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 33-year-old black woman with advanced acquired immunodeficiency syndrome (AIDS) presented with rapidly progressive muscle weakness and serologic and radiologic evidence of central nervous system Toxoplasma infection. Muscle biopsy revealed an inflammatory infiltrate predominantly composed of macrophages and T suppressor/cytotoxic cells. Human immunodeficiency virus major core protein (p24) was also detected in macrophages and damaged muscle cells around the inflammatory infiltrates. The patient improved clinically with glucocorticoid therapy for polymyositis and pyrimethamine and clindamycin therapy for toxoplasmosis.
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PMID:Inflammatory myopathy and acquired immunodeficiency syndrome. 246 39

We have used automatic decomposition electromyography (ADEMG) to study 41 muscles in 29 patients with well-defined peripheral and central motor disorders. In motor neuron diseases motor unit action potentials (MUAPs) showed increased amplitudes, firing rates and firing variability. Relatively large MUAPs sometimes were not identified by the computer program if they lacked sufficient high-frequency signal content, or were too variable in shape. In myopathies the MUAPs showed reduced amplitudes, durations and turns, and sometimes dramatic increases in firing rates. Also, the mean number of MUAPs per recording site was often increased, indicating excessive recruitment. In polymyositis (the best studied myopathy) the nature and magnitude of the MUAP shape and firing abnormalities were usually similar at different levels of contractile force, suggesting that motor units are affected without regard to recruitment order. In upper motor neuron paresis (multiple sclerosis), the shape properties of the MUAPs were normal, but mean firing rates were reduced, and firing variability increased. These findings confirm many of the traditional criteria for distinguishing neurogenic from myopathic disease electrophysiologically at the level of the individual MUAP. In addition, they demonstrate the potential diagnostic sensitivity of MUAP firing rate measurements for detecting neuromuscular dysfunction, and for differentiating between some cases of central and peripheral paresis, but not for distinguishing peripheral neurogenic from myopathic weakness, since firing rates tend to increase in both. Increased firing rate variability may be a marker of central or peripheral neurogenic weakness.
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PMID:Motor unit firing rates and firing rate variability in the detection of neuromuscular disorders. 247 26

A case of myasthenia gravis accompanied with polymyositis and malignant thymoma, detected immune complexes in the sera and around the muscle fibers, was described. A 37-year-old woman was admitted to Shinshu University Hospital in September, 1987 because of dyspnea, dysphagia and muscle weakness. She first noticed her right blepharoptosis 3 weeks before admission. Weakness of all four limbs and myalgia of lower extremities were noticed one week later. These symptoms got worse and nocturnal dyspnea, dysphagia and easy fatigability at mastication appeared. On admission, she looked ill and neurological examination revealed left blepharoptosis, bilateral facial weakness, weakness of all four limbs, more prominent in proximal muscles and tenderness of lower extremities. Edrophonium test was positive, improving her muscle weakness. Laboratory examination revealed the elevated serum levels of CK, the increased titre of circulating immune complexes and high titres of acetylcholine receptor antibodies and anti-skeletal muscle antibodies. Electromyographic study showed myogenic pattern and Harvey-Masland test revealed waning at low frequency stimulation. Muscle biopsy showed marked perivascular infiltration of lymphocytes, accompanied by phagocytosis and interstitial fibrosis. IgG deposits were shown around the muscle fibers exclusively around the infiltrates of mononuclear cells. Granular deposits of C3 were also shown specifically around the muscle fibers exclusively around the infiltrates of mononuclear cells. Thymectomy was performed on September 21, 1987. Invasion of thymoma, predominantly lymphocytic type, to right lung and pericardium was observed histologically. After thymectomy, she got better. Immunological data and immunohistochemical examination of the present case suggest that in the case of myasthenia gravis accompanied with polymyositis and malignant thymoma, immune complexes may play a primary role on the pathogenesis of myositis.
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PMID:[Detection of immune complexes in the sera and around the muscle fibers in a case of myasthenia gravis and polymyositis]. 253 18

Inclusion body myositis (IBM) was suspected on light microscopic grounds in 48 of 170 consecutive patients with inflammatory myopathies. One or more vacuoles containing membranous material, groups of atrophic fibres, and an autoaggressive endomysial inflammatory exudate occurred in 100, 96 and 92% of the muscle specimens. All three of these features were present in 88% of the specimens. Electron microscopy confirmed the presence of filamentous inclusions in 40 of 43 patients. The inclusions are typically near vacuoles and a minimum of three vacuolated fibres must be scrutinized to detect them with confidence. There is no electromyographic pattern that can reliably distinguish IBM from other inflammatory myopathies. The typical clinical features in the patients diagnosed by histological criteria as IBM were: insidious onset after age 50 yrs with painless, proximal lower extremity weakness; slow but relentless progression with selectively severe involvement of quadriceps, iliopsoas, tibialis anterior, biceps and triceps muscles; relatively early depression of the knee reflexes; and a normal or mildly elevated serum creatine kinase level. The male: female ratio was 3:1. Distal weakness occurred in about 50%, but only in 35% was it as great or greater than proximal weakness. Significant associated illnesses include other autoimmune disorders (15%), diabetes mellitus (20%), and diffuse peripheral neuropathy (18%). Prednisone treatment at dose levels frequently effective in polymyositis failed to prevent disease progression in those patients observed for 2 or more years. Our findings support the notion that IBM is a distinct entity in which a set of pathological features is associated with a constellation of clinical findings.
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PMID:Inclusion body myositis. Observations in 40 patients. 254 78

A 55-year-old Japanese male who developed acute polymyositis and chorioretinitis due to toxoplasmosis is described. The patients was well until one month prior to the present admission, when he had an onset of painful swelling of lymphnodes in the posterior cervical region, proximal muscle weakness, myalgia and a partial defect in the visual field of the right eye. He admitted that he had had a chance to eat half-cooked mutton while he had visited Saudi Arabia 40 days before. He was unable to go up and down the stairs at the peak of the illness. Serum CPK was 2050 u/l (N = 5-50) on January 11, 1989. These symptoms improved spontaneously except for the visual field defect. He was admitted to our hospital on January 31, 1989. On admission, neurological examination was unremarkable except for retinal exudate in the right eye which appeared consistent with the clinical diagnosis of toxoplasma chorioretinitis. Serum CPK was 103 u/l, and EMG showed myogenic changes. The IgM-immunofluorescent (IFA) anti-Toxoplasma gondii antibody titer was elevated to 640, and IgG-immunofluorescent antibody to 20480 after IgM-IFA. These clinical and serological findings indicate acute and recent Toxoplasma gondii infection. It appeared likely that Toxoplasma gondii directly caused acute myositis and chorioretinitis. Clinical manifestations of toxoplasma myositis may mimic those of idiopathic polymyositis, however, the clinical course of the former is usually self-limited probably because of generation of antibodies which will inhibit the growth of the organism.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acute acquired toxoplasmosis presenting as polymyositis and chorioretinitis in a Japanese male]. 260 34

There have been few cases of polymyositis in patients with AIDS, and polymyositis is rarely a cause of myoglobinuria. We studied a 20-year-old homosexual man with recurrent myoglobinuria. He was asymptomatic between episodes. Each episode was accompanied by muscle pain, limb weakness, high serum levels of creatine kinase, and pigmenturia. Muscle biopsy showed active necrosis without inflammation or abnormalities of glycolytic or other energy-generating enzymes. Antibodies to HIV were present in serum. Clinical evidence of AIDS has not developed in 2 years. Recurrent myoglobinuria may be another consequence of HIV infection.
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PMID:Recurrent myoglobinuria and HIV seropositivity: incidental or pathogenic association? 260 81

A 67-year-old woman was admitted to our department because of 5 years' duration of proximal muscle weakness. Serum CK was high, and EMG showed myogenic pattern, and muscle biopsy revealed remarkable inflammatory cells infiltrating around the destroyed muscle fibers. Her muscle weakness and hyperCKemia markedly improved by corticosteroid therapy, suggesting that the diagnosis was compatible with polymyositis (PM). In addition, serum calcium was high and phosphate was low. Serum parathormone level significantly elevated. The findings of diagnostic imaging procedures including echography, scintigraphy, and computed tomography of the parathyroid glands suggested presence of parathyroid adenoma with cystic degeneration in the thyroid tissue. There was only one case report of PM associated with primary hyperparathyroidism (PHP) as the literature referred. In this case, we could not prove direct relationship between PM and PHP. The association might have been coincidental. However, PHP might have played some role in the pathogenesis of muscular involvement, or there might be a similar immunological mechanism as seen between PM and malignancy. It is possible that association of PM and PHP is more frequent than generally considered. It may be necessary to pay more attention to find out the association of PM and PHP.
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PMID:[A case with polymyositis associated with primary hyperparathyroidism]. 261 6

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

We report a sporadic case of 12 years old boy with facioscapulohumeral dystrophy (FSHD), sensorineural hearing loss and exudative angioma of bilateral retina. His hearing loss was noted at 9 years, followed by muscle weakness of his right upper extremity at 11 years. Complete neurological examination at 12 years revealed FSH type distribution of muscle weakness with high serum CK level (330 U/L), moderate sensorineural hearing loss and exudative angiomas of bilateral retina. The biopsy from biceps brachii muscle showed advanced dystrophic changes with a dense inflammatory cell infiltration predominating on perivascular distribution and type II fiber predominance. The features of infiltrating lymphocytic surface antigen seen in this case were compatible with those of FSHD rather than those of polymyositis. In the literature, the association of FSHD with hearing loss and retinal vessel abnormalities has been documented on 15 cases as an unusual form of FSHD. However, it has otherwise been noted that the associations of FSHD and hearing loss or retinal vessel abnormalities are unequivocally frequent, Whenever special attention has been made. Morphological examination with light and electron microscopies on the muscle specimen in this patient did not demonstrate any recognizable abnormality such as arterio-venous shunt or thickening of vessel wall basal lamina. However, it cannot be completely excluded that exudation around the abnormal vessel wall in the muscle may play an initial role in the pathogenesis of FSHD. Further morphological survey on vessel abnormalities may be necessary in the FSHD muscle.
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PMID:[A case of facioscapulohumeral muscular dystrophy with sensorineural hearing loss and retinal angioma]. 262 25


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