Recognition of thyroid disease in the fetus

Article Abstract:

Hypo- or hyperthyroidism (insufficient or excess secretion of thyroid hormones, respectively) can be present in newborn infants. In such cases, the conditions have been present during fetal life, as well. Hyperthyroidism is recognized in newborns because its effects are more obvious, and because the mothers of these infants usually have Graves' disease (associated with goiter, hyperthyroidism, and other changes). Hypothyroidism is more difficult to detect and is usually the result of abnormal development of the thyroid gland. The effects of these conditions in prenatal life are beginning to be understood. A research report in the February 21, 1990 issue of The New England Journal of Medicine presents data gathered via sampling of fetal blood from the umbilical cord (cordocentesis) that show the normal levels of thyroxine (thyroid hormone, with powerful physiological effects), thyroid-stimulating hormone (TSH or thyrotropin, released by the pituitary gland to stimulate the production of thyroxine), and thyrotropin-releasing hormone (made in the hypothalamus, part of the brain). Fetuses were studied at different stages of gestation to learn more concerning the development of feedback loops in this highly interdependent system. The results indicated that the thyroid and pituitary glands become increasingly capable of secreting their respective hormones, but that TSH production does not respond to thyroxine levels, as it does in adult life. The physiologic consequences of these facts are discussed. When thyroid disease is suspected in a fetus, both mother and fetus must be carefully evaluated. The mother's levels of TSH and thyroxine should be regulated, and any medication that might affect the fetus should be discontinued or given in lower doses. Another article in the same Journal issue describes the successful treatment of such a case. In most cases involving maternal thyroid disease, cordocentesis is not necessary, and fetal health can be evaluated by maternal blood testing and clinical evaluation. (Consumer Summary produced by Reliance Medical Information, Inc.)

Methods, Diagnosis, Fetus, Prenatal influences, Prenatal diagnosis

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The pathogenesis of autoimmune thyroid disease

Article Abstract:

Autoimmune diseases occur when the immune system mounts an attack against normal cells and tissues. When an autoimmune reaction affects the thyroid gland, the severity of the condition is usually based on how the response affects the secretion of thyroid hormones. Treatment involves replacing hormones not being produced in sufficient quantities, or countering increased hormone production. There is no treatment for the underlying cause of autoimmune-related abnormal hormone secretion. The two main autoimmune thyroid diseases are Graves' disease and chronic autoimmune thyroiditis. They are caused by similar mechanisms, but result in opposite clinical manifestations. In Graves' disease, thyroid-stimulating hormone (TSH) is activated by immune system abnormalities, resulting in hyperthyroidism (over-active thyroid). In chronic autoimmune thyroiditis, the thyroid is inactivated and causes in hypothyroidism (under-active thyroid). In both conditions, antibodies attach to the TSH molecules and alter their activity, and immune cells known as T cells accumulate in the thyroid. These T cells are activated when the antigen-HLA complex binds with the antigen-HLA receptors on the T cells. The antigen is the structure the T cell recognizes as foreign, and the HLC complex is a component necessary for T cell binding. In the July 25, 1991 issue of The New England Journal of Medicine, a study by Davies et al. provides a clearer picture of the involvement of T cells in autoimmune thyroid diseases. It appears that in autoimmune thyroid diseases the genes that produce T cell receptors in the thyroid are not all expressed; only a few of the possible types are actually made. The few receptor types that are made seem to be more likely to react with normal thyroid cells. It is possible that infection or stress may play a role in this phenomenon. Future work, similar to that of Davies, should help to increase the understanding of autoimmune thyroid diseases. (Consumer Summary produced by Reliance Medical Information, Inc.)

Evaluation, Antigen receptors, T cell, T cell antigen receptors, Graves' disease, Thyroiditis, Autoimmune, Autoimmune thyroiditis

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Thyrotropin-receptor mutations and thyroid dysfunction

Article Abstract:

Mutations in the thyrotropin-receptor gene resulting in inherited hyperthyroidism or hypothyroidism may shed light on how the hormone thyrotropin stimulates thyroid hormone secretion. A child with congenital hyperthyroidism was found to have a gain-of-function mutation that overrode the normal braking action of the inactive thyrotropin receptor. The mutation causing hyperthyroidism and an enlarged thyroid is fairly rare, occurring mostly in persons with Graves' disease. In another case, three sisters inherited loss-of-function mutations of the thyrotropin-receptor gene, causing resistance to the action of thyrotropin and underlying hypothyroidism. Very high levels of thyrotropin masked the hypothyroidism experienced by the three sisters. Secretion of thyroid hormone was low due to thyroid resistance to thyrotropin because of an inability of thyrotropin to bind to the mutated receptors. More serious cases of hypothyroidism due to mutation of the thyrotropin receptor may be identified in the future.

Editorial, Abnormalities, Causes of, Hormone receptors, Thyrotropin

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