Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An 11-year-old girl with diffuse goiter is presented. She had no clinical evidence of thyrotoxic symptoms or signs of palpitation, excessive sweating, tachycardia or finger tremor. Both the serum T4 (24.0 micrograms/dl) and T3 (282ng/dl) were high, and thyroid 131I uptake rate (63.2%) was significantly elevated, but T3/T4 ratio was not elevated (11.8). BMR was measured three times and remained within normal limits. Her serum TSH was 1.9 microU/ml, and a TRH stimulation test resulted in a normal rise of serum TSH (13.4 microU/ml). The TSH secretion was not suppressed by medication (p.o.) of 75 micrograms of L-triiodothyronine given for 8 days. The autoantibodies of T4, T3 and TSH were negative. No sign of pituitary tumor was observed by plain X-ray film. No defect in her sight-field was found. From these clinical figures and data, Refetoff's syndrome was suspected. She was eumetabolic without any treatment, but the goiter gradually enlarged and dysphagia developed. A large dose of L-thyroxine (450 micrograms/day) was given for a period of one year and four months. She has been eumetabolic. Her goiter disappeared and the dysphagia completely subsided. After she was given large doses of L-T4, her serum TSH was reduced to 0.07 microU/ml and was slightly elevated to 0.24 microU/ml at 30 min after i.v. infusion of 500 micrograms TRH. Thyroid 123I uptake rate was suppressed to 8.3%. According to Refetoff's papers, this case was classified as being in the group with generalized resistance to thyroid hormone.
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PMID:[A case report of Refetoff's syndrome]. 259 12

A 22-year old man with a goiter and clinical manifestations of mild thyrotoxicosis (finger tremor, palpitation, tachycardia) was diagnosed as a syndrome of inappropriate secretion of TSH. Serum concentrations of T4, free T4, T3 and TSH were 24.1 micrograms/100 ml, 4.07 ng/100 ml, 261 ng/100 ml and 1.72 microU/ml, respectively. Thyroidal 131I uptake at 24 hr was 80%. The BMR was within the normal range. He had a normal TSH response to TRH (500 micrograms) with a peak level of 23.8 microU/ml. The basal level of alpha-subunit of TSH was not elevated (0.35 ng/ml). Oral 1-T3 administration (75 and 150 micrograms daily) raised serum T3 concentration, reduced basal TSH and blunted TSH response to TRH. The diurnal variation of TSH was maintained. There was no evidence of abnormalities in the secretion of other pituitary hormones. These findings were compatible with thyroid hormone resistance. However, the presence of a microadenoma in the pituitary gland was suspected with CT scan. Bilateral and simultaneous venous sampling for TSH from inferior petrosal sinus showed no gradient in TSH concentration indicating that a TSH secreting pituitary tumor was unlikely. These data suggest that inappropriate TSH secretion in the present patient is resulted from resistance to thyroid hormone. In the present study selective venous sampling is useful to differentiate the thyroid hormone resistance from a TSH secreting tumor.
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PMID:A case of refetoff syndrome: selective venous sampling for TSH is useful in differentiating thyroid hormone resistance from TSH secreting tumor. 271 78

Incubation with T3 results in a dose-dependent increase in growth rate of cultured GC cells, a GH-producing rat pituitary tumor cell line. The T3-induced increase in growth rate results mainly from shortening of the G1 period from 79.4 +/- 4.3 (SD) h in cells grown in T3-depleted medium (-T3) to 10.0 +/- 0.9 h. This effect can also be demonstrated in synchronized populations. Addition of T3 (0.3 nM) to cells synchronized in early G1 in the absence of T3 shortened the G1 period, estimated from graphic data, from more than 40-50 h to 13.4 +/- 2.1 h (n = 7). To determine the mechanism of this T3 effect, GC cells were grown in Dulbecco's modified Eagle's medium containing 10% serum plus or minus T3 (0.3 nM) and synchronized at the beginning of the G1 period by mitotic selection. Mitotic cells (85-100%), obtained by controlled mechanical shaking, were isolated by centrifugation and replated. The end of G1 was determined by the onset of DNA synthesis with [3H]thymidine as assessed by autoradiography (percent labeled nuclei). L-T3-induced shortening of G1 was detectable at 0.05 nM T3, half-maximal at physiological T3 (0.17 nM), and maximal between 0.3 nM and 1.0 nM T3. Addition of cycloheximide, 0.025 microgram/ml or 1.0 microgram/ml, decreased protein synthesis by 50% and 90%, respectively, and attenuated the T3 effect on G1 by 80-90%. The attenuation of the T3 effect on G1 by cycloheximide at a dose which inhibited protein synthesis suggests that T3-induced shortening of G1 may require new protein synthesis. Since glucocorticoids decrease the effect of T3 on induction of alpha-aminoisobutyric acid transport, their effect on T3-induced shortening of G1 was determined in G1-synchronized GC cells and in asynchronous cultures. Cortisol, 100 nM, significantly decreased the growth rate of asynchronous GC cells and attenuated the effect of T3 in G1-synchronized cells. Finally, T4 also decreased the length of G1 in a dose-dependent manner with a half-maximal effect at 40.0 nM. The half-maximal effect of T4 occurred at a nuclear iodothyronine concentration that was comparable to that achieved in incubations with 0.17 nM T3 (half-maximal dose). Thus, half-maximal shortening of G1 in synchronized GC cell cultures occurred at iodothyronine concentrations required for half-maximal occupancy of nuclear T3 receptors and for half-maximal induction of GH synthesis, growth rate, alpha-aminoisobutyric acid uptake, and depletion of the nuclear T3 receptor.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:L-Triiodothyronine (T3) stimulates growth of cultured GC cells by action early in the G1 period: evidence for mediation by the nuclear T3 receptor. 298 70

We report a 47-year-old Japanese man who presented with visual disturbance due to a pituitary tumor with suprasellar extension. The patient had mild secondary hypothyroidism preoperatively, and was started on administration of levothyroxine sodium immediately before transsphenoidal surgery. After the operation, levothyroxine sodium was continued for several months. Pathological examination of the surgical specimen, together with endocrinological investigation revealed that the suprasellar tumor was a FSH-producing pituitary adenoma. Since 3 months after the operation, he has developed muscle weakness and finger tremor. He was found to be thyrotoxicosis, and levothyroxine sodium was discontinued. Seven weeks after levothyroxine sodium was discontinued, thyrotoxicosis continued, with a positive thyrotropin binding inhibitory immunoglobulin (TBII) and a high diffuse 123I-uptake by the thyroid. He was started on thiamazole 30 mg/day. Although his thyroid dysfunction improved within 2 months, hyperthyroidism worsened repeatedly on attempts to discontinue thiamazole, and he required continuous treatment at 2.5 mg/day. Patients with occult autoimmune thyroiditis rarely progress to thyrotoxicosis after operations on other endocrine organs such as the adrenal or parathyroid gland. In patients with pituitary adenoma, thyroid function and thyroid-associated autoantibodies should be investigated pre- and post-operatively.
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PMID:Manifestation of primary hyperthyroidism after pituitary adenomectomy: a case report. 962 7

A 34-year-old woman suffered from palpitation, easy sweating, heat intolerance, increased appetite, irregular menstrual cycle and hand tremor for 1 year. Thyroid function tests showed elevated serum thyroxine (T4), tri-iodothyronine (T3) and thyrotropin (TSH). Computerized tomography (CT) revealed pituitary tumor with supraseller extension. Thyrotropin releasing hormone (TRH) test showed blunted TSH response with elevated baseline level and paradoxical growth hormone (GH) response with elevated baseline level. T3 suppression test (T3 60 microg per day x 10 days) showed no inhibition of TSH (11.1 microU/mL, normal range < 6.2 microU/mL). She received transphenoidal approach and removal of tumor which measured 0.5 x 0.3 x 0.2 cm. Histopathologically, it was a pituitary adenoma which was immunoreactive for TSH, GH, follicular stimulating hormone (FSH) and luteinizing hormone (LH). To our knowledge, this case is the first case of TSH-secreting pituitary adenoma in Taiwan.
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PMID:Thyrotropin-secreting pituitary adenoma with growth hormone hypersecretion. 1252 14