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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Authors describe an adult case of hypothyroid myopathy which occurred after a Hashimoto's thyroiditis. Ultrastructural examination of the deltoid muscle showed two fundamental changes: 1) large collections of mitochondria generally normal in shape, structure and size, especially in the subsarcolemmal sapce of the muscle fibre; 2) glycogen deposits both beneath sarcolemmal membrane and between myofibrils. Histochemical examination reveals an increased activity of mitochondrial oxydative enzymes, such as NADPH and SDH especially in subsarcolemmal regions of many type I fibres. The histogram is normal. It seems that the multiplication of skeletal muscle mitochondria may be compensatory to the slowing down of metabolic activities. This, however, is ineffective because it involves the mitochondria localized more superficially in the fibres with a loosely coupled oxydative phosphorylation. Glycogen accumulations are probably due to deficiency of the thyroid hormone; in fact stimulation of carbohydrate metabolism by thyroxine is well known. The abnormal functioning of the muscular mitochondria and the defective utilisation of glycogen are the most important factors in the pathogenesis of muscular weakness of hypothyroid myopathy.
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PMID:[Hypothyroid myopathy: histochemical and ultrastructural features with physiopatological correlations (author's transl)]. 15 85

Every patient with myxedema has hypothyroidism, but not every hypothyroid patient has myxedema. It often is possible to diagnose myxedema on clinical grounds alone. Characteristic symptoms are weakness, cold intolerance, mental and physical slowness, dry skin, typical facies, and hoarse voice. Results of the total serum thyroxine and free thyroxine index tests usually will confirm the diagnosis. L-thyroxine is the treatment of choice for myxedema, but it must be given to elderly patients with extreme caution. The transition from the hypothyroid to the euthyroid state brings about changes that put an added burden on the heart. The patient's clinical status and results of thyroid function tests determine the proper maintenance dose. Myxedema coma is rare but often fatal. It occurs most often in elderly women and may be mistaken for one of the chronic debilitating diseases common to this age group. Primary treatment is prompt administration of adequate doses of thyroid hormone--either l-throxine given intravenously of L-triiodothyronine given by nasogastric tube. It also is essential to identify and treat the condition precipitating the coma.
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PMID:Diagnosing and treating myxedema and myxedema coma. 62 51

Two patients with proximal muscle weakness and marked elevations of serum muscle enzymes were initially believed to have polymyositis; however electromyography and muscle biopsies were normal. Both patients were subsequently found to have hypothyroidism. Each regained her muscle strength, and serum enzymes normalized with thyroid hormone replacement. Because muscle weakness and an elevated creatine phosphokinase occur in most patients with hypothyroidism, thyroid dysfunction must be considered in the differential diagnosis of polymyositis.
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PMID:Hypothyroidism presenting as a polymyositis-like syndrome. Report of two cases. 99 45

To investigate respiratory muscle strength in patients with hypothyroidism, global respiratory muscle strength was assessed by measuring mouth pressure during PImax and PEmax efforts. Maximum pressures, VC, FEV1, FVC, T3, T4, and TSH were measured in 43 hypothyroid patients. Measurements were made before and three months after replacement therapy with thyroxine. The results showed that the mean value of PImax and PEmax increased after treatment. Significant change was found in the mean value of VC, FEV1, and FVC after treatment but not in the FEV1/FVC ratio. A highly statistically significant linear relationship was found between PImax and TSH and between PEmax and TSH as well as between PImax and T3 and PEmax and T3. We conclude that hypothyroidism affects respiratory muscle strength and that this weakness is linearly related to thyroid hormone levels. Respiratory muscle weakness is present in both inspiratory and expiratory muscles and is reversible with treatment.
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PMID:Respiratory muscle strength in hypothyroidism. 162 51

Hyperthyroidism is accompanied by significant dysfunction of both proximal and distal skeletal muscles. The purpose of this study was to quantitate the degree of muscle weakness in newly diagnosed patients with Graves' disease and to assess the response to treatment. Ten patients were prospectively studied with objective measures of strength and endurance of proximal and distal muscles while hyperthyroid (stage I), after 2 weeks of propranolol (stage II), and about 6 months later when euthyroid (stage III). Propranolol treatment for 2 weeks resulted in a subjective decrease in weakness, which was accompanied by a statistically significant improvement in grip strength (P less than 0.01), shoulder strength (P less than 0.02), and grip endurance (P less than 0.01) but not shoulder endurance. Muscle function further improved and attained control levels when the patients were chemically and clinically euthyroid. In contrast, a control group subjected to the same muscle testing protocol before and after 1 week of propranolol treatment showed no improvement in grip, shoulder strength, or shoulder endurance but had decreased grip endurance (P less than 0.01) and increased subjective weakness. These results confirm that muscle weakness commonly is associated with hyperthyroidism and can be quantitatively profound. In contrast to the effects of beta-blockade in normal controls, propranolol partially improves muscle weakness in thyrotoxic patients. We conclude that thyroid hormone and catecholamines in concert mediate the muscle dysfunction of hyperthyroidism.
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PMID:Hyperthyroid myopathy and the response to treatment. 168 15

We have reported two cases of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) associated with Graves' disease. Case 1: a 45-year-old woman noticed a diffuse goiter, palpitation and emaciation in 1977. Laboratory studies confirmed that she had Graves' disease, and she was treated with antithyroid drug. In 1986, when the hyperthyroidism was subsided, she showed progressive symmetrical weakness and numbness in her limbs, and she was almost in tetraplegia at 1987. Markedly slowed motor and sensory nerve conductions and elevated CSF proteins as well as clinical manifestations confirmed the diagnosis of CIDP. Following corticosteroid-pulse therapy and plasmapheresis resulted in good recovery in both motor and sensory impairment, though two-times of relapses were observed. Case 2: a 33-year-old man first noticed weakness in his legs in 1977, motor and sensory disturbances progressed for 12 years. Slowed nerve conduction, high CSF proteins and two-times of relapses in early phase indicated that the CIDP was the diagnosis. In 1989 he complained general fatigue, hyperhidrosis and body-weight loss. The serum thyroid hormone levels were high, and other laboratory studies confirmed the presence of Graves' disease. The cases with both CIDP and Graves' disease has rarely been reported. The background mechanism of this association is not well understood, but the susceptibility to CIDP and Graves' disease may be related to the HLA antigens and immunoglobulin Gm allotypes of which are the genes linked to the major histocompatibility complex and controlling immune responses. The present two cases commonly shared several HLA-DR antigens, but their significance should be confirmed by examining many cases.
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PMID:[Two cases of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) associated with Graves' disease]. 178 65

We studied 20 patients afflicted with primary hypothyroidism and treated with thyroid hormone replacements, with the aim of evaluating the clinical, biochemical, EMG and anatomo-pathological effects. Cramps, as well as subjective and objective proximal muscular weakness, disappeared. Seric CPK was normalized in all cases after 1-8 weeks of treatment. EMG myopathic patterns faded away in all cases. Anatomopathological changes took longer to observe; 5 cases with new biopsy showed an isolate atrophy of type II fibers, one of them after 18 months in treatment; type I fibers had mitochondrial accumula without change compared to the initial biopsy. There was a clear tendency for the destroyed fibers to become normalized and for the structures similar to the "core" to vanish.
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PMID:[Thyroid myopathy. Effect of treatment with thyroid hormones]. 210 62

The clinical and electrodiagnostic findings before and during 6 years of therapy are reported in a 59-year-old man with severe hypothyroidism. He had severe sensory neuropathy, carpal and tarsal tunnel syndromes, mild motor neuropathy and moderately severe myopathy. The sensory signs and symptoms disappeared in the 3rd and 4th years of treatment, respectively. Muscle cramps and pain subsided within 2 years, but mild proximal muscle weakness and atrophy persisted. The sensory distal latencies remained slightly prolonged and the electromyographic changes improved. This case shows that thyroid hormone replacement eliminates the neuropathic manifestations of severe hypothyroidism. In contrast, the myopathic features, such as weakness and muscle wasting, may persist despite maintenance of the euthyroid state.
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PMID:Hypothyroid neuropathy and myopathy: clinical and electrodiagnostic longitudinal findings. 239 52

Myocardial infarction is very rare in women under the age of 40 amounting to only .3-.57% of cases according to Polish studies, and it is 10 times less in women than in men. Nevertheless, the use of contraceptives has been implicated in triggering it by diminishing the synthesis of antithrombin III. The use of alcohol can cause the reduction of the fibrinolytic activity of the blood. The case of a 33- year old female patient, a laborer in a brewery is presented, who sought medical help from the company medical staff after 2 weeks of generalized weakness, vertigo, chest pain, and loss of breath under strain. Physical labor had to be discontinued. EKG (electrocardiogram) showed extensive primary and secondary myocardial infarction in progress. She had been taking contraceptives for 3 weeks (1 pill of Femigen once a day). She was drinking 50 g of alcohol daily in the form of 1 liter of beer. She did not smoke, and no circulatory disorder was ascertained. Laboratory tests showed no disorder of aminotransferase or LDH activity, but fibrinogen level (23.5 mcmol/1), antithrombin III level (.124 g/l), and fibrinolysis time (320 minutes) values were abnormal. There was no disorder in the lipid and carbohydrate metabolism, and thyroid hormone level was normal. traditional therapy was prescribed for 2-3 weeks of the infraction: nitrates, rest and avoidance of physical exertion. After administration of castor oil, 2 weeks late an EKG test showed the normalization of all parameters of blood coagulation, and the HDL cholesterol level also dropped. The concomitant use of contraceptives and alcohol can increase the risk of myocardial infraction, therefore they should not be used together, but if such a situation occurs, the control of blood coagulation parameters must be undertaken.
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PMID:[A case of extensive myocardial infarction in a young woman as a complication of oral contraceptives and alcohol]. 245 8

A patient with Graves' disease associated with severe muscle weakness who was finally diagnosed as polymyositis by pathological examination of the muscle is reported. A 28-year-old women was incidentally found to have hyperthyroidism when she consulted a hospital for the evaluation and treatment of anemia in 1979. She was treated with methimazole for approximately a month when she stopped the medication by herself. Approximately two yr later (Nov. 4, 1981) she consulted another hospital with complaints of palpitation and muscle weakness. Diagnosis of hyperthyroidism due to Graves' disease and thyrotoxic myopathy were made, followed by the treatment with radioiodine (4 mCi of 131I). She was further treated with propylthiouracil (PTU). Four yr after the treatment, serum thyroid hormone concentration declined to the lower level than normal and serum TSH concentration increased. She was subsequently treated with synthetic I-T4. Despite the fact she became euthyroid with the treatment, muscle weakness as well as elevated concentrations of muscle enzymes were not improved. Muscle biopsy was made in July 1983, and she was diagnosed as immune polymyositis and treatment with prednisolone and cyclophosphamide in addition to PTU or I-T4, was started. With the treatment, serum LDH decreased to the normal range. However she still has muscle weakness and serum concentrations of CPK and aldolase are still in higher levels than normal range.
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PMID:A case of Graves' disease associated with polymyositis. 209 Jun 76


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