUGR with absent end-diastolic flow in the umbilical arteries is due to a failure of oxygen transport from intervillous space to umbilical vein. Failure of the fetoplacental circulation to extract oxygen from the intervillous space under such circumstances means intervillous PO2 is closer to maternal arterial values than under physiological conditions. Correspondingly the placental villi are chronically exposed to a higher oxygen tension than under normal circumstances--the term `hyperoxia', relative to normal intraplacental oxygenation, is proposed to describe this situation. Both the trophoblast and villous core react to increased oxygen despite fetal hypoxia. These results challenge the generally accepted concept of `placental hypoxia' in all circumstances where fetal hypoxia might arise. Therefore three categories are proposed for the origins of fetal hypoxia: (1) preplacental hypoxia; (2) uteroplacental hypoxia; and (3) postplacental hypoxia. Examples for these three disease states are listed in this review and the structural reaction patterns of placental villi to these differences in oxygenation are discussed.