Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:4.1.2.13 (aldolase)
 3,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 25-year-old woman with a 2 years history of painful enlargement of the left calf visited our clinic because of ache in the left calf which became severe enough to interfere her walk. She had no history of trauma to the calf, and family history was negative for muscle disease. Physical examination showed an enlarged left calf muscle with pain which was evoked by stretching of the Achilles tendon. There was no muscle weakness or neurological abnormality. Laboratory tests were all within normal limits, including erythrocyte sedimentation rate and serum enzymes such as creatine kinase and aldolase. The CT scan revealed an isolated round-shaped low density area in the left calf muscle, which showed up as a markedly high signal intensity on T2 weighted images of MRI. The lesion was confirmed to be the lateral head of the gastrocnemius muscle. The specimen obtained from the affected muscle demonstrated degenerative and inflammatory changes together with excess fibrosis. There was no sarcoid lesion or malignancy. From the above results, the present case was thought to have isolated focal myositis. Prednisolone 80 mg (40 mg, twice, at 4-day intervals) was given to the left femoral artery without any trouble. Thereafter the patient became free from pain and difficulty in walking, and the lesion demonstrated by CT scan disappeared in 15 days. However, the high signal intensity on T2 weighted images faintly remained until the 54th day after the treatment. In summary, MRI is more sensitive than CT scan for detection of isolated focal myositis, which might be successfully treated by arterial injection of prednisolone within a short period than any other conventional methods.
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PMID:[A case of isolated focal myositis successfully treated by arterial injection of prednisolone--its findings by CT scan and MRI]. 208 34

To devise a clinical laboratory policy for serum aldolase (ALD) requests, the use of ALD alone and in conjunction with serum creatine kinase (CK) was studied in 126 consecutive patients. Both enzymes were normal in 76 cases (60.3%); CK was normal but ALD was raised in 19 cases (15.1%); ALD was normal but CK raised in nine cases (7.1%); and both were raised in 16 (12.7%). The spectrum of disease was similar irrespective of the enzymes elevated. The role of ALD in the diagnosis and monitoring of muscle disease is in those cases where CK falls within the reference range.
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PMID:Serum aldolase with creatine kinase in current clinical practice. 210 48

A case of severe infantile form of congenital nemaline myopathy who developed extensive fatty replacement of the skeletal muscles was described. A girl was born with severe hypotonia and flaccidity of the extremities. She was put on a ventilator because of the severe respiratory insufficiency. Muscle biopsy performed at 3 months of age revealed numerous nemaline rods in myofibers. She had an anoxic episode at 2 years of age and fell into a vegetative state after that. Serum creatine kinase and aldolase levels were normal. At 8 years of age, X-ray CT scan of the skeletal muscles revealed diffuse and severe fatty replacement of the skeletal muscles of the trunk and extremities; this was far more extensive than in the case of Duchenne muscular dystrophy of similar age. Second muscle biopsy performed in the anterior tibialis muscle at the age of 8 years revealed atrophic muscle fibers and extensive proliferation of connective and fatty tissues. Electron microscopy revealed, numerous rod-containing muscles fibers with severe disorganization and loss of myofilaments. Sural nerve biopsy performed at the same time showed decreased number of large myelinated fibers. Although a possibility could not be excluded completely that the episode of anoxia and chronic debilitation may have contributed to these pathological neuromuscular findings, it was presumed that severe degeneration and fatty replacement of the skeletal muscles progress rapidly after birth in some cases of severe infantile form of congenital nemaline myopathy.
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PMID:[A case of severe infantile form of congenital nemaline myopathy with extensive fatty replacement of the skeletal muscles]. 217 91

The eosinophilia-myalgia syndrome associated with the use of oral preparations of the amino acid L-tryptophan was recognized in late 1989. We describe the clinical and laboratory manifestations, pathological findings and early clinical course of 20 patients with the eosinophilia-myalgia syndrome. Prominent clinical findings included severe myalgias limiting function, fatigue, rashes, edema and weight gain, weight loss, muscle weakness and shortness of breath. Laboratory findings included eosinophilia (often marked), normal erythrocyte sedimentation rate, and elevated aldolase with normal or low creatine kinase values. On biopsy fascial inflammation was always seen consisting of lymphocytes, histiocytes and eosinophils in a perivascular distribution. Invasion of the vascular wall by lymphocytes was seen in 20%. Capillary and arteriolar endothelial cell thickening was found in most cases on electron microscopy and endothelial cell necrosis or mural invasion by lymphocytes was seen in 25% of cases. Two patients improved with no therapy. Ten patients responded to therapy with prednisone alone. Three patients have had progressive disease and one of these died. The relationship of this syndrome to previously described disease entities associated with eosinophilia is discussed.
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PMID:Eosinophilia-myalgia syndrome associated with L-tryptophan use. 227 99

Seven patients who developed a syndrome of eosinophilia, connective-tissue disease, and cutaneous abnormalities while ingesting tryptophan were examined. Other clinical manifestations commonly seen were pulmonary symptoms, fever, lymphadenopathy, and the development of myopathy. Laboratory features included mild elevations of aldolase and lactate dehydrogenase levels, with essentially normal creatine kinase levels, erythrocyte sedimentation rates, and C-reactive protein levels. Biopsy findings included features of scleroderma, small-vessel vasculitis, fasciitis, and myopathy. Discontinuation of tryptophan administration and implementation of corticosteroid therapy were of some benefit in relieving the intense myalgias and cutaneous findings that developed. Although temporally related to tryptophan ingestion, it is unclear whether this substance, a metabolite, or a contaminant were causal. We speculate that the pathogenesis of this syndrome may relate to abnormalities in tryptophan metabolism.
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PMID:Tryptophan-associated eosinophilic connective-tissue disease. A new clinical entity? 230 82

A rare case of myotonic dystrophy with mechanical derangement in a 48-year-old male is reported. The patient was admitted to Fuzisawa City Hospital because of chest discomfort. On physical examination, he had the typical facial appearance of myotonic dystrophy, and displayed grip myotonia. The blood pressure was 120/60 mmHg and the pulse 51, regular. A systolic ejection murmur at the cardiac base, an early diastolic blowing murmur along the left sternal border, and a pansystolic murmur at the apex were heard. The deep tendon reflexes were all normal. Elevation of serum creatine kinase and aldolase were noted. Chest X-ray films suggested moderate cardiomegaly. An electrocardiogram showed sinus bradycardia, atrioventricular block and left bundle branch block, suggesting diffuse involvement of the conduction system. An echocardiography confirmed the presence of left ventricular enlargement, thickened aortic valves, mitral regurgitation, and aortic regurgitation. Selective coronary angiography revealed no abnormalities. Left ventriculography demonstrated diffuse hypokinesis of the entire ventricle. Light microscopy of biopsied right myocardium revealed prominent interstitial fatty infiltration, mild interstitial fibrosis, and variation in the nuclear size. A 22-year-old son also had myotonic dystrophy and had an echocardiography indicative of thickened valves with aortic regurgitation. Myotonic dystrophy is a autosomal dominant disease. Cardiac involvement selectively disturbs the conduction system, sinus node, and to a lesser extent myocardium. Although the presence of aortic regurgitation could be a mere coincidence, we believe that this did not occur by accident, because the patient's son also had aortic regurgitation.
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PMID:[A case of myotonic dystrophy associated with intracardiac conduction abnormalities and aortic regurgitation]. 237 32

Changes in muscle proteins in serum after exercise were studied to evaluate the use of such proteins as indicators of increased muscle membrane vulnerability. Seventy-one women were asked to perform bicycle exercise for 45 min at a moderate load; four proteins (creatine kinase - CK, myoglobin - Mb, aldolase - Ald and pyruvate kinase - PK) were measured in serum up to 24 h after exercise. Twenty-one women were carriers of Duchenne's muscular dystrophy (DMD); these are known to show an elevated serum CK activity at rest, as well as increased CK response after exercise. Fifty women without a family history of neuromuscular disease were tested to obtain normal values: they showed a small peak (18%) of CK activity 8 h after exercise, and an even smaller peak of Mb (9%) 1 h after exercise. The mean post-exercise increase for both CK and Mb in the 21 DMD carriers was significantly higher than in controls; the maximum of Mb, on average 70% of baseline levels, was reached 1 h after exercise and was higher than that for CK (48%), which was reached 8 h after exercise. It is concluded that myoglobin levels after exercise are a good index of increased vulnerability of the muscle membrane.
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PMID:Myoglobin is a sensitive marker of increased muscle membrane vulnerability. 239 44

The topology of the interfaces between actin monomers in microfilaments and three glycolytic enzymes (glyceraldehyde-3-phosphate dehydrogenase, aldolase and phosphofructokinase) was investigated using several specific antibodies directed against precisely located sequences in actin. A major contact area for glyceraldehyde-3-phosphate dehydrogenase was characterized in a region near residue 103. This interaction altered, by long-range conformational changes, the reactivity of antigenic epitopes in the C-terminal part of actin. The interface between actin and aldolase appeared to involve a sequence around residue 299 in the C-terminal region of actin. The interaction of phosphofructokinase, in contrast, modified the reactivity of all antibodies tested. Finally, the phosphagen kinases arginine kinase and creatine kinase showed no interaction with the microfilament.
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PMID:Antigenic probes locate binding sites for the glycolytic enzymes glyceraldehyde-3-phosphate dehydrogenase, aldolase and phosphofructokinase on the actin monomer in microfilaments. 248 31

Eight- and nine-week-old Hungarian Landrace pigs were tested with halothane as described by Laky et al. (1985). Immediately after the test blood samples were taken for determination of the activity of serum creatine kinase (CK), creatine kinase MB (CK-MB) isoenzyme, aldolase (ALD), lactate dehydrogenase (LDH) and alpha-hydroxybutyrate dehydrogenase (alpha-HBDH). Elevated creatine kinase, creatine kinase MB isoenzyme and aldolase activities indicating enhanced susceptibility to stressors were found in 92% of the halothane reacted and 16% of the halothane non-reacted animals. In these individuals the activities of lactate dehydrogenase and alpha-hydroxybutyrate dehydrogenase were also high. Data of the literature show a close relationship between enhanced susceptibility to stressors and halothane reaction in pigs. It was suggested, therefore, that determination of the activity of appropriate serum enzymes might be used for detecting this enhanced susceptibility.
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PMID:Activities of some serum enzymes in halothane reacted and non-reacted pigs. 262 95

Pneumatic cuff with manometer has become a routine apparatus being applied in surgery of the hand. Ischaemia of the upper extremity procured by means of pneumatic cuff with controlled pressure maintained for 30 minutes to 2 hours and 20 minutes appeared to be safe. The following enzymes were studied: lactic dehydrogenase (LDH) creatine kinase (CPK), aldolase and total protein as well as its electrophoretic decomposition, moreover seromucoid and also 9 selected glycoproteins. There were changes indicating metabolic disturbances during the time from the 3 rd h. upon the removal of the cuff to as late as the third 24-hours inclusive. Significant deviations were disclosed with regard to the rise in levels of: creatine kinase, alpha 1 and alpha 2 globulins, protein of acute phase (inflammatory)--seromucoid and 5 glycoproteins as well as a drop in albumins level. The rise in the value of metabolic enzymes was more significant when the application of the cuff was longer than 1 hour. A similar behaviour was observed in some of the selected glycoproteins qualified to the acute phase proteins. In patients, in whom the cuff was applied for 2 hours or longer, there were transient side effects of ischaemia, which under proper management terminated without traces. In own material neither local nor general permanent changes were noted after imposed ischaemia, which is ample evidence that the technique of ischaemia used in the cited time compartments is safe and useful in surgical procedure involving the extremities particularly the upper ones. Nevertheless, disclosed deviations in a number of metabolic parameters show that some injury to ischaemic tissues is found to take place.
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PMID:[Effect of tourniquet ischemia of the arm on changes in selected parameters of muscle metabolism]. 263 95


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