Maturation of the secretion of thyroid hormone and thyroid-stimulating hormone in the fetus

Article Abstract:

To learn more concerning fetal thyroid function, 62 fetuses at different stages of gestation were studied by cordocentesis (sampling blood from the umbilical cord using ultrasound guidance). Maternal blood samples were taken just before cordocentesis was performed. The fetal blood samples studied had been obtained for therapeutic reasons that were unrelated to the purpose of the study. Of interest were the levels of: thyroid-stimulating hormone (thyrotropin, which stimulates the thyroid to produce its hormones); T3 and T4 (thyroid hormones, which exert powerful physiological effects); and thyroxine-binding globulin (one of the proteins to which thyroxine is bound; thyroxine can be in either the free or bound form). Results showed that the concentrations of all these hormones in the fetus increased during gestation. No changes that correlated with the duration of pregnancy were noted in the mothers, although their levels of T3 and T4 were higher than those in normal nonpregnant adults. In most cases, fetal concentrations of thyroid-stimulating hormone were higher, and levels of T3 were lower than in adults. Fetal levels of T4 and of thyroxine-binding globulin were lower than the maternal levels, reaching adult values by approximately 36 weeks' gestation. A discussion is presented on the interaction among these hormones and on aspects of their physiological control. It is likely that the increase in fetal hormone levels that takes place in the second trimester is the result of maturation of the pituitary, thyroid, and liver; these organs mature independently. As gestation continues, the fact that increasing levels of thyroid hormone do not cause a reduction in levels of thyroid-stimulating hormone (as is the case in the normal negative feedback loop) may mean that the fetal pituitary gland (from which thyroid-stimulating hormone is released) is not yet able to respond appropriately to this stimulus. (Consumer Summary produced by Reliance Medical Information, Inc.)

Measurement, Fetus, Thyroid hormones, Thyrotropin

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Immunoendocrine interactions and autoimmunity

Article Abstract:

The causes of autoimmune disease (which results when the body's own immune system fails to distinguish between foreign proteins and its own tissues) are not known. Such disorders result from genetic, constitutional (having to do with the whole body), and environmental conditions. Autoimmune diseases run in families, but genes for susceptibility to particular diseases probably do not exist. Rather, genetic predispositions give way to frank diseases when other factors trigger them. In autoimmune thyroid disease, infectious agents and iodine taken in with the diet have been implicated. Constitutional factors, such as defects in the immune system and endocrine changes associated with aging, are reviewed. Most autoimmune diseases are more prevalent in women; androgens (male sex hormones) suppress autoimmunity. Thus, there may be a hormonal contribution to these disorders. Glucocorticoids (hormones produced by the adrenal gland) suppress the immune system, in part by redistributing T cells (cells of the immune system) from the circulation into lymphoid organs. This results in fewer T cells becoming activated when an immune response is mounted. Another immune effect of the endocrine system is the stimulation of glucocorticoid secretion by interleukin-1 (produced by white blood cells). A report in the June 14, 1990 issue of The New England Journal of Medicine revealed that three women who had developed a Cushing's syndrome (hypersecretion of glucocorticoids) also developed an apparent autoimmune thyroid disorder. The effects of pregnancy on the immune system are described as a clear example of endocrine-immune interactions. (Consumer Summary produced by Reliance Medical Information, Inc.)

Reports, Immune system, Endocrine gland diseases, Endocrine diseases, editorial

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Molecular mimicry and autoimmunity

Article Abstract:

Molecular mimicry may play a role in some autoimmune diseases but there is little evidence that it is an important role or that a treatment can be designed to prevent autoimmune diseases. Autoimmune diseases occur when the immune system attacks the body. This is normally not supposed to happen. Researchers have speculated that this may occur when people are infected by a certain micro-organism. The body creates antibodies to fight the organism. However, the organism may have proteins that mimic the structure of natural proteins in the body. Therefore, the antibodies attack the natural proteins.

Health aspects, Mimicry (Biology)

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