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1.
Ginecol Obstet Mex ; 65: 300-4, 1997 Jul.
Artigo em Espanhol | MEDLINE | ID: mdl-9312519

RESUMO

The preeclampsia-eclampsia syndrome is a vasospastic disorder and probably has a placental origin. Once the hypertensive syndrome is established the uteroplacental blood flow is reduced as well as the intervillous blood flow. Since 18-24 weeks of gestation and before the symptoms of preeclampsia become overt, changes in placental flow velocity can be detected with Doppler technics. The placental theories for the etiology of preeclampsia are focused on the hypoxic effect in the trophoblastic tissue of second trimester. The placental ischemic changes are evident and seen in the uteroplacental bed. They are interrelated with the stages of trophoblastic invasion of the spiral arteries during the 14 and 20 weeks. When the trophoblastic invasion is over, the spiral arteries become a high resistance system. The defect observed in preeclampsia is the lack of invasion of the trophoblast to the maternal arteries. The diminished placental perfusion probably creates endothelial damage. This damage has several effects: decreased prostaglandin production, activated coagulation cascade, stimulated fibrin aggregation, and increased vascular permeability. The ideal laboratory test for preeclampsia shall predict the onset of this entity. Recent findings seem promising. The fibronectin concentration increases 2-3 wks. prior to the clinical manifestation of preeclampsia. Severe hypertension shows an abnormal decrease in fibronectin levels. Hypocalciuria has been described as an early predictor in the development of preeclampsia. Other agents undergoing extensive evaluation as predictors are: uric acid, b-thromboglobin, prolactin and atrial natriuretic peptide. Recently high levels of b-HCG (human corionic gonadotrophin) have been linked to a lack of trophoblastic invasion during the second trimester, therefore this is a potential marker for those patients that will eventually develop preeclampsia.


Assuntos
Eclampsia/etiologia , Pré-Eclâmpsia/etiologia , Adulto , Cálcio/urina , Permeabilidade Capilar , Gonadotropina Coriônica/análise , Eclampsia/diagnóstico , Feminino , Humanos , Hipertensão/complicações , Pré-Eclâmpsia/diagnóstico , Valor Preditivo dos Testes , Gravidez , Segundo Trimestre da Gravidez , Prognóstico , Síndrome , Trofoblastos/metabolismo , Ácido Úrico/análise
2.
Ginecol Obstet Mex ; 65: 258-61, 1997 Jun.
Artigo em Espanhol | MEDLINE | ID: mdl-9273338

RESUMO

Uterine arteriovenous malformation (AVMs) are fairly rare. Seventy four cases have been reported in the medical literature. The clinical presentation of this entity is quite diverse. The approach to uterine AVM requires clinical alertness and to make the diagnosis a high index of suspicion is required. Prompt treatment is often essential. This article reviews the entire literature on uterine AVM emphasizing the various clinica presentations and treatment modalities available for the gynecologist.


Assuntos
Malformações Arteriovenosas/etiologia , Embolização Terapêutica , Doenças Uterinas/etiologia , Adolescente , Adulto , Idoso , Malformações Arteriovenosas/diagnóstico , Malformações Arteriovenosas/terapia , Feminino , Humanos , Pessoa de Meia-Idade , Útero/irrigação sanguínea
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