Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027121 (myositis)
 4,538 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 15 patients with rheumatoid arthritis (RA) and in 12 age- and sex-matched normal subjects, we evaluated inspiratory muscle strength and respiratory control system. Inspiratory muscle strength was assessed by measuring maximal inspiratory pressure (MIP). Respiratory drive was assessed by evaluating surface electromyographic activity of the diaphragm (EMGd) during both room-air breathing and hypercapnic rebreathing. Compared to the predicted value (mean +/- 1.65 SD), MIP was significantly reduced in nine patients (60%). All told, we noticed a significant inverse relationship in the patients between MIP and duration of steroid therapy (p less than 0.01). During room-air breathing, both EMGd and mouth occlusion pressure (P0.1), expressed both in actual values and as percentage of MIP, were significantly greater in patients than in the normal control group (p less than 0.001 for both). Both EMGd and P0.1 (%MIP) response slopes to CO2 were significantly greater in patients than in the normal control group (p less than 0.01 and p less than 0.001, respectively) and significantly related to the functional stage of disease. During quiet breathing and for a PETCO2 of 60 mm Hg, both EMGd (p less than 0.01 and p less than 0.05, respectively) and P0.1 (%MIP) (p less than 0.01 and p = 0.001, respectively) were inversely related to MIP. These results indicate that RA patients may exhibit inspiratory muscle weakness and increased respiratory drive. Steroid myopathy and rheumatoid myositis could explain the reduction in MIP, whereas neural afferents arising from respiratory muscle, lung, or joint receptors could be involved in the observed increase in neural drive.
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PMID:Inspiratory muscle strength and respiratory drive in patients with rheumatoid arthritis. 238 91

Twenty-two chronic alcoholic patients were assessed by neurologic examination and muscle biopsy. The patients manifested proximal muscular weakness to a variable extent. One case presented as an acute bout of myopathy, according to the Manual Muscle Test, MMT. The most prominent histologic feature observed was muscle atrophy (95.3%) better evidenced through the ATPase stain with the predominance of type II A fibers (71.4%). Lack of the mosaic pattern (type grouping) seen in 76% of the cases and an important mitochondrial proliferation with intrasarcoplasmatic lipid accumulation in 63% of the patients. In case of acute presentation of muscle weakness the pathological substrate is quite different, i.e. presence of myositis mainly interstitial characterized by lymphoplasmocytic infiltrate and several spots of necrosis like Zencker degeneration. Based on histologic criteria, our data suggest that: the main determinant of muscle weakness seen in chronic alcoholic patients is neurogenic in origin (alcoholic polyneuropathy); the direct toxic action of ethanol under the skeletal muscle is closely related to the mitochondrial metabolism; the so-called acute alcoholic myopathy has probably viral etiology.
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PMID:[Histochemical study of the skeletal muscle in chronic alcoholism]. 248 Jul 68

A man with IgG1 multiple myeloma developed fever, confusion, and progressive muscle weakness resulting in paralysis. Echovirus type 11 was isolated from cerebrospinal fluid, pleura, pleural fluid, and muscle, and muscle biopsy disclosed changes consistent with viral myositis. Immunologic evaluation revealed low serum levels of polyclonal IgG subtypes 1 and 3, reduced blood levels of T-helper/inducer and T-suppressor/cytotoxic cells, and a complement abnormality involving the function of the classical pathway C3 convertase, C4b2a. Therapy with intravenous immunoglobulin was associated with clinical recovery. This is the first reported case of disseminated central nervous system enteroviral infection in an adult with a B-cell malignancy, and in association with a documented complement abnormality. The findings suggest the efficacy of immunotherapy in this disease.
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PMID:Disseminated echovirus infection in a patient with multiple myeloma and a functional defect in complement. Treatment with intravenous immunoglobulin. 252 14

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

The authors report two male patients with inclusion body myositis (IBM) and review the features of this condition in the literature. This is an uncommon type of idiopathic myositis which involves males more often than females; it usually develops in elderly patients; its course is very slow; it is usually associated with distal weakness; neurophysiological studies show a mixed "myogenic" and "neurogenic" pattern; and it is usually unresponsive to corticosteroids. The diagnosis is basically made on the basis of the histological features, mainly consisting of vacuoles surrounded by a basophilic haze in histochemical stains of frozen tissue and, particularly, by the presence of characteristic microfilaments in ultrastructural studies.
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PMID:[Myositis with inclusion bodies: a little-known variety of idiopathic inflammatory myopathy]. 255 35

Toxic myopathies are an uncommon manifestation of chemotherapeutic agents. Most myopathies are characterized by a weakness affecting proximal limb-muscles more than distal ones. Steroids, chloroquine and ipecac syrup are the most common drugs inducing myopathies. Toxic myositis is rare and reported with D-penicillamine abuse. Myotoxicity of local agents injection such as anesthetics, steroids or antibiotics is also known. Congenital myopathies such as malignant hyperthermia, hypokalemic periodic paralysis or paroxysmal myoglobinuria may also be induced by drugs but are very rare.
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PMID:[Muscular diseases in relation to drug consumption]. 256 73

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

Antibodies to a 56 kDa nuclear protein have been found in the sera of 85% of patients with myositis using an immunoblotting technique. This auto-antibody appears to be relatively disease-specific though more frequently detectable in both adult and childhood onset dermatomyositis. In adult patients with myositis the anti-56 kDa antibody level reflects disease activity. This antibody is thus much more frequently found than previously described disease-specific autoantibodies in patients with myositis such as the Jo-1 antibody, and may represent a useful diagnostic aid in patients with muscle weakness.
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PMID:Autoantibodies against a nuclear 56 kDa protein: a marker for inflammatory muscle disease. 261 71

This article reviews the clinical features and emphasises the treatment of polymyositis and dermatomyositis. Pharmacological intervention with corticosteroids and immunosuppressive agents is discussed. In addition, strategies regarding the initiation and subsequent tapering of these drugs are provided, and an algorithmic approach to the management of myositis is provided. Therapeutic modalities for patients with refractory disease are considered, and the potential adverse effects of such treatment are discussed. Since patients with myositis often have disease-related complaints other than muscle weakness, a practical treatment approach for these problems is also outlined.
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PMID:Current management of polymyositis and dermatomyositis. 265 93

Dermatomyositis in childhood is an uncommon disease, affecting muscle and skin. The disease usually has an insidious onset; the proximal muscle groups are classically more affected than the distal group. If left untreated, the disease will either spontaneously arrest or will progress until the child is completely bedridden, with death secondary to hypoventilation and aspiration. For a definitive diagnosis 3 or 4 of the following criteria (plus rash) are required: 1) symmetrical limb girdle weakness; 2) muscle biopsy evidence of myositis and muscle necrosis; 3) elevation of muscle enzymes; 4) electromyographic changes of myositis. The main pathologic feature of juvenile dermatomyositis is vasculitis affecting small arteries and veins of muscle, skin and gastrointestinal tract. Whether muscle from patients with polymyositis contains a specific auto antigen or is contaminated with an immunogenic infectious agent such as a virus (coxsackie virus, for instance) remains unclear. Childhood dermatomyositis is almost uniformly responsive to steroid treatment; there is a good chance of remission with minimal risk of secondary complications with an initial low dosage of prednisone (1 mg/kg/day). The use of additional drugs such as azathioprine, methotrexate or cyclophosphamide is reserved for patients who are either not completely responsive to steroids or difficult to wean off steroids. Cyclosporine A has been proposed to achieve a reduction in steroid dosage.
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PMID:[Dermatomyositis in children]. 271 39


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