Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026850 (muscular dystrophy)
 5,870 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The AA. have carried out in patients affected by proved myocardial infarct, by other cardiac diseases and by muscular dystrophy the following enzymes determinations: total CPK, total LDH, SGOT, SGPT, HBDH, CPK isoenzymes by column chromatography (Mercer's method) and LDH isoenzymes either by column chromatography (Mercer's method) and by electrophoretic separation. Some results concerning the appearance of the CK-MB isoenzymes during the acute period of the myocardial infarction are described.
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PMID:[Determination of CPK isoenzymes by column chromatography (author's transl)]. 102 94

Duchenne muscular dystrophy is one of the best known forms of muscular dystrophy. The incidence in different countries varies from 130 to 390 per million male live births. Becker variety may be considered a mild form of Duchenne dystrophy, with an incidence 10 times lower. A sex linked recessive inheritance is involved in both forms, the affected gene is placed at locus X21. The incidence of both forms in Chile is similar to that reported worldwide, and has been increasing since 1950. Increased CK and LDH levels are confirmed in patients, and overall, they are also higher in female carriers. However only 26% of carriers have increased CK levels and 21% increased LDH levels, compared to normal subjects. Electromyograms show myopathic characteristics in all carrier women. The scope of a prospective clinical, genetic and epidemiologic study currently underway is discussed.
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PMID:[Duchenne and Becker muscular dystrophy in Chile]. 134 81

For the purpose of clarifying the cause of white muscle disease (WMD) in calves, tocopherol and selenium levels and blood glutathione peroxidase (GSH-Px) activity were measured on 10 calves with WMD and nine of their dams. The main clinical symptoms of the 10 calves with WMD were motor disturbances including recumbency and stiffness. Serum enzyme activities (GOT, GPT, CPK, LDH) in calves with WMD increased markedly, and this increase was also observed in some of their dams. Serum tocopherol levels of calves with WMD were low, 70% of which showing deficient levels of less than 70 micrograms/100 ml. Serum selenium levels of all the calves were lower than 35 ppb, indicating a deficiency, and were accompanied by low blood GSH-Px activity. alpha-Tocopherol and selenium concentrations in organs were very low. Dams of calves with WMD showed low serum tocopherol levels, 22% of which indicating deficient levels below 150 micrograms/100 ml. Serum selenium levels in dams showed a marked decrease to under 20 ppb, and also low blood GSH-Px activity. Feedstuffs supplied in the farms to affected calves indicated very low alpha-tocopherol contents (below 3 mg/100g DM) and low selenium concentrations below 50 ppb in DM. It was concluded that WMD in calves was attributable to nutritional muscular dystrophy caused by deficiencies in tocopherol and selenium in feedstuffs supplied to their dams.
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PMID:Studies on serum tocopherol, selenium levels and blood glutathione peroxidase activities in calves with white muscle disease. 258 29

Nine children with Duchenne muscular dystrophy were given Sanorex (mazindol), a growth hormone inhibitor, daily for 6 months. There was no significant change in their muscle function, but there was a significant reduction in weight gain and in levels of growth hormone, somatomedin C, hair zinc, serum zinc, and serum LDH. Selenium and glutathione peroxidase in the serum increased significantly. Thirteen other children with growth hormone deficiency had a significant reduction in hair selenium following growth hormone administration. These results show a significant relationship between growth hormone and selenium nutritional status and confirm our previous reports indicating an effect of growth hormone on zinc nutritional status. It is possible that prolonged therapy with a growth hormone inhibitor would attenuate the course and improve the longevity of patients with muscular dystrophy.
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PMID:Growth hormone inhibition causes increased selenium levels in Duchenne muscular dystrophy: a possible new approach to therapy. 649 89

Two autopsy cases of congenital muscular dystrophy of Fukuyama type (F-CMD) were described. The first case was diagnosed clinically and pathologically as its typical case. Neither his family history nor the history of his prenatal period were contributory. He had suffered from muscle weakness and atrophy since his birth. Serum CPK was markedly elevated. EMG and muscle biopsy proved dystrophic changes of the skeletal muscles. In addition, he manifested mental retardation and attacks of convulsion. EEG failed to elicit remarkable changes, but PEG represented ventricular dilatation. He died of respiratory insufficiency at age 12. His postmortem examination showed variegated anomalies in the nervous system. Extensive micropolygyria was present in the cerebrum and cerebellum accompanied by adhesions between the bilateral cerebral hemispheres. Assymmetry of the longitudinal fibers was pointed out in the pontine base. Anterior horn cells were atrophic and moderately depopulated. On the other hand, the second patient was an atypical F-CMD case in symptoms, signs and pathology. His grand-mothers on both father's and mother's sides wee first cousins. His three siblings showed no similar disorders. His mother developed slight gestational toxicosis in the sixth and seventh months of pregnancy. His muscle weakness, contracture of the bilateral hip-joints and clubfoot had been observed since his birth. Physical and neurological examinations at age 6 showed deformity of the skull, myopathic face, macroglossia, high-arched palate, pigeon chest, scoliosis of the thoracic spine. In addition, generalized muscular atrophy, hypotonia and areflexia were recognized. Pseudohypertrophy of the muscles was absent. Sensation was intact to all modalities. Serum CPK and LDH were moderately increased.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[2 autopsy cases of congenital muscular dystrophy of Fukuyama type--a typical and an atypical cases]. 652 23

The genotype difference (dystrophic vs nondystrophic) in the LDH isozymes is observed in kidney. These differences are evident only at birth and at early developmental stages (before the expression of dystrophic symptoms). The tissue specific genotype differences for PK are limited to the thigh muscle (M form) and heart (L form), after the onset of the condition. These differences may reflect the pleiotropic effect of the dy2J locus during the temporal regulation of these and other enzymes implicated in muscular dystrophy (MD).
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PMID:Dystrophic mutation (dy2J) affecting regulation of lactate dehydrogenase (LDH) and pyruvate kinase (PK) in C57BL/6J mice. 715 75

The LDH isoenzyme pattern was investigated in biopsy material of muscles of children suffering from progressive muscular dystrophy and other neurogenic muscular disorders. An absence or pronounced activity loss of LDH 5 was observable in most of the cases. The proportion of subunits was the same in the diseased and the control muscles. Comparing the measured isoenzyme patterns with those expected from a random coupling of of the subunits, a lower percentage of LDH 5 and a higher one of LDH 4 was detected. The cause of the absence of LDH 5 is not a disturbance of M subunit synthesis but the post-translational inhibition of the tetramer forming process of the synthetised M subunits.
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PMID:LDH isoenzymes in muscle diseases. 744 85

Authors have treated with allopurinol ten children with progressive muscular dystrophy, whose ages were between 15 months to eleven years. An initial and monthly clinical evaluation of muscular strength, Gowers's sign and pseudohypertrophy was performed. Monthly determinations of CPK, LDH, aldolase, GOT and serum urate; every two months electromyography was also made. In three patients a complete recovery of strength, Gowers's sign was found and at the same time pseudohypertrophy diminished; the age average was three years and four months. In four patients a partial recovery was found; the age average was nine years and four months. In three patients there was no answer to treatment, they were contracted and had deformities, being age average ten years. No variations on monthly controls of CPK, LDH, aldolase and GOT were observed. On these facts their opinion is that allopurinol is an effective drug in the treatment of progressive muscular dystrophy and that its' effectivity is better when treatment is initiated early and, of course, before patients present deformities and contractures.
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PMID:[Allopurinol in progressive muscular dystrophy (author's transl)]. 746 88

Estimation of the enzymes CPK and LDH, with their isoenzymes, is useful in diagnosing myocardial infarction and monitoring its progress. However, increases of CPK-MB and LDH1, may be not associated with acute myocardial infarction, as in hypothyroidism, muscular dystrophy, polymyositis, malignant disease. We report a case of hypothyroidism with increased CPK-MB and LDH1. At the beginning the diagnosis was difficult because of altered electrocardiogram associated with one event of "burning" localized altered at the anterior thorax. This case illustrates that plasma enzyme activity and isoenzyme profiles should be interpreted with caution when clinical and instrumental (eco 2D) findings are not entirely associated with myocardial infarction.
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PMID:[The enzymatic and electrocardiographic changes falsely indicative of an acute myocardial infarct during hypothyroidism]. 813 81

A case of muscular dystrophy in a 1-year-old male castrated Domestic Shorthair cat is presented. The most striking clinical features were regurgitation, a stiff gait, an increased muscle tone and exercise intolerance. Serum biochemistry panels showed a marked increase in the muscle specific enzyme creatine kinase, and moderately elevated levels of LDH, AST and ALT. Spontaneous electrical activity of skeletal muscles in the form of "bizarre high frequency discharges" and "myotonia-like repetitive discharges" were registered. Gross pathology revealed a marked hypertrophy of the skeletal muscles. The main histopathological changes were myofiber necrosis and calcification, variation in fiber size, hypertrophied muscle fibers of type I and type II and fiber splitting. Indirect immunofluorescence showed dystrophin deficiency. Feline muscular dystrophy resembles the X-linked human Duchenne muscular dystrophy (DMD). Besides the X-linked muscular dystrophy in the mouse and Golden Retriever the feline muscular dystrophy could represent another valuable animal model for the study of DMD.
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PMID:[Muscular dystrophy in a cat]. 824 6


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