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Results for “HYPERTHYROIDISM”

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At least 37 records · Page 2Linked to original sources

PubMed1987

The decrease in non-specific suppressor T lymphocytes in female hyperthyroid Graves' disease is secondary to the hyperthyroidism.

There has recently been considerable interest generated in the significance of changes in the peripheral blood T lymphocyte subsets in patients with autoimmune thyroid disease. Previously, monoclonal antibodies that recognized T cells (Leu 1+ cells), T helper/inducer cells (Leu 3a+ cells), and T suppressor/cytotoxic cells (Leu 2a+ cells), have been used to enumerate these subsets. Using 2 new monoclonal antibodies (anti-Leu-8 and anti-Leu-15), in addition to the above 3 antibodies, and 2-colour flow cytometry, we have enumerated the total T, T helper/inducer, T suppressor/cytotoxic, T helper (Leu 3a+8-), T inducer (Leu 3a+8+), T suppressor (Leu 2a+15+), and T cytotoxic (Leu 2a+15-) cells in 22 patients with hyperthyroid Graves' disease, 38 patients with 131I-treated Graves' disease and 10 patients with Hashimoto's thyroiditis. All patients and controls were female. We found that hyperthyroid patients with Graves' disease had significantly lower T suppressor/cytotoxic cells (p less than 0.05) than did controls, and that this was mainly due to a decrease in T suppressor cells (p less than 0.01). Furthermore, patients with severe hyperthyroidism had a more significant decrease in T suppressor/cytotoxic (p less than 0.001) and T suppressor (p less than 0.001) cells, and an increase in the T helper/inducer:T suppressor/cytotoxic (p less than 0.01) and T helper:T suppressor (p less than 0.01) cell ratios. Patients who were euthyroid more than 1 year after 131I therapy for Graves' disease had normal T cell subsets and ratios, whether or not TSH receptor antibody or other thyroid auto-antibody titres were elevated. Ten females with Hashimoto's thyroiditis also had normal T cell subsets.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1989

Concurrent hyperthyroidism and hyperparathyroidism: influence of hyperthyroidism on serum magnesium, free calcium and parathyroid hormone.

A patient with concomitant primary hyperparathyroidism and Graves' disease with hyperthyroidism was observed during treatment with carbimazole. His serum free calcium levels was initially elevated (6.3mg/dl, normal 4.5-5.3 mg/dl) whereas his serum magnesium level was depressed (1.6 mg/dl, normal 1.7-2.8 mg/dl), but immunoreactive parathyroid hormone levels were only slightly increased (96 pg/ml, normal less than 86 pg/ml). During therapy with carbimazole, the patient became euthyroid and serum free calcium levels decreased to 6.0 mg/dl whereas serum magnesium levels increased to 2.3 mg/dl, and parathyroid hormone increased to values clearly indicative of hyperparathyroidism (185 pg/ml). A subtotal thyroidectomy and parathyroidectomy corrected both diseases in this case. These observations suggested that hyperthyroidism per se causes a decrease in serum magnesium levels and also potentiates the osteoclastic effects of parathyroid hormone resulting in an exacerbation of hypercalcemia which in turn produced a relative inhibition of hormone secretion by the abnormal parathyroid tissue.

Adult↗

PubMed1983

Thermoregulation in hyperthyroid rats: mechanism underlying the lack of hypothermic response to morphine in hyperthyroid animals.

Previous experiments in our laboratory demonstrated that morphine, at doses which produced pronounced hypothermia in normal rats, not only failed to decrease but instead increased body temperature in thyroxine-treated animals. The present studies were undertaken to further investigate these initial findings. In animals treated chronically with subcutaneous thyroxine, basal body temperatures were elevated and morphine induced only hyperthermia whether given subcutaneously (10 mg/kg) or centrally (30 micrograms) into the anterior hypothalamus. Basal oxygen consumption, which reflects metabolic heat production, was significantly elevated when compared to controls. In response to morphine, control animals showed decreased oxygen consumption while thyroxine-treated animals showed a slight increase. In both groups of animals, changes in core temperatures reflected changes in oxygen consumption. These results indicate that hyperthyroid animals fail to decrease body temperature in response to morphine because they are unable to decrease metabolic heat production. Morphine, acting at central hypothalamic sites, reduces heat production in normal animals, but in thyroxine-treated animals morphine cannot overcome the increased thermogenesis.

Animals↗

PubMed1991

High levels of serum soluble interleukin-2 receptors in hyperthyroid patients: correlation with serum thyroid hormones and independence from the etiology of the hyperthyroidism.

The serum levels of soluble interleukin-2 receptors (s-IL-2R) and soluble CD8 antigens (s-CD8) were measured in 33 patients with Graves' disease (GD), 29 with toxic nodular goiter (TNG), 6 with toxic adenoma (TA), and 12 with hypothyroidism, as well as in 11 patients with infectious mononucleosis (known to have high s-IL-2R and s-CD8 levels) and 34 normal controls. Serum levels of T3 and T4, both total and free, and of TSH were simultaneously determined. s-IL-2R levels were significantly higher in all patients with hyperthyroidism (mean +/- SD, 3276 +/- 1273 U/mL for GD, 4183 +/- 1832 for TNG, and 1671 +/- 648 for TA) compared to normal control values (P less than 0.001 for GD and TNG and P less than 0.01 for TA), while in the euthyroid state they were within the normal range (535 +/- 240 U/mL). Hypothyroid patients had significantly lower s-IL-2R levels compared to normal controls (P less than 0.05). A positive correlation (P less than 0.001) between serum s-IL-2R levels and total/free T3-T4 levels was found in these groups of patients, while no correlation between s-CD8 levels and s-IL-2R/T3/T4 was found. These findings suggest an association between hyperthyroxinaemia and activation of human lymphocytes in vivo.

Adenoma↗

PubMed1989

[Hypophyseal hyperthyroidism. Non-tumoral hypersecretion of thyroid stimulating hormone with clinical hyperthyroidism].

A case of hyperthyroidism due to inappropriate TSH secretion in a 45-year-old man is presented. The diagnosis was confirmed by measurement of increased serum TSH values using three different assays, increased T4 and T3 values, the clinical picture, and the effect of anti-thyroid treatment. Nuclear magnetic resonance and computerized tomographic scans of the pituitary fossa showed no abnormalities. Treatment with long-term oral thyrotropin-releasing hormone, oral triiodothyronine, and short-term subcutaneous Sandostatin injections resulted in partial suppression of TSH without however adequate clinical effect. Treatment with thyroxin, bromocriptine, and triiodothyroacetic acid did not alter the parameters. It is concluded, that the inappropriate TSH secretion may be due to a pituitary microadenoma.

Humans↗

PubMed1985

[Transient neonatal hyperthyroidism in the child of a treated hyperthyroid mother. Subsequent appearance of sexual precocity].

We report a newborn female with neonatal hyperthyroidism, born to a mother with Graves disease treated with potassium iodide and carbimazole. At four months she had some breast development, a bone age advance of one year, and elevated levels of FSH and estradiol. Later on the prolactin level was also raised, while LH and TSH values continued low. Posteriorly, irregular cutaneous pigmentation, brown in colour, was evident on the neck and trunk, and a McCune-Albright syndrome was suspected. The relationship between these conditions and treatment of them is discussed.

Carbimazole↗

PubMed1983

A lysosomal study of cold-induced hyperthyroidism in the rat: comparison to human hyperthyroid tissue.

Prolonged exposure to cold in the adult rat is considered an acceptable model to study experimental hyperthyroidism. In our experiments adult rats were exposed to cold (1 degree to 4 degrees C) for various periods of time, after which their thyroid tissue and plasma were assayed for lysosomal enzyme activity. In additional animal experiments we examined the cold-exposed rats during propranolol treatment. After 2 weeks of exposure to cold, rat thyroid glands were hypertrophied and hypervascular. There was a significant increase in all three lysosomal enzymes measured in the rat thyroid tissue compared to age-matched controls. The percent of enzyme activity found in the various subcellular fractions did not change. The plasma triiodothyronine concentration increased slightly in the cold-exposed rats, whereas there was no change in thyroxine or lysosomal activity. Propranolol had no effect. In separate experiments human thyroid tissue from patients with diffuse toxic goiter or histologically normal thyroid tissue was examined. Similar to cold-exposed rat thyroid tissue, diffuse toxic goitrous tissue showed a twofold to threefold increase in lysosomal enzyme activity compared to control tissue. These data suggest that increased thyroidal lysosomal enzyme synthesis is one of the factors operative in the increased secretion of active thyroid hormones in Graves' disease.

Animals↗

PubMed1962