International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics · 2013
Optimal treatment of hypothyroidism associated with live birth in cases of previous recurrent placental abruption and stillbirth.
Клинический случайСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Vanes Neil K, Charlesworth Dorreh, Imtiaz Rabia, Cox Philip, Kilby Mark D, Chan Shiao Y
Аннотация
OBJECTIVE: To examine the clinical management of and placentas from pregnant women with hypothyroidism and obstetric history of recurrent stillbirth in order to identify possible etiologic mechanisms.
METHODS: Two cases involving 26-year-old women with hypothyroidism and history of recurrent stillbirth are reported. Placentas from all of the women's pregnancies were compared in order to identify histologic similarities.
RESULTS: In both cases, multifocal hemorrhagic infarctions and abruptions were seen, indicating progressive uteroplacental ischemic damage leading to stillbirth. Thrombophilia, infection, and diabetes tests were all negative. With meticulous monitoring and normalization of thyroid function by end of first/early second trimester in subsequent pregnancies, there were live births and no evidence of infarction on placental histology.
CONCLUSION: The 2 reported cases raise the possibility of uteroplacental ischemia and placental abruption being mechanisms by which hypothyroidism can lead to stillbirth; they also highlight the potential of minimizing this risk via adequate levothyroxine treatment from early pregnancy.
METHODS: Two cases involving 26-year-old women with hypothyroidism and history of recurrent stillbirth are reported. Placentas from all of the women's pregnancies were compared in order to identify histologic similarities.
RESULTS: In both cases, multifocal hemorrhagic infarctions and abruptions were seen, indicating progressive uteroplacental ischemic damage leading to stillbirth. Thrombophilia, infection, and diabetes tests were all negative. With meticulous monitoring and normalization of thyroid function by end of first/early second trimester in subsequent pregnancies, there were live births and no evidence of infarction on placental histology.
CONCLUSION: The 2 reported cases raise the possibility of uteroplacental ischemia and placental abruption being mechanisms by which hypothyroidism can lead to stillbirth; they also highlight the potential of minimizing this risk via adequate levothyroxine treatment from early pregnancy.