Clinical Observations on Some Aspects of Hydatidiform Moles

Chun, Deborah M.; Braga, C.; Chow, C.; Lok, L.

doi:10.1111/j.1471-0528.1964.tb04263.x

Cited by 83 publications

(18 citation statements)

References 12 publications

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“…A fetus is not required, because preeclampsia occurs with hydatidiform mole, 29 and preeclampsia is also reported for pregnancy implanted outside the uterus. 30 The syndrome resolves after delivery or attrition of the placenta.…”

Section: Role Of the Placentamentioning

confidence: 99%

Redefining Preeclampsia Using Placenta-Derived Biomarkers

et al. 2013

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Section: Role Of the Placentamentioning

confidence: 99%

Redefining Preeclampsia Using Placenta-Derived Biomarkers

et al. 2013

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“…The accumulated evidence strongly suggests that the causative agent is the placenta (2,3). For example, preeclampsia can occur in hydatidiform mole (4), where no fetus is present.…”

Section: Introductionmentioning

confidence: 99%

Preeclampsia is associated with abnormal expression of adhesion molecules by invasive cytotrophoblasts.

Zhou

Damsky²,

Chiu³

et al. 1993

J. Clin. Invest.

521

250

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In normal human pregnancy, invasion of the uterus and its arterial system by cytotrophoblasts extends through the entire decidua and the adjacent third of the myometrium. Our previous work showed that during the first trimester of pregnancy, invasion is accompanied by a marked change in the expression of cell adhesion molecules by invasive cytotrophoblasts. In the pregnancy disorder preeclampsia, cytotrophoblast invasion is limited to the superficial decidua, and few arterioles are breached. The purpose of this study was to determine whether cytotrophoblast expression of adhesion molecules in this disorder is also abnormal. Placental bed biopsy specimens from normal pregnancies and those complicated by preeclampsia were stained with anti-integrin antibodies. The results showed that adhesion molecule switching by invasive cytotrophoblasts is abnormal in preeclampsia, which suggests that this subpopulation of trophoblast cells fails to differentiate properly. A likely result is that the delicate balance of adhesive interactions that normally permit cytotrophoblast invasion is tipped in favor of those which restrain this process, with the net effect of shallow uterine invasion. (J. Clin. Invest. 1993. 91:950-960.)

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“…The condition appears to originate in the placenta ( 1 ), as the disorder is always cured by emptying the uterus, and it may also develop without a fetus, as with hydatidiform mole (2).…”

Section: Introductionmentioning

confidence: 99%

Pre-eclampsia is associated with an increase in trophoblast glycogen content and glycogen synthase activity, similar to that found in hydatidiform moles.

Arkwright¹,

Rademacher²,

Dwek³

et al. 1993

J. Clin. Invest.

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Pre-eclampsia is a placental disorder, but until now, biochemical details of dysfunction have been lacking. During an analysis ofthe oligosaccharide content ofsyncytiotrophoblast microvesicles purified from the placental chorionic villi of 10 primigravid women with proteinuric pre-eclampsia, we found an excess of glycogen breakdown products. Further investigation revealed a 10-fold increase in glycogen content (223±117 ,tg glycogen/ mg protein), when compared with controls matched for gestational age at delivery (23±18 ,ag glycogen/mg protein) (P < 0.01). This was confirmed by examination of electron micrographs of chorionic villous tissue stained for glycogen. The increase in glycogen content was associated with 16 times more glycogen synthase (1,323±1,013 relative to 83±96 pmol glucose/mg protein per min) (P < 0.001), and a threefold increase in glycogen phosphorylase activity (2,280±1,360 relative to 700±540 pmol glucose/ mg protein per min; P < 0.05).Similar changes in glycogen metabolism were found in trophoblast microvesicles derived from hydatidiform moles. Glycogen accumulation in villous syncytiotrophoblast may be a metabolic marker of immaturity of this cell which is unable to divide. The implications of these findings with regard to the pathogenesis of pre-eclampsia are discussed. (J. Clin. Invest.

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Clinical Observations on Some Aspects of Hydatidiform Moles

Cited by 83 publications

References 12 publications

Redefining Preeclampsia Using Placenta-Derived Biomarkers

Redefining Preeclampsia Using Placenta-Derived Biomarkers

Preeclampsia is associated with abnormal expression of adhesion molecules by invasive cytotrophoblasts.

Pre-eclampsia is associated with an increase in trophoblast glycogen content and glycogen synthase activity, similar to that found in hydatidiform moles.

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