Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of acute idiopathic myopericarditis with transient severe swelling and akinesis of the interventricular septum on echocardiograms was reported. A 35-year-old man was admitted to our CCU because of cardiogenic shock five days after the onset of "common cold". Electrocardiograms revealed low voltage and ST-segment elevation in all leads except for a VR and a VL. Serum CPK, GOT and LDH were slightly elevated. Echocardiograms showed severe asymmetrical septal hypertrophy (ASH, 20 mm), akinesis of the interventricular septum and moderate pericardial effusion. With improvement of the clinical course and of the hemodynamic data, the thickness and wall motion of the interventricular septum became normal. Serum antiviral antibodies were not elevated throughout the course. Transvenous percutaneous right ventricular endomyocardial biopsy revealed degeneration and fragmentation of the myofibrils with interstitial cellular infiltration and edema in the subacute phase (8th hospital day), but showed only focal fibrosis in the chronic phase. Coronary arteriograms and left ventriculograms in the chronic phase (50th hospital day) were normal. From these findings we can conclude that the severe transient ASH is due to myocardial inflammatory swelling.
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PMID:[Acute idiopathic myocarditis having myocardial inflammatory swelling demonstrated by echocardiography: a case report]. 383 77

A non-hereditary slowly progressive neuromuscular disease occuring in a 39-year-old male, consisting of an asymmetrical wasting of the muscles of the shanks, is reported. Neither clinical nor electromyographic criteria can safely distinguish whether a primary neurogenic or a primary myogenic process is causally involved. The initial rise in serum CPK-activity indicates a myopathic origin. The lightmicroscopic aspect of the muscle-biopsy shows a muscular atrophy which resembles a primary neurogenic pattern with grouped clusters of atrophic fibers as well as a myopathic or rather myositic tissue-pattern with randomly scattered atrophic fibers. In addition there are numerous vacuoles which are equivalent to concentric lamellae of dense material in electronmicroscopy. Numerous fibrillary inclusions as well in the cytoplasm as in the cell-nucleus correspond to typical alterations in the so-called "inclusion body myositis". The disease is critically discussed as a nosological entity among neuromuscular disorders.
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PMID:[Ultrastructural and clinical studies in "inclusion body myositis" (author's transl)]. 624 16

Two brothers, 25 and 19 years old, were affected by asymmetrical hypertrophic cardiomyopathy. The older brother had waddling gait and weakness of the proximal girdle muscles, while the younger had a broad-based gait and weakness of selected limb girdle muscles. EMG exam was myopathic. Serum enzyme, CPK and aldolase were elevated. Histochemical reactions in muscle revealed "core-like" areas, subsarcolemmal rims of mitochondria and lipid accumulation. Succinate-dehydrogenase stain showed a lack of activity in both biopsies, with the exception of intrafusal fibers. Microphotometric quantitative measurements confirmed the defect in both biopsies. Biochemical measurements of several mitochondrial enzymes in muscle showed a reduced activity of succinate-dehydrogenase (33%) and succinate-cytochrome C reductase (36-47%) which are both components of complex II. On myocardial biopsy lipid and mitochondrial abnormalities were found. This mitochondriopathy represents a new phenotype of partial complex II defect.
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PMID:Hypertrophic cardiomyopathy with mitochondrial myopathy. A new phenotype of complex II defect. 851 73

Dermatomyositis is an inflammatory myopathy of unknown aetiology. Muscle involvement may eventuate later in the disease course in some patients, who may present with typical skin disease without clinical signs of myopathy and are referred to as dermatomyositis sine myositis. A 48 year old female presented with intermittent urticaria like rashes, diffuse asymmetrical swelling of proximal limbs, pain in small joints of hands and fatiguability. Initial laboratory work-up for immune markers was negative. Three years later, she developed heliotrope rash and periorbital oedema with no evidence of muscle weakness and was labeled as amyopathic dermatomyositis. After an interval of one year, she developed profound weakness and significantly raised CPK. Patient responded well to steroids and Azathioprine and improved both clinically and biochemically.
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PMID:An elusive case of dermatomyositis. 2917 76