Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

A case in reported of the clinical syndrome of polymyositis in a young man. The syndrome masked pulmonary tuberculosis. Sudden appearance of pains and weakness of the muscles of the shoulder and abdominal muscles was accompanied by fever up to 40 degrees C, and macular rash on the trunk and extremities. During the disease right-sided pneumonia developed and regressed after treatment with antibiotics (tetracyclines, penicillin). Laboratory investigations showed high ESR, high leucocyte count, high levels of transaminases, CPK and LDH, and in cutaneo-muscular++ biopsy specimen scan subepidermal infiltrations were present. The patient was treated with corticosteroids with a striking improvement of the general condition. During this treatment left-sided pleural effusion developed. Bacteriological examination of the pleural fluid, including tests for acid-fast bacilli, was negative in direct examination, but these bacilli were cultured from fluid. No malignant cells were found. After antituberculous treatment the condition of the patient and the biochemical parameters became normal.
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PMID:[Polymyositis in pulmonary tuberculosis]. 262 70

A case of 16-year-old female with myalgia and myoglobinuria following prolonged exercise was reported. Neurological examination revealed mild weakness of proximal muscle in the lower extremities. Serum CK, LDH, myoglobin were significantly increased during the attacks. On biopsy, the muscle fibers contained myriad lipid-filled vacuoles, in predominantly type 1 fibers. Electron microscope examinations revealed numerous lipid droplets adjacent to mitochondria and glycogen particles. Carnitine level in the patient's muscle was markedly reduced (under 5% of control), but the serum carnitine concentration was normal. The muscle carnitine palmityl transferase level was not depressed. A forearm ischemic test resulted in normal lactate production. On exercise tolerance test by a bicycle ergometer, mild exercise (15-30 watts for 15 minutes) induced myalgia and marked elevation in serum CK, lactate and pyruvate, while severe exercise showed no increase in serum CK level. The findings suggest that the energy production system in the skeletal muscle was impaired. However, the enzyme activities of NADH oxidation in mitochondria and the anaerobic glycolysis pathway were within normal limits. During fasting (36 hours), there was a normal production of ketone bodies, suggesting that hepatic metabolism of lipids was normal. She showed good response to L-carnitine therapy.
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PMID:[Muscle carnitine deficiency associated with myalgia and rhabdomyolysis following exercise]. 274 89

A case of polymyositis with repeated dysphagia and muscle weakness associated with peculiar findings of skin was reported. The patient was a 67-year-old man. His birth and development was normal. There was no family history of neuromuscular disease. On 26th March 1987 he was admitted to a hospital because of dysarthria and dysphagia after fever and diagnosed as having viral myositis. His conditions improved spontaneously with bed rest and he left hospital on 14th April. On 23rd April he had chill and sore throat with fever. On 27th he was admitted to the same hospital because of dysarthria and muscle weakness of the proximal portion of the upper limbs. These symptoms also improved with bed rest. He had repeated these symptoms several times and then he was admitted to our hospital on 12th June. On examination he showed the skin pigmentation under the right eye and the eruption in the back of hands and the buttocks. Muscle weakness was observed in the proximal portion of the upper limbs and the neck flexor. Laboratory tests in admission were as follows: sGOT 49 mU/ml, sGPT 104 mU/ml, LDH 1064 mU/ml, CPK 565 mM/ml, aldolase 25.2 IU/1/37 degrees C. Electromyography showed the typical myogenic changes and biopsy of left biceps brachii revealed inflammatory cells in the muscle fiber which are specific to polymyositis. Immuno-histochemical study is performed to analyse the subpopulation of mononuclear cells in biopsied muscle and skin. Mononuclear cells infiltrated into perimysium, endomysium and epidermis were positive for T11 and T8, but less positive for T4, B1 and Leu11. On the basis of these findings he was diagnosed as having "polymyositis syndrome".
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PMID:[A case of polymyositis with repeated dysphagia and muscle weakness associated with peculiar findings of skin]. 280 15

A 34-year-old woman noted difficulty of gait initiation, then dilated finger opening and hyperhidrosis appeared. Her stature was a muscular habitus, and muscle stiffness and myokymia were found in all muscles of the extremities. Her stiffness persisted during sleep. Her calf muscles were large and a contracture was noticed in ankle joints. There was no evidence of wasting and weakness. A remarkable delay in voluntary relaxation of the contracted muscles without percussion myotonia was recognized. Tendon reflexes of lower extremities were absent. Laboratory examination revealed elevation of CPK, LDH, myoglobulin, aldolase and basal metabolic rate (BMR). An extraband of CPK isoenzyme between MB and MM fraction was observed. The thin layer gel filtration technique and immunofixation technique showed that this extraband was complexes of CPK and IgA, and light chain of the CPK linked IgA was lambda type. All other laboratory tests were normal for the following: urinalysis, ESR, a blood count, liver function, kidney function, glucose, rheumatoid factor, CRP, thyroid function, parathyroid function, serum electrolytes, ECG, EEG, cranial CT, without slight elevation of IgA, and CSF protein. In needle EMG and surface EMG spontaneous discharges were recorded at rest. These discharges consist of normal motor unit potentials, doublets, and triplets in needle EMG. The discharges were markedly reduced after the median nerve block with xylocaine. In needle EMG, myotonic discharge was not observed. Nerve conduction velocities were within normal ranges. According to these data, she was diagnosed as having Issacs' syndrome (continuous muscle fiber activity syndrome). Carbamazepine, 200 mg daily was administrated and showed a dramatic reversal of the symptoms.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of Isaac's syndrome--continuous muscle fiber activity syndrome]. 373 Jan 94

A 36 year old woman was admitted to the hospital in November 1983 because of her inability to walk. For 3 months prior to admission, she took oral contraceptives (OCs) as a treatment for amenorrhea. 2 months prior to admission, she had general malaise, anorexia, and unsteady gait. 1 month before her admission, tingling and numbness began in the fingertips and spread up to the forearms, a tight feeling around the waist developed, and walking became ataxic. On admission to the hospital, she was thin and pale with greying hair. Her mind was clear and there were no abnormalities of the cranial nerves. Her extremities were hypotonic but not wasted. Slight muscle weakness of the hands and feet was noted. There was myokymia in both legs. Deep tendon reflexes of the extremities were absent. The plantar responses were extensor and lack of coordination in the extremities was noted. There was a definite glove and stocking type of hypesthesia to pinprick and cotton wool. Vibration sense was decreased below T11 and lost in both legs. There was a marked loss of position sense to passive movement in the legs and some impairment in the hands. Laboratory examination revealed mild magaloblastic anemia, elevated LDH, borderline low concentration of vitamin B12 in the serum, increased excretion of methylmalonate in the urine, achylia, positive antiparietal cell antibody and positive anti-intrinsic factor antibody. Cyanocobalamin absorption by the Schilling test was 5.6% after intrinsic factor, 11.3%. The diagnosis of pernicious anemia was made. Upper gastrointestinal studies showed typical carcinoid tumors of the stomach. Cerebrospinal fluid was normal. Peripheral nerve conduction studies demonstrated normal or slightly decreased motor conduction velocities and absent sensory action potential. Sural nerve biopsy was performed. Myelinated fibers were moderately decreased in number to 5554/mm squared and pronounced loss of large myelinated fibers was demonstrated in fiber histogram. Teased method of the single fiber showed mainly axonal degeneration. Anemia and neurologic function improved rapidly with parenteral hydroxocobalamin therapy and 1 month after treatment commenced, she was able to walk without assistance. The clinical significance of peripheral nerve involvement of subacute combined degeneration of the spinal cord was discussed, as the peripheral nerve affection is only poorly understood in contrast to the myelopathy. This was followed by discussion of the possible effect of the OCs and gastric carcinoid to neurological manifestation of pernicious anemia. (author's modified)
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PMID:[Subacute combined degeneration of spinal cord. Significance of peripheral nerve involvement]. 401 64

Sixty steroid-treated patients with asthma were evaluated for the presence of muscle weakness by use of both manual muscle testing and the Cybex II isokinetic dynamometer. The patients were compared to age and sex-matched sedentary control subjects. Forty-eight percent of the patients (12/25) taking greater than or equal to 40 mg per day of prednisone had hip flexor strength greater than or equal to 2 SD below the mean of age and sex-matched control subjects by Cybex testing (CT). Sixty-four percent of the patients (16/25) taking greater than or equal to 40 mg per day of prednisone were found on manual muscle testing to have hip flexor weakness. Only one patient taking less than 30 mg per day of prednisone was found to have muscle weakness. Biochemical parameters, including CPK, aldolase, SGOT, LDH, and LDH isoenzymes were measured to assess the degree of steroid-induced muscle damage. They neither correlated with the degree of hip flexor weakness as measured by CT, nor did they discriminate between patients receiving small doses and large doses of steroids. Changes in urinary excretion of creatine did not help to confirm the diagnosis of steroid myopathy. Although CT provides an objective means of assessing muscle strength in these patients, at this time no definitive chemical test is available for the diagnosis of steroid myopathy.
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PMID:Steroid myopathy: incidence and detection in a population with asthma. 401 54

Tremolite is an amphibole which has been implicated in a variety of disease patterns in different parts of the world. It occurs in a number of phases, which are chemically identical but have specific physical characteristics. In an attempt to clarify the epidemiological findings, tremolite fibres of 3 specific forms--A, B and C--were characterized and studied for biological activity by: (i) in vivo intrapleural injection of rats (2 separate experiments--1 with poor survival). (ii) in vitro enzyme release from mouse peritoneal macrophages (iii) in vitro giant-cell formation in A549 cultures (iv) in vitro cytotoxicity for V79-4 cells. Sample C, which contained more long thin fibres than A and B, was alone in producing mesotheliomas. C, but not A or B, induced LDH and B-glucuronidase enzyme release, and induced giant cells. A was not cytotoxic, B moderately cytotoxic and C as highly cytotoxic as UICC crocidolite. The in vivo studies were marred by being split between 2 experiments, of which the second had poor survival. We are aware of the weakness of our in vivo data, but as Tremolite C was being considered for commercial use on the European market we felt it timely to submit our findings for publication.
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PMID:Biological effects of tremolite. 628 Jul 41

Two autopsy cases of congenital muscular dystrophy of Fukuyama type (F-CMD) were described. The first case was diagnosed clinically and pathologically as its typical case. Neither his family history nor the history of his prenatal period were contributory. He had suffered from muscle weakness and atrophy since his birth. Serum CPK was markedly elevated. EMG and muscle biopsy proved dystrophic changes of the skeletal muscles. In addition, he manifested mental retardation and attacks of convulsion. EEG failed to elicit remarkable changes, but PEG represented ventricular dilatation. He died of respiratory insufficiency at age 12. His postmortem examination showed variegated anomalies in the nervous system. Extensive micropolygyria was present in the cerebrum and cerebellum accompanied by adhesions between the bilateral cerebral hemispheres. Assymmetry of the longitudinal fibers was pointed out in the pontine base. Anterior horn cells were atrophic and moderately depopulated. On the other hand, the second patient was an atypical F-CMD case in symptoms, signs and pathology. His grand-mothers on both father's and mother's sides wee first cousins. His three siblings showed no similar disorders. His mother developed slight gestational toxicosis in the sixth and seventh months of pregnancy. His muscle weakness, contracture of the bilateral hip-joints and clubfoot had been observed since his birth. Physical and neurological examinations at age 6 showed deformity of the skull, myopathic face, macroglossia, high-arched palate, pigeon chest, scoliosis of the thoracic spine. In addition, generalized muscular atrophy, hypotonia and areflexia were recognized. Pseudohypertrophy of the muscles was absent. Sensation was intact to all modalities. Serum CPK and LDH were moderately increased.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[2 autopsy cases of congenital muscular dystrophy of Fukuyama type--a typical and an atypical cases]. 652 23

A female patient presented with severe hypokalemia and muscle weakness following chronic abuse of laxatives (Folia Sennae). Parenteral substitution of potassium resulted in complete normalisation of the clinical signs and of the pathologically elevated serum concentrations of CPK, LDH and GOT. The importance of laxatives as a possible cause of severe hypokalaemic conditions is underlined by this case report.
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PMID:[Laxative-induced hypokalemic myopathy. A case history]. 693 Jul 55


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