Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report on a 43-year-old patient with short stature (hyposomia), allegedly the result of vitamin-D-resistant rickets, previously treated for ankylosing spondylitis. In addition, a uricostatic drug therapy was also necessary because of hyperuricemia with gout attacks. Further examinations revealed the accurate diagnosis: Rathbun's disease. Hypophosphatasia is a hereditary disorder characterized by a deficiency of liver/bone/kidney alkaline phosphatase activity in serum and tissues with defective bone mineralization, bone deformities, short stature, early loss of teeth, and craniosynostosis. In our patient radiographic features were spinal hyperostosis, but with syndesmophytes, chondrocalcinosis of peripheral joints and intervertebral discs, calcific periarthritis and premature closure of skull sutures. Curved ribs and short stature were suggestive of rickets. The aim of this case report is to demonstrate the close relations between hypophosphatasia and spondylitis ankylosans in respect to radiology and clinical symptoms.
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PMID:[Rathbun syndrome (hypophosphatasia). Clinical aspects: dwarfism and Bechterew symptoms]. 179 58

The pretreatment characteristics of 265 multiple myeloma patients treated between 1977 and 1983 were evaluated as potential prognostic factors for survival. Patients whose diagnosis was based on bone marrow plasmacytosis (greater than 30%) were noticed to have poorer survival (P less than 0.001). Although classification of patients according to stage has traditionally been used to identify prognostic groups, differences in survival were noted only between Stage III and Stage I or II patients using one of two common staging systems. Multivariate analysis using Cox's proportional hazards model identified the following prognostic factors in order of importance: plasmacytosis (hazard ratio [HR] = 2.2, 95% confidence interval [CI] = 1.49 to 3.27), hypercalcemia (HR = 1.68, CI = 1.22 to 2.32), hypoalbuminemia (HR = 1.51, CI = 1.15 to 1.99), alkaline phosphatase (HR = 1.62, CI = 1.18 to 2.23), hyperuricemia (HR = 1.46, CI = 1.09 to 1.96), and renal insufficiency (HR = 1.48, CI = 1.08 to 2.04). All patients were followed from 2 to 7.5 years and 130 (49%) survived over 2 years. Logistic regression analysis demonstrated that hyperuricemia, hypoalbuminemia, renal insufficiency, plasmacytosis, gender, alkaline phosphatase, and hypercalcemia were significant predictors of 2-year survival. Knowledge of these factors could be of value in predicting prognosis and planning therapy in patients with multiple myeloma.
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PMID:Prognostic factors in multiple myeloma. 204 58

Two patients with chronic neutrophilic leukemia, a rare myeloproliferative syndrome, are reported with a review of the literature. The major features of the 34 collected cases (including the two patients reported here) were persistent leukocytosis simulating a leukemoid reaction, hepatosplenomegaly, hyperuricemia, increased vitamin B12 blood level, increased leukocyte alkaline phosphatase and absence of the Philadelphia chromosome. Infection was the leading cause of death. Concomitant multiple myeloma was found in eight patients.
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PMID:[Chronic neutrophilic leukemia: apropos of 2 cases and review of the literature]. 208 13

A 57-year-old man complains of a reduced exercise tolerance and bone pain for years. There is a past medical history of hyperuricemia and anemia of unknown etiology. In a routine examination a leukocytosis of 64,000 per ml, increased number of thrombocytes and an elevated level of lactic dehydrogenase is found. The suspected diagnosis of myeloproliferative disorder, in the present case of chronic myelogenous leukemia, is confirmed by a diminished neutrophil alkaline phosphatase activity, bone marrow biopsy and the demonstration of the Ph1 (Philadelphia) chromosome. Magnetic resonance imaging reveals an infiltration of the bone marrow. After the initial treatment with busulfan the white cell count is lowered.
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PMID:[Weakness, bone pain]. 236 65

A group of 72 patients with chronic renal failure (22 non-dialysed and 50 hemodialysed) were studied for the behaviour of the threshold of vibratory sensibility in upper and lower limbs at frequencies of 125 and 250 Hz. The patients dialysed were examined just before hemodialysis. All the patients were studied for the following parameters: concentration of calcium, inorganic phosphates, PTH, creatinine, uric acid in the blood serum and the activity of general alkaline phosphatase and its thermolabile fraction (osseous). The patients dialysed differed from the patients non-dialysed in higher creatinine, uricemia and the activity of alkaline phosphatase, both general and its "osseous" fraction. But they did not differ significantly in the concentration of phosphates, PTH and calcemia . Two thirds of patients with chronic renal failure, both dialysed and non-dialysed, revealed a significant increase in the threshold of vibratory sensibility, better marked in lower limbs then in upper limbs. As opposed to patients non-dialysed, patients dialysed did not show a significant correlation between the level of PTH in blood serum and the threshold of vibratory sensibility. Dialysotherapy did not influence significantly the frequency of disorders in vibratory sensibility. Considering the fact of almost identical frequency of disorders in vibratory sensibility both in patients dialysed and non-dialysed and also the lack of correlation between the level of lesion of vibratory sensibility and the concentration of PTH in blood serum, the participation of parathormone in the pathogenesis of uremic neuropathy seems to be doubtful.
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PMID:[Study of vibration sensation in the aspect of disorders of calcium-phosphate metabolism in patients with chronic renal failure]. 264 22

The metabolic effects of ethanol are due to a direct action of ethanol or its metabolites, changes in the redox state occurring during its metabolism, and modifications of the effects of ethanol by several nutritional factors. Ethanol causes hyperglycemia or hypoglycemia depending whether or not glycogen stores are adequate, inhibits protein synthesis, and results in a fatty liver and elevations in serum triglyceride levels. Increases in serum lactate, results from the increased reduced nicotinamide-adenine dinucleotide/nicotinamide-adenine dinucleotide + (NADH/NAD+) ratio, and hyperuricemia probably occurs owing to the increased turnover of adenine nucleotides after ethanol ingestion. Ethanol decreases thiamine absorption and decreases the enterohepatic circulation of folate. Acetaldehyde, the major metabolite of ethanol, increases the degradation of pyridoxal 5'-phosphate by displacing it from its binding protein and making it susceptible to hydrolysis by membrane-bound alkaline phosphatase. Chronic ethanol administration also results in decreased vitamin A stores and reduced bone mass and blood levels of 25-hydroxyvitamin D. The mechanism whereby ethanol affects these vitamins and their associated enzymes is unknown.
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PMID:The effect of ethanol and its metabolites on carbohydrate, protein, and lipid metabolism. 329 39

The metabolic effects of ethanol are due to a direct action of ethanol or its metabolites, changes in the redox state occurring during its metabolism, and modifications of the effects of ethanol by nutritional factors. Ethanol causes hyperglycemia or hypoglycemia depending on whether glycogen stores are adequate, inhibits protein synthesis, and results in fatty liver and in elevations in serum triglyceride levels. Increases in high-density lipoprotein cholesterol after ethanol ingestion may explain the lower risk of myocardial infarction and death from coronary disease after moderate drinking. Increases in serum lactate, resulting from the increased NADH/NAD+ ratio, and hyperuricemia, most likely the result of increased turnover of adenine nucleotides, are common transient effects of ethanol ingestion. Causes of vitamin deficiencies in alcoholism are decreased dietary intake, decreased intestinal absorption, and alterations in vitamin metabolism. Ethanol decreases thiamine absorption and decreases the enterohepatic circulation of folate. Acetaldehyde increases the degradation of pyridoxal 5'-phosphate by displacing it from its binding protein and making it susceptible to hydrolysis by membrane-bound alkaline phosphatase. Ethanol decreases hepatic vitamin A concentration and its conversion to active retinal, and modifies renal metabolism of vitamin D.
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PMID:Metabolic effects of alcohol. 388 Dec 85

True reference values (TRV) should ultimately be determined in blood from inactive, unstimulated rats but in practice, acceptable reference values (ARV) may be established using blood from decapitated or anesthetized animals if one is cognizant of variations associated with blood sampling procedures. Data reported here illustrate some variations in serum biochemical values following decapitation or anesthesia. Decapitation does not provide serum in which ARV for sodium, potassium or lactate dehydrogenase can be found but ARV can be determined for glucose, insulin and several other parameters. It is suggested that both TRV and ARV for serum electrolytes be determined using serum from cannulated rats. All three anesthetics raised glucose levels and ether and halothane increased alkaline phosphatase activity. Both halothane and Innovar-VetR decreased insulin:glucose ratios suggesting inhibition of insulin release from the pancreas. Innovar-VetR also produced hypoxia due to severe respiratory depression and bradycardia as well as hyperuricemia, hyperglycemia and hyperphosphatemia. Techniques most likely to provide ARV should be of the shortest possible duration, afford least respiratory and cardiovascular suppression and minimize stimulation of the sympathetic nervous system.
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PMID:Variation of rat serum biochemical values following decapitation or anesthesia with ether, halothane or Innovar-VetR: rapid Innovar-VetR-induced hyperuricemia and hyperglycemia. 704 81

Analysis of 2,547 cases of multiple myeloma (MM) reported in China in 1980s showed that the clinical manifestations are characterized by multipliey. High misdiagnosis rate (69%) and multiple complications. While the monoclonal protein had more than 25 immunological type, IgG myeloma was the commonest (43.1%). Light chain subgroup trended to have higher incidence of renal damage (76.9%). Plasma cell leukemia eventually developed in 30 cases. In order to improve diagnosis and avoid misdiagnosis, the key points are 1, to better the recognition of clinical features of MM. 2. patient should receive urine Bence-Jones protein, immunoglobulins, immunoeletrophresis, bone X-ray and multiple site bone marrow puncture whenever one of such manifestations as unexplained anemia, skeletal pain, proteinuria, elevation of ESR, hyperviscosity syndrome, hypercalcemia, hyperuricemia, elevation of alkaline phosphatase, pathological fractures and diffuse osteoporosis. 3. immuno-binding electrophoresis and immunofluorence antibody detection should be done for suspected cases with normal immunoglobulin level.
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PMID:[On the diagnosis of multiple myeloma an analysis of 2,547 domestic cases]. 765 87

The mechanism of crystal deposition in joints varies with the chemical nature of the crystal. Crystallisation of monosodium urate, characteristic of gout, requires a neutral pH and supersatured tissues, which is the basis for the clinical definition of the upper limit of normal blood uric acid level. The appearance of crystals also is dependent on time since crystallisation of monosodium urate is very slow. Inhibitory or promoting factors could intervene and explain rare cases of gout without hyperuricemia or the rapid crystallisation which seems to characterise some types of drug-induced gout. Crystal deposits of calcium pyrophosphate dihydrate form mainly in the cartilage where they seem favoured by ageing or by trauma, which could deplete cartilage of crystallisation inhibitors, notably proteoglycans. High pyrophosphate levels within cartilage also play an important role. The appearance of these pyrophosphates in the interstitial cartilagenous medium would be in large part due to the activity of an ectoenzyme, nucleoside triphosphate pyrophosphatase; increased activity of this ectoenzyme could be responsible for some chondrocalcinosis. Chronic hypercalcaemia can also be involved in the pathogenesis of cartilage deposition of calcium pyrophosphate dihydrate by raising the calcium-pyrophosphate product, or by decreasing the activity of alkaline phosphatase, an enzyme responsible for breakdown of extracellular pyrophosphates. The pathophysiology of calcium phosphate deposits is poorly understood. For some authors, these deposits occur within matrix vesicles, but for others, within collagen fibres. Increase in the calcium-phosphate product can also be a cause, for example, during renal osteodystrophy or vitamin D intoxication.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Mechanism of crystal deposition in the joints]. 817 67


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