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)

Fingerprint inclusions, circular structures of unknown origin, mitochondrial changes, dilatation of the sarcoplasmic reticulum, rods of Z-line material, elongated T-systems, honeycombs, and myelin figures were present in some damaged muscle fibres. Many damaged fibres showed loss of myofilaments and groups of atrophied fibres occurred. The muscle biopsy was from the left biceps brachii and presented also the changes of polymyositis. The patient had muscle weakness, malignant hypertension, alcoholism, polyarthropathy, and evidence of mild peripheral neuropathy.
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PMID:Fingerprint inclusions and circular structures in the muscle. Report of a case. 22 37

A woman presented with severe weakness and wasting involving only one arm. A definite diagnosis was not made until almost six years later when she developed proximal weakness in the legs as well, and a muscle biopsy showed changes of polymyositis. Asymmetry of weakness in polymyositis has been noted previously in the literature, but is rare. In previous reports asymmetry as marked as in the present case has not been noted.
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PMID:Polymyositis presenting with severe weakness involving only one arm. 28 77

A 54-year-old woman had muscle disease that terminated fatally with complete body paralysis. The patient had renal failure, which progressed concurrently with her muscle weakness. Myoglobinuria was not demonstrated during the active stage of her illness. Renal biopsy specimens demonstrated immune deposits in the glomeruli, and, at autopsy, there was a generalized glomerulonephritis. We believe the muscle disease was a consequence of acute rhabdomyolysis, hyperacute polymyositis, or virus infection. Regardless of the nature of the muscle disease, an immune mechanism may have been responsible for the associated renal failure.
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PMID:Muscle disease associated with renal failure. 30 32

A 40-year-old woman with clinical and laboratory features of myasthenia gravis, hyperthyroidism, and polymyositis responded to treatment with prednisone alone. Symptoms of myasthenia gravis appeared first followed by hyperthyroid symptoms. Triiodothyronine, thyroxine, and thyroid uptake were elevated as were serum levels of CPK, SGOT, SGPT, and LDH. Muscle biopsy specimen showed mild type II fiber atrophy and a small focus of inflammatory cells. Two weeks after initiation of prednisone, 100 mg every other day, the ESR declined from 44 to 12 mm/hr, serum enzyme values became normal, and the weakness improved. Over the ensuing four months, the thyroid function values returned to normal and the patient no longer needed any anticholinesterase drug. At present, she is functionally normal except for mild defects in eye movement and she takes no medication. Physicians should consider treating patients who have several concurrent autoimmune diseases with prednisone to see if all conditions can be brought under control with one simple therapy.
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PMID:Prednisone use in concurrent autoimmune diseases. 42 Jun 18

A 14-year-old boy had a protracted illness characterized by bilateral tenderness and weakness of the extremities; the illness was considered to be a connective tissue disease similar to polymyositis. Not until nine months later, when the patient had new cardiac murmurs, pulmonary edema, and then a cerebrovascular accident, was the true nature of his illness suspected. The diagnosis of left atrial myxoma with the triad of constitutional, obstructive, and embolic effects was confirmed by echocardiographic studies and cardiac catheterization. The tumor was successfully removed.
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PMID:Atrial myxoma mimicking a collagen disorder. 42 37

A case of eosinophilic polymyositis is reported. Tender muscle swelling was followed by proximal weakness, creatinine kinase elevation, and electromyographic features typical of polymyositis. Severe myocarditis, pericarditis and heart failure were present. Muscle biopsy specimen showed active myositis with eosinophil infiltrate. Unlike previous cases, blood eosinophils count was normal. The clinical response to corticosteroids was excellent, and a relapse occurring as steroid dose was lowered responded rapidly to an increased dose of prednisolone. Eosinophilic polymyositis may be a component of a general systemic illness with prominent cardiac involvement.
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PMID:Eosinophilc polymyositis. 50 94

Six patients with eosinophilic fasciitis are presented. This syndrome is characterized by indurative swellings of arms and legs, with rapidly progressing difficulties in extending elbows, wrists, and fingers, and often limited motion of shoulders and ankle joints. Pain when contracting muscles, and weakness of proximal muscles and hand grip are common features. The frequent occurrence of localized skin lesions has presented differential diagnostic difficulties to systemic sclerosis and to polymyositis. Visceral involvement and Raynaud's phenomena, however, are absent or mild. Blood eosinophilia, hypergammaglobulinemia, and unspecific signs of inflammation are found. Biopsy of muscle fascia gives characteristic histopathological findings of cell infiltrations (mostly mononuclear cells, frequently eosinophils) and vascular proliferation, in the middle layer of a thickened fascia. Skin changes are prevalent, but not conclusive for the diagnosis, and myositis in some patients might be difficult to distinguish from polymyositis. The importance of the clinical recognition of eosinophilic fasciitis and the inclusion of fascia in diagnostic muscle biopsies, is underlined.
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PMID:Eosinophilic fasciitis. Review and report of six cases. 53 17

Four adolescents with Hodgkin's disease also developed autoimmune diseases. There were two idiopathic thrombocytopenic purpura (ITP), one polymyositis, and one scleroderma. The first two patients developed ITP in the absence of a spleen, and with their Hodgkin's disease in remission. The first patient with Hodgkin's disease has been continuously free of cancer for over five years. The second patient was a 17-year-old male whoe Hodgkin's disease recurred, but whose disease was in remission at the time the ITP occurred. The polymyositis occurred in an 18-year-old youth when he was in his initial remission for his Hodgkin's disease, but his disease subsequently recurred two years later. This youth presented with Coombs positive autoimmune hemolytic anemia. The polymyositis did not respond to therapy, and he is left with severe muscle wasting and weakness; however, the polymyositis is now quiescent. The scleroderma occurred in an 18-year-old female who had been continuously free of Hodgkin's disease for eight years. The scleroderma did not respond to drug therapy and she now has moderate skin changes, but remains in continuous remission of her Hodgkin's disease. Although there are a few reports of Hodgkin's disease and concurrent autoimmune disorders, physicians dealing with cancer in adolescents should be aware of this association.
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PMID:Autoimmune disorders complicating adolescent Hodgkin's disease. 57 59

Myoglobin was detected in the sera of patients with dermatomyositis, polymyositis, scleroderma, and systemic lupus erythematosus (LE) with active myopathy. Overall, myoglobinemia was detected in 74.1% of sera taken from patients with active myositis before therapy, with slightly greater frequency in the groups with dermatomyositis and polymositis. With steroid therapy, this frequency fell to 43.4% and to 9.5% in patients in clinical remission not requiring therapy. Serum enzyme (creatine phosphokinase, lactic dehydrogenase, and SGOT) activity was higher in samples containing myoglobin, but there was considerable overlap between those with and without myoglobinemia. Sequential serum determinations in six patients demonstrated rapid reduction in the levels of serum myoglobin with therapy, usually before enzyme values had returned to normal. In one patient followed up for 30 months, myoglobinemia correlated with clinically observed exacerbations of rash and weakness to a greater degree than did enzyme determinations.
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PMID:Myoglobinemia in inflammatory myopathies. 57 36

A patient with polymyositis responded initially to steroid therapy. A muscle biopsy disclosed features of primary myopathy and group atrophy. The patient became refractory to therapy and died with relentlessly progressive weakness. The autopsy disclosed lower motor neuron involvement and degeneration of the spinocerebellar tracts. There was loss of Purkinje cells, which may have occurred secondary to an anoxic episode prior to death. The case is unique because of the limited involvement of the lower motor and spinocerebellar systems.
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PMID:Lower motor neuron disease with spinocerebellar degeneration. 61 94


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