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)

In spring 1981, thousands of people living in Madrid were intoxicated by adulterated edible oil containing oleoanilide and probably other toxic substances. Due to increasing international travel Swiss doctors may also be faced with this particular disease. The case is reported of a 28-year-old woman who presented in May 1981 with a highly febrile influenza-like syndrome after consuming the adulterated oil while in Madrid. In the following weeks she developed myopathy, characterized by muscular weakness and pain, aldolase elevation and typical electromyographic disturbances, as well as edema and general discomfort. The white cell count showed eosinophilia up to 2170/mm3. Five months later, the symptoms are still continuing. Other members of the family have been exposed to the oleoanilide and exhibited various abnormalities which constitute a new clinical syndrome different from previously reported intoxications by industrial oil.
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PMID:[Poisoning by adulterated edible oil]. 732 94

We described a 50-year-old woman with late-onset nemaline myopathy with focal mononuclear cell infiltrates in her muscle biopsy. She developed difficulty in climbing stairs, and elevating her arms for 5 months after the onset of the disease. On admission, neurological examination revealed moderate weakness and atrophy in the proximal limb and neck muscles. Laboratory studies were within normal limits except mildly elevated serum CK and aldolase levels. Electromyography showed myopathic changes in the right triceps and quadriceps muscles examined. A biopsy from the left biceps brachii muscle revealed increased variation in fiber size, with numerous basophilic atrophic fibers. There were some foci of mild mononuclear cell infiltration. Most of basophilic fibers contained nemaline bodies on modified trichrome stain. On electron microscopy numerous nemaline bodies were present in fibers with marked myofibrillar degeneration. Azathioprine and prednisolone administration was not effective to improve her condition. As mononuclear cell infiltration has been occasionally described in the previously reported patients of adult-onset nemaline myopathy, inflammatory process may have some roles in formation of nemaline bodies on the way of acute myofibrillar degeneration.
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PMID:[A patient of late-onset nemaline myopathy with mononuclear cell infiltration]. 783 55

Didemnin B (NSC 325319), a cyclic depsipeptide isolated from a Carribean sea tunicate, exhibited potent antitumor activity in preclinical studies. After determining the maximum tolerated dose in our previous phase I/II trial, we conducted a phase II study of this drug in patients with previously treated small cell lung cancer; the starting dose was 6.3 mg/m2 intravenously over 30 min every 28 days. The major side effects were in the neuromuscular system and included severe muscle weakness, myopathy and/or myotonia by electromyography, and elevation of creatine phosphokinase and aldolase levels. We also observed modest increases in bilirubin and alkaline phosphatase levels. There were minimal hematologic toxic effects. No response was observed among 15 evaluable patients, leading us to conclude that didemnin B was toxic but inactive in patients with previously treated small cell lung cancer at the stated dose and schedule. A review of the literature revealed no significant antitumor activity in cancers of the colon, breast, ovaries, cervix, or lung (non-small cell) or in renal cell carcinoma. Further clinical trials for didemnin B may not be warranted at the stated dose and schedule.
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PMID:Phase II clinical trial of didemnin B in previously treated small cell lung cancer. 789 44

Dermatomyositis (DM) developed in a 35-year-old woman after 2 months of psoralen ultraviolet-A (PUVA) therapy for presumed psoriasis. Her disease was characterized by symmetrical proximal muscle weakness and cutaneous lesions compatible with DM. In addition, laboratory abnormalities included a positive antinuclear antibody, and elevated levels of creatine kinase and aldolase. This is the first report of DM developing during PUVA therapy.
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PMID:Dermatomyositis occurring during psoralen A (PUVA) therapy. 818 50

We describe two siblings with distal myopathy with rimmed vacuoles, who died suddenly presumably due to fatal arrhythmia. Case 1. A 26-year-old man with a 4 year-history of progressive muscle weakness and wasting was hospitalized in April, 1989. The family history showed that his younger brother had the same disease, but his parents, not consanguineous, and other family members had no neuromuscular diseases. On admission, neurologic examination showed muscle weakness and atrophy in the distal portions of four extremities. No myotonia or fasciculation was present. The deep tendon reflexes were absent except diminished bilateral PTR. Sensation and co-ordination were normal. The creatinine kinase (CK) level was moderately elevated to 691 IU/l, and the aldolase mildly to 6.9 IU/l. Normal laboratory values included serum electrolytes, glucose and thyroid function study. An ischemic forearm exercise test revealed a normal rise in serum lactate and pyruvate concentrations. The glucose response after glucagon was normal in the fasting state. An electrocardiogram and chest film were normal. An electromyogram revealed myopathic changes with mild neuropathic changes, including positive sharp waves and fibrillation potentials at rest. The muscle biopsy specimen from the left anterior tibial muscle showed scattered fibers with rimmed vacuoles and moderate variation in fiber size. Neither fiber necrosis nor inflammatory cellular infiltration was seen. Regenerating fiber was not present. An electron microscopic examination showed numerous lamellar bodies of various size. Nerve biopsy was normal. He was diagnosed as having distal myopathy with rimmed vacuoles. Muscle weakness progressed gradually over the next two years, but his general condition was good. He asked to receive the corticosteroid therapy, and rehospitalized.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Distal myopathy with rimmed vacuoles and sudden death--report of two siblings]. 826 2

High dose glucocorticoid may induce a significant myopathy with loss of thick myofilament from muscle, particularly if administered in conjunction with depolarizing drugs. Remarkably, the effect of chronic low dose glucocorticoid in muscle is vastly different, although it may induce changes in muscle glycogen metabolism as evidenced in animal experimental trials. However, there is no clear confirmation that these changes could develop similarly in patients. We evaluate clinical, functional, histological and metabolic muscle changes during chronic low-dose glucocorticoid treatment in 11 asthmatic patients. Remarkably, these patients did not develop clinical symptoms of myopathy nor significant muscle weakness or morphological changes in muscle histology. However, glycogen concentration and the activity of the main regulatory enzymes of glycogen metabolism, aldolase and creatine kinase were modified in comparison with controls. An increase in the synthesis and muscle cell deposition of glycogen and a decrease in the muscle glycogen degradation process have been suggested. These changes were not related with malnutrition. There was not correlation between histological and biochemical changes. We conclude that chronic treatment with glucocorticoid causes clear changes in glycogen metabolism in the skeletal muscle, resulting in glycogen muscle storage. The significance of these biochemical changes is unknown, but it can be well an associated phenomenon with glucocorticoid treatment.
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PMID:Patients with chronic glucocorticoid treatment develop changes in muscle glycogen metabolism. 881 73

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

We reported a case of polymyositis manifested after beta-interferon therapy for chronic viral hepatitis type C. In November 1992, a 62-year-old female was diagnosed as having chronic viral hepatitis type C. In January 1993, she was treated with beta-interferon(total 2.52 x 10(8)IU). In March 1993, after the treatment, she noticed weakness and atrophy of her lower extremities. Neurological examination revealed proximal dominant muscle weakness and atrophy of the extremities. Increased levels of serum CK and aldolase were disclosed on admission. By needle EMG, a low voltage with short duration interference pattern was noted. February 7, by muscle biopsy of the right quadriceps, necrotic myofibers, marked variation in fiber diameter, stromal mononuclear cell infiltration, and endomysial fibrosis was detected. The immunological stain of infiltrating cells in the muscle fibers revealed CD4:CD8 ratio as 64:55, whereas in conventional polymyositis CD8 cells dominate CD4 cells. Diagnosis of polymyositis was made and oral prednisolone 60 mg a day was started. Her symptoms and signs improved gradually and she was discharged after 2 months. Many adverse effects due to immunological disturbances caused by interferon treatment have been reported, but polymyositis due to interferon has been very rare. When interferon will be prescribed, manifestation of polymyositis should be considered.
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PMID:[Polymyositis after interferon beta treatment of chronic hepatitis type C]. 868 84

A 69-year-old woman was admitted to our hospital because of slight fever, general fatigue, joint pain and proximal muscle weakness. Severe elevation of serum enzyme levels of CPK, transaminase and aldolase was noted. The chest roentgengram showed diffuse reticular and nodular infiltrates. Histological examination of the transbronchial lung biopsy specimens revealed alveolitis and organizing pneumonia. Daily administration of 80 mg predonisolone was effective for both lung findings and myositis.
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PMID:[A case of polymyositis presenting histological picture of bronchiolitis obliterans organizing pneumonia with transbronchial lung biopsy specimens]. 872 Feb 70

Oral L-carnitine has been reported to lower the elevated serum myoglobin of renal failure in chronic peritoneal dialysis patients, and intravenous L-carnitine can improve muscle fatigue and cramps in chronic hemodialysis patients. In this study oral L-carnitine, 1.98 g/day, was administered to 6 chronic hemodialysis patients for 8 weeks. Serum levels of myoglobin, creatine kinase, and aldolase, as well as skeletal muscle symptoms (cramps during dialysis, fatigue, and weakness) were monitored biweekly for 12 weeks. Mean baseline serum myoglobin level was 337 +/- 34 ng/mL. By 6 and 8 weeks mean serum myoglobin was 234 +/- 39 and 233 +/- 40 ng/mL, significantly lower by the Friedman test (p < 0.05). Four weeks after carnitine was discontinued, mean serum myoglobin had risen to 320 +/- 118 ng/mL. Serum creatine kinase and aldolase levels were normal throughout the study. All 6 patients noted improvement in muscular symptoms, with maximal effect at 8 weeks, although 2 patients did not improve until 2 to 4 weeks after carnitine was stopped. We conclude that oral L-carnitine may lower serum myoglobin and improve muscle cramps and weakness in hemodialysis patients. The maximal effect of carnitine on myoglobin occurs 2 weeks before the maximal improvement in muscular symptoms.
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PMID:Effect of oral L-carnitine on serum myoglobin in hemodialysis patients. 882 May 5


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