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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Synaptosomes from rat cerebral cortex were impregnated in the zinc iodide--osmium (ZIO) solution. The fine structural localization of the ZIO impregnation product was studied and, in addition, the function-dependent features of the reaction were examined after electrical stimulation or potassium chloride treatment. It was revealed that: (i) Aldehyde prefixation resulted in an increase in the number of reactive synaptic vesicles in all types of synaptosomes; (ii) Electrical stimulation decreased the number of reactive vesicles in a voltage dependent manner; (iii) Potassium chloride treatment also reduced the reactivity of vesicles; the reduction was dependent on the concentration of potassium and duration of treatment; (iv) Experimental interventions leading to the release of neurotransmitters from the synaptic vesicles and to fatigue of the nerve terminals also resulted in a decrease of the ZIO-reaction product of synaptic vesicles in a manner proportional to the strength of stimuli.
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PMID:Studies on the fine structural localization of zinc iodide-osmium reaction in the brain. III. Some characteristics of localization in the synaptosomes. 34 39

In primidon-treated patients there are significantly decreased serum concentrations of total and free thyroxin, protein bound iodine and base line serum TSH values. In primidon-treated children T3-resin test values, concentration of thyroxin-binding protein and total cholesterol are identical to those of the control group. Degree of diminution in serum concentration of protein bound iodine, total and free thyroxin and base line TSH was independant of the primidon dose per day. Probably the demonstrated alteration in the thyroid function tests studied, is mainly caused by phenobarbital, the major metabolite of primidon and not directly by unmetabolized primidon. It is suggested that the high protein-binding capacity of phenobarbital results in a competitive displacement of protein bound thyroxin comparable to that of DPH. Phenobarbital is know to be a stimulator of the drug metabolizing enzyme system in the liver. This effect may be the cause of an increased turnover of T4 which results in a decreased serum concentration of total and free T4 at last. It seems possible that there is a balance in serum concentration of thyroid hormones on a lower level. Normal euthyroid state may be presumed, if T4-secretion raises, but there is no clue for an increased pituarity response. In contrast to the normal group in primidon-treated children the base line serum TSH values are decreased. It is supposed that another effect of primidon is responsible for this fact. There may be an influence of primidon treatment on hypothalamic pituarity axis. Our findings do not indicate clearly a hypothyroid state in primidon-treated patients; further investigations should give an answer to the guestion, if side effects as tiredness, decreased impetus and constipation are not partly caused by alterations in thyroid hormone system.
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PMID:[The effect of primidone treatment of thyroid hormones in epileptic children and adolescents (author's transl)]. 40 30

Nuclear medicine has a place in the study of brain trauma, brain tumours, stroke, dementia epilepsy and depression. The development of new tracers labelled with widely available radionuclides, such as technetium-99m (99Tc) and iodine-123, has played a key role here. Practical methodology can now be implemented in the routine setting. Additional applications are reviewed in the context of brain death, encephalitis, post-viral fatigue syndrome, Parkinson's disease and schizophrenia.
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PMID:The role of nuclear medicine in neurology and psychiatry. 146 80

Postpartum thyroid dysfunction (PPTD) refers to the syndromes of transient hyperthyroidism, transient hypothyroidism, or both, occurring sequentially in the first 12 months postpartum. Approximately 5 to 9% of women develop the disorder in this period. PPTD is most often subclinical but some women will experience symptoms such as lack of energy and depression in the hypothyroid phase. The thyroid gland, which normally enlarges during pregnancy, will remain enlarged or enlarge further in the postpartum period in a significant number of affected women, instead of returning to the prepregnancy size as in unaffected women. The gland is painless and histologically demonstrates lymphocytic infiltration. PPTD is strongly associated with the presence of antimicrosomal and/or antithyroglobulin antibodies, which occur in up to 76% of cases. Antibody activity tends to increase in the postpartum period and to peak at the time of onset of the disorder. TSH receptor antibodies are not seen and the gland has low radioiodine uptake, distinguishing PPTD from Graves' disease. The HLA associations are controversial, as is the role of dietary iodine. The etiology of PPTD is almost certainly immunological, reflecting the phenomenon of rebound from the relative immune tolerance of pregnancy. Detection of the disorder is important in order to reassure or treat those who are symptomatic and because PPTD may recur in subsequent pregnancies. In addition, up to one third of affected women will go on to develop permanent hypothyroidism 2 to 4 years later. The role of screening for PPTD remains to be clarified.
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PMID:Postpartum thyroid dysfunction. 152 73

There is an increasing use and variety of beta-adrenoceptor blocking agents (beta-blockers) available for the treatment of hyperthyroidism. Recent comparative studies suggest that atenolol (200mg daily), metoprolol (200mg daily); acebutolol (400mg daily), oxprenolol ( 160mg daily), nadolol ( 80mg daily) and timolol (20mg daily) produce a beneficial clinical response equal to that seen with propranolol ( 160mg daily). Most beta-blockers reduce resting heart rate by approximately 25 to 30 beats/min, although a lesser reduction is seen with those possessing intrinsic sympathomimetic activity such as oxprenolol and pindolol. While earlier studies employing large doses of intravenous propranolol concluded that beta-blockade reduced myocardial contractility, more recent non-invasive studies suggest that the predominant cardiac effect is on heart rate. In patients with cardiac failure, beta-blockers may, however, produce a profound fall in cardiac output. Nevertheless, in combination with digoxin they may be useful in controlling the atrial fibrillation of thyrocardiac disease. beta-Blockers improve nervousness and tremor (although to a lesser extent with cardioselective agents) and severe myopathy, and they also reduce the frequency of paralysis in patients with thyrotoxic periodic paralysis. There is often subjective improvement in sweating but usually no major effect on eye signs. Recent studies show a 10% reduction in oxygen consumption/basal metabolic rate with long term oral use of selective or nonselective beta-blockers. In addition, many agents (propranolol, metoprolol, nadolol and sotalol but not acebutolol, atenolol or oxprenolol) reduce circulating tri-iodothyronine (T3) concentration by between 10 and 40%, although the clinical significance of this effect (if any) is not established. beta-Blockers may also have endocrinological effects on gastrin, cyclic AMP, catecholamines and other hormone levels. Given in adequate dosage, propranolol has been shown to control thyrotoxic hypercalcaemia. Minor side effects (nausea, headaches, tiredness, etc.) are quite common but overall beta-blockers are well tolerated by the thyrotoxic patient. The major use of these drugs is in symptomatic control while awaiting definitive diagnosis or treatment. As an adjunct to antithyroid drugs or radioactive iodine, beta-blockers will produce a satisfactory clinical response in the weeks to months before these forms of therapy produce a euthyroid state. beta-Blockers are more convenient than antithyroid drugs in the control of patients receiving therapeutic radioiodine, in that continuous therapy and assessment of biochemical response is possible.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Use of beta-adrenoceptor blocking drugs in hyperthyroidism. 614 1

A 47-year-old housewife was admitted to our hospital because of general fatigue and constipation suggesting hypothyroidism. For 3 years before admission, general fatigue, arrhythmia, dry skin, drowsiness, cold intolerance and hypermenorrhea occurred insidiously. She had habitually taken considerable amounts of seaweed every day, e.g. more than 50 g of " Kombu " for more than 5 years and at least 1 g of " Wakame " for 6 months. On admission, serum thyroxine (T4) was 1.3 micrograms/dl, serum triiodothyronine (T3) was 47 ng/dl, TSH was 132 microunits/ml, and 123I thyroidal uptake was 60% at 3 hr. and 75% at 24 hr. Anti-thyroglobulin hemagglutination antibodies and anti-thyroid microsomal hemagglutination antibodies were both negative. When seaweed was omitted from her diet, T4 rose to 6.3 micrograms/dl and T3 rose to 113 ng/dl, whereas TSH lowered to 11 microunits/ml in 2 weeks. The seaweed-free diet was continued and 4 months later, when she had become euthyroid, an open biopsy of the thyroid gland was carried out. Histological examination of the specimen revealed a marked colloid deposition without characteristic features of Hashimoto's disease. Five months after admission, with the daily administration of 100 mg potassium iodide (KI), the effects of inorganic iodide on thyroid function had begun to be seen. On the 16th day of the KI regimen, palpitation and tachycardia (pulse rate 160/min.) with multifocal ventricular premature beat appeared, and T4 on the 11th day was 5.9 micrograms/dl, which was clearly lower than the pretreatment level of 8.4 micrograms/dl. KI was discontinued on the 16th day, and one week after the withdrawal, T4, T3 and TSH all returned to the pretreatment level. For more than 3 years on a seaweed-free diet, she remained euthyroid without any thyroid regimen. To see the effects of inorganic iodide on thyroid function after this long period on a seaweed-free diet, KI was again administered. One hundred mg/day KI for 14 days followed by 200 mg/day for 21 days had virtually no effect on T4, T3 and free T4 and she remained well. None of the perchlorate discharge tests performed on 3 occasions during the 6 month period after the initiation of the seaweed-free diet showed a discharge.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A case of iodide myxedema observed for 3 years under a low iodide diet--especially on the restoration of the mechanism of escape from the Wolff-Chaikoff effect]. 674 70

A 72-year-old man with epiphora secondary to bilateral canalicular stenosis resulting from long-term treatment with 0.125% to 0.25% echothiophate iodide (phospholine iodide) drops for glaucoma underwent bilateral conjunctivodacryocystorhinostomies with Jones' tubes. Within days after undergoing this surgery, he experienced severe unexplained diarrhea, fatigue, weight loss, and prostration. He cancelled his postoperative ophthalmic appointment because of "medical illness." He required admission to his local hospital where extensive studies were done in an attempt to establish the cause of this life-threatening condition. After stopping the echothiophate iodide drops, all symptoms disappeared within two days. Drug toxicity is a previously unreported complication of conjunctivodacryocystorhinostomy, and this case demonstrates that topical medications have enhanced systemic absorption after lacrimal surgery with placement of fistulizing prosthetic devices. One must be aware of this possible complication, not only with long-acting anticholinesterases, but with topical sympathomimetic drugs (especially in cardiac patients) as well as cycloplegic agents in children.
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PMID:Phospholine iodide toxicity and Jones' tubes. 739 39

Cases of hypothyroidism and hyperthyroidism associated with amiodarone therapy are described, and the mechanisms, clinical appearance, and management of amiodarone-induced thyroid dysfunction are discussed. A 72-year-old man with a history of recurrent ventricular tachycardia unresponsive to conventional antiarrhythmic drugs was started on amiodarone therapy. Initially he responded well, but after three months he began to have fatigue, dry skin, and intolerance of cold. His serum thyroid-stimulating hormone (TSH) concentration had risen from 4.4 microU/mL before amiodarone therapy began to 20 microU/mL, consistent with hypothyroidism. He was started on sodium levothyroxine for thyroid hormone replacement; the dosage was adjusted in accordance with subsequent TSH measurements. His hospital course was complicated by congestive heart failure. The second patient was a 43-year-old man with a history of atrial fibrillation who developed hyperthyroidism when placed on amiodarone therapy. He had persistent sweating, intolerance of heat, restlessness, and tachycardia. Thyroid function tests confirmed the presence of hyperthyroidism. The patient was treated with propylthiouracil and propranolol, and amiodarone was discontinued. He remained unresponsive to the propylthiouracil, which was discontinued, and was scheduled for radioactive iodine treatment. The mechanism of amiodarone-induced thyroid dysfunction may involve the large iodine content of the drug. Amiodarone-induced hypothyroidism may range in severity from mild symptoms to severe myxedema; the skin, hair, and nails are particularly affected. Persons with clinical hyperthyroidism secondary to amiodarone treatment show the signs and symptoms of a hypermetabolic state resulting from thyroid hormone excess. Amiodarone-induced hypothyroidism is treated with levothyroxine and hyperthyroidism with antithyroid drugs. Amiodarone can cause thyroid dysfunction, which can have serious consequences.
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PMID:Amiodarone-induced thyroid dysfunction. 825 59

We report herein a case of amyloid goiter associated with rheumatoid arthritis in which hypothyroidism was observed. A 52-year-old housewife who had suffeed from rheumatoid arthritis for 15 years was referred to our hospital because of general fatigue. On admission, a large goiter was observed. Laboratory data showed primary hypothyroidism. Renal biopsy and gastric mucosa biopsy showed amyloid deposition of AA-type. Thyroid biopsy showed massive amyloid involvement. Although the findings of iodine-123 scintigraphy, technetium-99m pertechnetate scintigraphy, computed tomography and magnetic resonance image studies were similar to those for goiter associated with chronic thyroiditis, tallium-201 chloride scintigraphy gave a differing result, demonstrating absent uptake at 3 hours in this case. Replacement therapy with levothyroxine relieved the symptoms. This case was unusual in that amyloid goiter presented clinically as hypothyroidism. Absence of tallium-201 chloride uptake at 3 hours may be a diagnostic specificity for amyloid goiter in differentiating its hypothyroidism from that caused by chronic thyroiditis.
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PMID:Amyloid goiter: radiological study in a case presenting hypothyroidism. 882 Sep 91

A fifty-year-old woman was admitted to our hospital because of palpitation and general fatigue. She had received hemithyroidectomy for thyroid papillary adenocarcinoma at 28 years of age. She had experienced episodes of repeated painless thyroiditis five times over the last 12 years. At her sixth episode of thyrotoxicosis, she was suspected to have Graves' disease and admitted to our hospital. Laboratory findings revealed thyrotoxicosis with positive thyroid stimulating antibody and high radioactive iodine uptake, i.e. Graves' disease. Painless thyroiditis often relapses but rarely develops into Graves' disease. This is a rare case in which repeated painless thyroiditis was followed by Graves' disease. The relation between painless thyroiditis and Graves' disease is discussed.
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PMID:A case of repeated painless thyroiditis followed by Graves' disease. 882 26


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