Increased need for thyroxine during pregnancy in women with primary hypothyroidism

Article Abstract:

The need of pregnant women with primary hypothyroidism (deficient thyroid hormone secretion) for extra thyroid hormone (thyroxine, or T4) beyond the usual maintenance level has not been well established. To better understand this issue, medical records were reviewed of 12 women (average age, 30.6) who received doses of thyroxine before conception and during pregnancy. Blood levels of free thyroxine and of thyrotropin (the hormone that stimulates production of thyroxine) were recorded. Results showed that, although they received the same daily thyroxine doses before and during pregnancy, the patients' levels of thyroxine decreased significantly, but not below the normal range, except in one patient. At the same time, the average maximal thyrotropin level increased dramatically beyond the pre-pregnancy level (a normal compensatory mechanism, which stimulates the production of more thyroid hormone). Nine patients had their thyroxine dose raised as a result; an average increase of 45 percent was required. Three months after delivery, thyroxine levels in all women were higher than they had been before and during pregnancy, and thyrotropin levels were lower than during pregnancy (but similar to the levels before pregnancy). The results raise questions regarding why earlier studies failed to detect the need for increased thyroxine in pregnant, hypothyroid women. One explanation is the recent development of tests that can detect thyrotropin levels with great sensitivity. Reasons for the increased need for thyroxine in pregnancy are also discussed. Thyroid hormone levels normally rise in pregnant women during the first three months of pregnancy, but these increases may be the result of the action of chorionic gonadotropin (a hormone of pregnancy), not a result of thyrotropin. However, hypothyroid women cannot manufacture more thyroid hormone in response to any regulating signal, and their hormone levels fall. Inadequate correction of thyroid hormone can affect both mother and fetus, although these mildly hypothyroid women would not be expected to develop complications (nor did they). However, some pregnancies, such as those involving an infant with congenital hypothyroidism, could require conscientious monitoring of thyroxine levels. (Consumer Summary produced by Reliance Medical Information, Inc.)

Care and treatment, Measurement, Testing, Physiological aspects, Drug therapy, Pregnant women, Dosage and administration, Endocrine gland diseases, Endocrine diseases, Thyrotropin

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Maternal thyroxine and congenital hypothyroidism

Article Abstract:

Hypothyroidism is an inherited disorder caused by the partial or total lack of thyroid organ development. When infants are born without thyroid function, they initially appear normal. However, within a few weeks, their condition deteriorates and signs of decreased or absent thyroid function (hypothyroidism) become obvious. Cretinism, a severe form of mental retardation, can develop if infants who are deficient in the hormone thyroxine are left untreated. It is suggested that these infants do not appear with symptoms initially because thyroid hormones are passed on from the mother during pregnancy. In one study, measurements of thyroxine levels were taken in infants born with an inherited disease which prevented them from secreting thyroxine. Any thyroxine found in the infants' blood was assumed to be acquired from the mother. The small amount of thyroxine found in the fetal blood seems to be enough to delay thyroid-deficiency symptoms for at least a week. This study confirms the importance of thyroid screening programs in infants to provide early effective replacement therapy.

Analysis, Case studies, Abnormalities, Maternal-fetal exchange, Prevention, Infants (Newborn), Newborn infants, Mental retardation, editorial

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Severe hypothyroidism caused by type 3 iodothyronine deiodinase in infantile hemangiomas

Article Abstract:

Babies with hemangiomas who develop hypothyroidism should be carefully examined. Hemangiomas are benign tumors that usually go away without treatment. Researchers describe the case of a baby with liver hemangiomas who had a deficiency of thyroid hormone. He needed 8 to 9 times more therapeutic thyroid hormone as babies who don't even have a thyroid gland. This indicated that some process in his body was destroying thyroid hormone very rapidly. His doctors discovered that his liver hemangiomas were producing type 3 iodothyronine deiodinase, an enzyme that converts thyroid hormone to its inactive form.

Causes of, Complications and side effects, Diseases, Infants, Hemangioma

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