Serum thyroglobulin concentration as an indicator for assessing thyroid stimulation in patients with Graves' disease during antithyroid drug therapy
Article Abstract:
Graves' disease is characterized by an enlarged thyroid gland and abnormal protrusion of the eyeballs. The regulation of blood levels of thyroglobulin, an iodine-containing protein released by the thyroid gland, was assessed in patients with Graves' disease. Thyroglobulin levels were assessed in relation to levels of the pituitary hormone thyrotropin, which stimulates the thyroid gland, and the presence of antibodies, or immune proteins, that specifically bind to receptors for thyrotropin (TRab). One hundred and thirteen patients were treated with the antithyroid drug methimazole and their thyroid activities were maintained at normal levels for at least 10 months. Blood levels of thyroglobulin averaged 116 nanograms per milliliter (ng/mL) in nine patients with normal thyrotropin levels and no TRab, 249 ng/mL in 18 patients with TRab but normal thyrotropin levels, and 399 ng/mL in six patients with TRab and undetectable thyrotropin levels. In another 39 patients treated with methimazole, thyroglobulin levels were correlated with the levels of TRab but not thyrotropin. Among 14 patients with hypothyroidism or low thyroid activity due to excessive treatment with methimazole, thyroglobulin levels increased with rising thyrotropin levels, but became normal with supplements of the thyroid hormone thyroxine. Among eight patients with recurrent hyperthyroidism or increased activity of the thyroid gland, thyroglobulin measured 188 ng/mL and TRab at almost 28 percent. Patients with normal thyroid activity or mild recurrence of hyperthyroidism maintained low levels of thyroglobulin and TRab. These findings suggest that thyrotropin and abnormal factors that stimulate the thyroid gland control the release of thyroglobulin in patients with Graves' disease. Measurement of thyroglobulin levels provides a means of assessing the activity of the thyroid gland. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1990
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Biochemical basis of thyroid hormone action in the heart
Article Abstract:
The thyroid hormone triiodothyronine (T3) has direct and indirect physiological effects on the heart. Direct effects of T3 may be nuclear, involving the cell nucleus, or extranuclear, independent of the nucleus. Extranuclear T3 effects do not require the binding of T3 to nuclear receptors (proteins on the nuclear membrane that specifically attach thyroid hormones) or increases in protein production. Extranuclear T3 effects influence the transport of amino acids, sugars, and calcium across the cell membrane. Nuclear T3 effects involve the binding of T3 to nuclear receptors and the activation of genes which are responsive to this thyroid hormone. The T3 nuclear receptors belongs to a group of specialized proteins, the ligand-activated transcription factor family, which are produced by a specific set of genes called the erythroblastosis A (cerb-A) genes. These proteins are similar to virus-produced erythroblastosis A (v-erb A) proteins, which cause a blood cell cancer in chickens. Three types of c-erb proteins that do not bind T3 and two forms that do bind T3 have been identified and have effects on T3-responsive genes. T3 increases the transcription or processing of genes controlling the speed of heart muscle contraction and relaxation; consequently, T3 increases the energy consumption of the heart. However, most of the energy consumed is used for heat production rather than contraction of the heart. This results in decreased efficiency of the heart in patients with hyperthyroidism, or increased activity of the thyroid gland. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1990
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Fatal nonthyroidal illness may impair nocturnal thyrotropin levels
Article Abstract:
Thyrotropin or thyroid-stimulating hormone (TSH) is a hormone released by the pituitary gland which acts to stimulate the thyroid gland. The effect of nonthyroidal illness on the circadian, or 24-hour, variation in the levels of TSH was assessed in 20 patients with sudden respiratory failure. Five of the six patients who died had abnormally low levels of the thyroid hormone thyroxine (T4), whereas only three of 14 surviving patients had low T4 levels. The levels of TSH measured at 8 in the morning were similar in both groups, although TSH levels at 9 P.M. and 11 P.M. increased in survivors and decreased in patients who died. Five of the six nonsurvivors and none of the surviving patients had a suppressed 1 A.M. TSH level, suggesting a relationship between suppressed 1 A.M. TSH level and death. The levels of cortisol, a hormone released by the adrenal gland, were higher only at 8 A.M. in patients who died as compared with patients who survived. The results suggest that fatal illness is associated with a suppression of the normal late night rise in TSH levels. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1990
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