The thyroid and pregnancy

Hall, R; Richards, C. J.; Lazarus, John

doi:10.1111/j.1471-0528.1993.tb15299.x

Cited by 30 publications

(8 citation statements)

References 38 publications

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“…(2,7,8,(11)(12)(13) Anderen vinden dan weer geen verschil in hCG-gehalten tussen brakers en niet-brakers, (15)(16) doch stellen wel een hoger oestradiolgehalte vast bij brakers. (17) Dit hogere oestradiolgehalte zou dan weer de verklaring vormen voor de hogere incidentie van hyperemesis bij obese vrouwen (verhoogde perifere conversie van androgenen naar oestrogenen) en de verminderde incidentie bij rooksters. (18,19) Evans kon in zijn studie bij 342 patiënten met variërende ernst van nausea en braken echter geen enkel verband tussen de schildklierdysfunctie en de graad van nausea en braken aantonen.…”

Section: Is There a Relation Between Hyperemesis Gravidarum And Hyperunclassified

Is Er Een Relatie Tussen Hyperemesis Gravidarum en Hyperthyroidie?

Leunen¹,

Velkeniers²,

Verlaenen

2001

Acta Clinica Belgica

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In patients admitted with hyperemesis gravidarum, we found 23% of the women to present a thyroid stimulation. This hyperthyroidism differs from the auto-immune hyperthyroidism, i.e. the patients have no thyroid antibodies, no classic clinical signs of thyrothoxicosis. Probably, the absolute hCG concentration and its biological activity plays a crucial role in the thyroid stimulation. This degree of thyroid stimulation has no influence on the severity of the hyperemesis gravidarum, neither on the outcome of the pregnancy.

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Section: Is There a Relation Between Hyperemesis Gravidarum And Hyperunclassified

Is Er Een Relatie Tussen Hyperemesis Gravidarum en Hyperthyroidie?

Leunen¹,

Velkeniers²,

Verlaenen

2001

Acta Clinica Belgica

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“…These complications include a premature birth with its own risk of psychomotor development, hypotrophy [8,9] associated with a higher level of maternal toxemia [10,11], a greater number of deaths in utero that could reach 20% in older studies (significantly higher in untreated mothers), and thyroid dysfunction [9,12,13]. The latter alone can be the source of all other complications and this justifies in utero screening to limit its consequences [14].…”

Section: Discussionmentioning

confidence: 99%

One Case of Fetal and Neonatal Variable Thyroid Dysfunction in the Context of Graves’ Disease

Brand

Liégeois

Langer³

2004

Fetal Diagn Ther

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Cases of maternal thyroid dysfunction are not always clearly identified during pregnancy. We report here the case of a 36-year-old patient with a history of treated Graves’ disease whose child successively presented with a hypo- and hyperthyroid dysfunction that was difficult to treat despite the administration of synthetic antithyroid drugs and β-blockers. The patient’s thyroid hormone levels were normal during pregnancy, while still secreting anti-TSH-receptor autoantibodies. With time, these antibodies went from an inhibiting to a stimulating activity. Fetal monitoring using only ultrasonography had been proposed to the patient. With such a follow-up associated with fetal blood sampling it would have been possible to treat already in utero the thyroid dysfunction. The management of such patients is not limited to the follow-up of the maternal thyroid hormones, but should also evaluate the activity of the anti-TSH-receptor autoantibodies around the 28th week of amenorrhea and their effect on fetal blood. Fetal and neonatal thyroid dysfunctions have a major impact, but they can be detected and treated in utero. The clinical, laboratory and ultrasound follow-up makes it possible to monitor patients who are at risk and to propose a therapeutic and obstetrical management.

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“…High levels of TSAb are associated with fetal hyperthyroidism, while TSBAb may cause hypothyroidism (Hall et al, 1993). However, in both cases permanent neurological deficit may follow (MacSweeney et al, 1978;Virtanen et al, 1989).…”

Section: Introductionmentioning

confidence: 99%