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)

An accurate differential diagnosis of ptosis results if one refers the functional disorders of the levator to the different levels of the motor unit: Muscle, synapsis, peripheral neuron and nucleus. Therefore ptosis can be classified into myogenic, synaptogenic and neurogenic forms. This classification is also based on electromyographic findings from the levator muscle. Myogenic forms of the ptosis are: Senile ptosis, chronic progressive ocular muscle dystrophy, acute exophthalmic myositis and affections of the levator together with general systemic myopathies. Synaptogenic forms of ptosis are: Botulism and myasthenia gravis. Neurogenic forms of ptosis are: Cortical ptosis, ptosis from lesions of the oculomotor nucleus (congenital ptosis, Moebius-syndrome), peripheral oculomotor palsy, ptosis in aberrant third nerve regeneration, sympathetic ptosis (Horner-syndrome), ptosis in cases of paradoxic innervation such as the Duane retraction-syndrome and the Marcus-Gunn-Jaw-Winking-syndrome (ptosis linked with jaw movement). According to the classification in myogenic, synaptogenic and peripheral-neurogenic forms of ptosis, the therapeutic possibilities (medical, surgical etc.) are discussed.
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PMID:[Differential diagnosis of ptosis (author's transl)]. 97 34

Neuromuscular disorders accompanied by a "myasthenic reaction", but without other symptoms of myasthenia gravis and no therapeutic response to cholinergic drugs may be called myasthenic syndromes. The abnormal fatigability can be shown in the electromyogram. Lasting voluntary contraction of a muscle shows a rarefication of the EMG-pattern. Sometimes during repetitive stimulation of the motor nerve a decrease in the amplitude of the muscle potential may occur. This decrease is poorly influenced by cholinergic drugs. Often this observation was present in patients with myositis and myotonic dystrophy, sometimes in other myopathies and seldom in neurogenic disorders. A failure in the neuromuscular transmission is discussed not only in myasthenia gravis, but also in myasthenic syndromes. But there may be another explanation. A decreased number of intact muscle fibers during lasting innervation will cause a more rapid fatigation of the muscle fibers and in this way there will be an exhaustion. It is discussed, whether the symptoms in myasthenic syndromes can be explained by an abnormal "fatigability".
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PMID:["Fatiguability" in myasthenic syndromes]. 104 94

We describe the cutaneous disorders in 172 patients with thymoma. Myasthenia gravis was the most common additional disease. Cutaneous disorders were found in 34 patients; 19 had skin disorders at the time of diagnosis of thymoma and 15 developed skin disorders after diagnosis of thymoma. Cutaneous fungal diseases were found in fewer than 10% of the patients (tinea pedis excluded). One patient with chronic mucocutaneous candidiasis was included in this group. Two patients with lichen planus, 2 with pemphigus, 2 with myositis, and 1 with lupus-like disease were also included in this study. Patients with skin disorders were no different than patients without these disorders with regard to thymoma histology, age at diagnosis, sex, or presence of myasthenia gravis. There were no associations between these variables and the patients who developed these skin disorders after diagnosis of thymoma. Thymectomy did not alter the clinical course with respect to cutaneous diseases.
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PMID:Dermatologic disorders in patients with thymoma. 244 57

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

Polymyositis and myasthenia gravis-like syndromes have been seen in patients with GVH disease following bone marrow transplantation. We therefore investigated the histopathology of muscle in mice with acute graft-versus-host disease in order to determine whether these conditions are caused by injury from the GVH reaction itself or are due to radiation and drugs used to prepare the host for transplantation. GVH reactions were induced by intravenously infusing 50 x 50(6) lymph node and spleen cells from A/J-strain donors into (C57BL/6 x A/J)F1-hybrid recipients. These mice developed an active inflammatory myopathy beginning 15 days after engraftment. The inflammatory infiltrates were focal in distribution, initially around perimysial blood vessels, and later around muscle fibers. The infiltrating cell population was composed of lymphocytes, plasmacytoid cells, and macrophages. Muscle cell necrosis was observed and was temporally related to elevations in serum creatine kinase. Similar histologic changes were present in the myocardium. Our findings support the notion that muscle involvement in patients with GVH disease is caused by the disease itself. Myositis accompanying experimental GVH disease in mice may hold promise as a model of autoimmune inflammatory myopathy.
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PMID:Inflammatory myopathy in F1 hybrid mice with acute graft-versus-host reactions. 275 59

During the last several years, there has been increasing interest in the use of intravenous immune globulin for immunosuppression. Although the mechanism(s) of action remains to be delineated, immune globulin therapy has been shown to be effective in some antibody-mediated disorders. In Rh disease, antibody-induced cytopenias, myasthenia gravis, and the clotting disorder associated with anti-factor VIII antibody, intravenous immune globulin has had therapeutic benefit. It was of interest that intravenous immune globulin may partially ameliorate the tendency toward dilation of the coronary vessels in Kawasaki disease. If this disorder represents a vasculitis of the small feeding vessels of the coronary arteries, could this agent influence other forms of collagen vascular disease? Pilot studies in dermatomyositis and polymyositis and systemic juvenile rheumatoid arthritis indicate benefit from intravenous immune globulin therapy. In these studies we used a high-dose protocol consisting of 1 gm/kg/day of immune globulin for 2 days every 4 weeks. In patients with either myositis or systemic juvenile rheumatoid arthritis, beneficial effects were seen. In the former group of patients, increased proximal muscle strength and reduction in creatine kinase levels were observed. In the latter group of patients a marked reduction in systemic features was observed. The amount of corticosteroids required was reduced in both groups of patients. These studies indicate the potential for intravenous immune globulin in collagen vascular disorders and the need for carefully controlled trials of this form of therapy.
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PMID:The use of intravenous immune globulin in collagen vascular disorders: a potentially new modality of therapy. 279 2

After a controlled, double blind multicenter trial of D-penicillamine in the treatment of rheumatoid arthritis, 148 patients were followed for an additional year in an open label trial. Complications of longterm D-penicillamine included rash, gastrointestinal manifestations, proteinuria, bone marrow depression, myasthenia gravis, myositis, acute febrile reaction and pemphigus foliaceus. With the exception of one patient with myasthenia gravis, all adverse reactions resolved after withdrawal of D-penicillamine. While the complications of D-penicillamine therapy are usually dose related, these reactions can occur at any time and at any dose. Continued and frequent longterm monitoring of D-penicillamine therapy is required.
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PMID:Toxicity of longterm low dose D-penicillamine therapy in rheumatoid arthritis. Cooperative Systematic Studies of Rheumatic Disease Group. 295 97

A 56 year old male presented after 2 months of muscle stiffness, pain and palpable lumps. Biopsy confirmed the presence of myositis. Myasthenia gravis and peripheral neuropathy became clinically apparent within days of commencing corticosteroid therapy. 4 months later, at operation, a locally invasive thymoma was found. This combination of features has not previously been described.
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PMID:A case of invasive thymoma associated with myasthenia gravis, myositis and demyelinating neuropathy. 358 2

A 48-year-old man presented with a malignant thymoma in combination with myositis, myasthenia gravis, a giant cell myocarditis and recurrent intractable ventricular tachycardias. Despite various therapies (chemical, electrical and surgical), arrhythmias supervened in the presence of a normal coronary arteriogram. Active myocarditis was believed to be the mechanism of the ventricular tachycardias.
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PMID:Intractable ventricular tachycardia in a patient with giant cell myocarditis, thymoma and myasthenia gravis. 379 92

An investigation was made into the occurrence of muscular atrophy and muscular pathology in a series of 170 patients with myasthenia gravis. The results can be summarized as follows: (1) Of the 148 patients with generalized myasthenia gravis, 14 showed local muscular atrophies. Of 10 biopsies from atrophic muscles, eight showed neurogenic changes, with or without lymphocytic infiltrations. One biopsy showed lymphocytic infiltrations only, and one showed type II-fibre atrophy (Table 1). No relationship was demonstrable between the presence of clilnical muscular atrophy and age, sex, duration of the disease, severity of the disease, presence of a thymoma, or drug resistant ophthalmoplegia. (2) In this group of patients 61 biopsies were examined from 46 individuals; 40 of these biopsies were taken from the quadriceps muscle. A thymoma was present in 17 patients. Examination disclosed neurogenic changes in 17 biopsies, lymphocytic infiltrates in 21, and myositis in one biopsy (Table 2). A distinct correlation was established between the presence of a thymoma and lymphocytic infiltrates, but none was demonstrable between thymoma and neurogenic changes (Table 3). (3) An enzyme-histochemical study was carried out in 35 cases, including 12 with neurogenic changes. A normal differentiation of type I- and type II-fibres was observed in eight instances, type grouping of type II-fibres in three, and type II-fibre atrophy in two cases. (4) In 21 patients and 19 controls, the smallest mean diameter was determined in the quadriceps muscle. Both type I- and type II-fibres proved to have a smaller mean diameter in the female patients than in the controls. In the male patients this could not be proven. (5) Of the eight patients who had died without disorders of ventilation, 90 muscle specimens were examined postmortem. Four of these patients had a thymoma. Lymphocytic infiltrations, found in 32 biopsy specimens, were mostly observed in the presence of a thymoma. Neurogenic changes were apparently unrelated to the presence of a thymoma (Tables 5 and 6). The post mortem examination included the spinal cord in five, and peripheral nerves in three cases. No abnormalities were found. (6) The muscular atrophy found in patients with myasthenia is not a myopathy but an affection of the lower motor neurone. Neurogenic changes were regularly found in the muscles of patients with myasthenia, even without muscular atrophy. The finding of these changes is no reason to reject the diagnosis. It is postulated that denervation occurs at the neuromuscular junction as a result of permanent absence of acetylcholine.
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PMID:Neurogenic muscle involvement in myasthenia gravis. A clinical and histopathological study. 470 58


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