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)

A 30-year old woman with a history of recurrent goiter, who had undergone two partial thyroidectomies, is described. She presented with tachycardia, nervousness and a fine tremor of the fingers. Initially, she had normal serum thyroid hormone levels: thyroxine (T4 (D)) 11.6 MUG/100 ML, TRIIODOTHYRONINE (T3) 138 ng/100ml, normal levels of binding proteins and a very high serum thyrotropin (TSH), 98 muU/ml. During follow-up T4 (D) increased to 17.2 mug/100 ml, T3 increased to 277 ng/100 ml, while TSH decreased to 11 muU/ml. There was an exaggerated response of TSH to a peak value of 550 muU/ml after intravenous administration of 200 mug thyrotropin-releasing hormone (TRH). Administration of 60 mg prednisolone daily resulted in a blunting of the response to TRH. Administration of 50 mug T3 daily for 1 month resulted in a fall in serum TSH from 98 to 50 muU/ml. Later, when the serum TSH level had fallen spontaneously to 20 muU/ml, administration of 100 mug T3 daily for two weeks resulted in a fall in serum TSH to 5.3 muU/ml. Treatment with 20 mg carbimazole daily for 3 weeks resulted in a decrease in serum T4 levels with a concomitant increase of serum TSH. There was no evidence of pituitary enlargement and other pituitary hormone levels were normal. All the relatives studied (father, sister, three children) had elevated T4 levels with normal basal TSH values. It is concluded from this study that our patient presents evidence of partial resistance to thyroid hormones.
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PMID:Familial partial target organ resistance to thyroid hormones. 6 Mar 46

We present a patient 52 years old with a symtomatology of three month's evolution with: rapid weight loss, weakness in legs fasciculated tremor increased by any physical effort, nervousness and anxiety. The isotopic exploration of thyroid in basal conditions and after estimulation with TSH shows a very small captation of iodide. The determination of T 4 shows a notable increase (24 U. U. Normal range is 7,5 to 10,5 U. U.). The clinical symtomatology biochemical and gammagraphic datum support the diagnostic of subacute thyroiditis and also the posterior evolution of symtomatology in spite of the absence of odynophagia and the increase of syze of the thyroid. We comment on the particularity of this clinical entity that could be confused with thireotoxicosis because of its atypical character of presentation.
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PMID:[A clinical report. Atypical subacute thyroiditis]. 55 34

Thyroid and adrenal function was assessed in euthymic bipolar patients, stable on prophylactic lithium for at least 1 year, before and after lithium discontinuation in a randomised double-blind placebo-controlled trial. All hormonal measurements were within the reference range, but a significant increase (P less than 0.001) in plasma thyroxine (T4) levels and a decrease (P less than 0.01) in TSH levels were observed 1 month after lithium withdrawal; cortisol concentrations showed a non-significant decrease in the same period. No relationship could be demonstrated between the magnitude of the change in hormone levels and the probability of relapse of manic symptoms. In the second part of this study, inositol was added for 11 days to the diets of bipolar patients being treated with prophylactic lithium and normal controls. No modification was shown in T4 and TSH in either group before or after inositol administration. Inositol did not alleviate other side-effects such as tremor and thirst in the patient group. This result suggests that short-term dietary inositol is not equivalent to lithium withdrawal and is of no value in reducing hormonal and other adverse effects of lithium prophylaxis.
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PMID:The effects of lithium discontinuation and the non-effect of oral inositol upon thyroid hormones and cortisol in patients with bipolar affective disorder. 191 59

Graves' disease was found in a 41-year-old, married male patient with Klinefelter's syndrome. The patient began having finger tremor 5 years previously, and developed palpitation and weight loss 3 months prior to examination. He had a diffuse goiter, exophthalmos, and atrial fibrillation. Plasma levels of T3, T4 and free T4 were 2.8 ng/ml, 16.6 micrograms/dl and 4.5 ng/dl respectively. [123I] uptake was 53%, and TSH receptor antibody was 75%. Although he had no gynecomastia, his general physical appearance was that of typical eunuchoism. Chromosome studies showed a karyotype of 47,XXY. A diagnosis of Graves' disease associated with Klinefelter's syndrome was made.
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PMID:A case of Graves' disease associated with Klinefelter's syndrome. 212 24

Associations between hyperthyroidism and Parkinson disease have been reported. The treatment of the hyperthyroid state seems to improve the extrapyramidal symptomatology. We report a case of a woman suffering from Parkinson disease and hypothyroidism. The treatment with thyroxine increased parkinsonian tremor. Dopamine regulation of TSH circadian and pulsatile release is not clear. These observations stress the possible role of thyroid hormones in regulating dopaminergic metabolism.
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PMID:[Dysthyroidism and Parkinson's disease]. 222 22

Pituitary apoplexy is characterized by a wide spectrum of clinical features. A quite rare case of painless thyroiditis, hypopituitarism and central diabetes insipidus (DI) followed by pituitary apoplexy was presented. A 61-year-old woman was admitted to our hospital in May, 1986 because of marked general malaise, polydipsia and weight loss which became progressively worse. Four months earlier she had experienced episodes of abrupt onset of severe headache associated with nausea and blurring vision. Physical examinations revealed a fine tremor, dry skin and nervousness. The thyroid gland was not palpable. Visual fields were intact. Her blood pressure was 105/64 mmHg with variable tachycardia. The routine laboratory studies were normal or negative except for hypoalbuminemia, hypocholesterolemia and hypernatremia. Erythrocyte sedimentation rate was 12 mm/hr. An impairment in corticotropin secretion was suspected from the low plasma cortisol and the low urinary excretion of 17-OHCS and the sufficient response to ACTH. Basal levels of GH and gonadotropin were also low, and responses to the stimulation tests (Insulin-stress, L-DOPA, and LH-RH) were all blunted. Brain computed tomographic scan and magnetic resonance imaging demonstrated a suprasellar mass that, after infusion, developed peripheral ring-like enhancement and large hyperintense pituitary mass, respectively. A diagnosis of pituitary apoplexy with anterior pituitary failure was made. However, the initial levels of thyroid hormones showed elevated as follows: Free T3 7.6 pg/ml, Free T4 3.3 ng/dl and T3-resin uptake 41.1%. TSH responses to TRH were all suppressed. TSH receptor antibody (TBII) was negative. Both antithyroglobulin and antimicrosomal antibodies were repeatedly positive. A thyroid scan with 99mTc revealed no uptake in the thyroid area. These findings led us to the diagnosis of "painless autoimmune thyroiditis". She had become hypothyroid without any medication. At that time radioactive 99mTc and 123I uptakes increased significantly. When hydrocortisone was substituted, daily urine output abruptly increased to about 10 liters with low osmolality, and the presence of DI was suspected. This diagnosis was confirmed by water deprivation and hypertonic saline infusion tests and subsequent pitressin test. She is currently quite well on L-thyroxine, hydrocortisone and desmopressin (1988). This association with pituitary apoplexy must be a rare occurrence, as a literature search has failed to find a similar case. The pathogenetic trigger of "painless thyroiditis" in this case may be responsible for some immunological change due to secondary adrenal insufficiency after pituitary apoplexy.
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PMID:[An unusual association of transient resolving thyrotoxicosis due to painless thyroiditis, hypopituitarism and central diabetes insipidus associated with spontaneous pituitary apoplexy]. 230 57

The relationships between lithium dosage, affective morbidity, side-effects, thyroid and renal function and biological markers for depression were examined in the context of a prospective double-blind lithium reduction study in patients receiving prophylactic lithium. Unipolar and bipolar patients on such treatment were randomly allocated to two groups over a period of one year, either continuing with their usual dosage of lithium or reducing their lithium dosage by up to 50%. Biological markers investigated included dexamethasone suppression test (DST) and 5-hydroxytryptamine (5-HT) transport into platelets (Vmax). Results showed no association between affective morbidity and lithium dosage/level. There was, however, an association between lower dosage/level of lithium and lower side-effects, including tremor and weight gain, lower TSH levels and lower 24 h urinary volume in these patients. Elderly patients, however, experienced significantly greater morbidity upon reduction of their lithium dosage. There was an association between increased Vmax of 5-HT transport and a reduction in morbidity. DST non-suppression was associated with lower mean weight for the whole year of the study.
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PMID:The efficacy of low-dose lithium: clinical, psychological and biological correlates. 251 Dec 99

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

The effects of TRIAC on peripheral thyroid hormones, TSH incretion and peripheral tissue parameters were investigated in 13 mildly obese patients (group I) and 10 volunteers of normal body weight (group II). TRIAC was administered 3 x 1 mg daily over a period of 8 days to both groups. In group I (on a 400 kcal low caloric diet) bTSH and fT4 decreased significantly whereas TT4 decreased only insignificantly. TT3 and fT3 rose significantly due to the cross-reactivity of the employed antibody. The peripheral tissue parameters cholesterol, ankle jerk and systolic time interval did not reveal any changes suggesting an increase in metabolic rate. The increase in heart frequency was not significant either. The significant rise in sex-hormone binding globulin was most probably associated with the weight reduction of 3.1 +/- 1.2 kg per week. In group II (on normal diet) bTSH and fT4 decreased significantly whereas TT4 decreased only insignificantly. As in group I, TT3 and fT3 rose significantly. Also in group II TRIAC did not cause alterations in the peripheral tissue parameters. In contrast to the obese group the volunteers in group II showed no significant rise in sex-hormone binding globulin and no reduction of body weight. Side effects such as nervousness, tremor or palpitations were not observed. Thus, TRIAC does not induce an increase in peripheral metabolic rate, not even under a TSH-suppressive dose as high as 3 x 1 mg per day.
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PMID:3,5,3'-Triiodothyroacetic acid (TRIAC) effects on pituitary thyroid regulation and on peripheral tissue parameters. 260 44

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


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