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)

An 81-year-old male with congestive heart failure and prostatic hypertrophy was found to have markedly elevated serum acid phosphatase (EC 3.1.3.2) and moderately elevated serum alkaline phosphatase (EC 3.1.3.1). Alkaline phosphatase isoenzyme analysis was performed to determine the organ source of the enzyme. There was an unsual slow-migrating alkaline phosphatase isoenzyme band in the serum of this patient suggestive of hepatic origin by a variety of biochemical tests.
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PMID:An unusual alkaline phosphatase isoenzyme in a patient with concomitant marked elevation of acid phosphatase without clinical evidence of prostatic carcinoma. 6 Oct 77

The historical and clinical features and the haematological and biochemical changes in 126 cats with hyperthyroidism are described; 125 of the cats were domestic short- or longhaired, and one was a chinchilla. There were 62 males and 64 females with a mean age of 13.0 years. The duration of signs ranged from two days to two years with a mean of 5.4 months. The historical and clinical features were weight loss, polyphagia, polyuria/polydipsia, tachycardia, hyperactivity, diarrhoea, respiratory abnormalities, other cardiac abnormalities, skin lesions, vomiting, moderately raised temperature, decreased activity, decreased appetite, congestive cardiac failure, haematuria and intermittently decreased appetite. Goitre was palpable in 123 cats. The serum total thyroxine concentrations of the cats were more than three standard deviations above the mean of the reference range. Serum total tri-iodothyronine concentrations ranged from 0.78 to 14.96 nmol/litre and were within the reference range in 11 of the cats. Mild hyperthyroidism was a much commoner cause of high normal or marginally above normal thyroid hormone concentrations than severe, concurrent, non-thyroidal illness. Other common biochemical changes were increased of serum alanine aminotransferase, urea, aspartate aminotransferase, alkaline phosphatase and lactate dehydrogenase. There were minimal changes in the red cell parameters. Leucocyte changes showed two trends: a mature neutrophilia, either with or without an accompanying leucocytosis often in association with a lymphopenia, or an eosinophilia, either with or without a lymphocytosis.
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PMID:Historical, clinical and laboratory features of 126 hyperthyroid cats. 141 11

4'-Epidoxorubicin (Epi-A) administered immediately prior to liver resection has been suggested as treatment for patients with primary liver carcinoma. Long-term toxicity was studied in rats given a single dose of Epi-A intravenously immediately prior to a standard partial hepatectomy (PH). After 52 weeks only 9% of the rats given 5 mg/kg + PH were alive, 79% of the rats given 2 mg/kg + PH and 92% of the PH control survived. The weight gain of the rats given 5 mg/kg + PH was only 17% of that of PH controls. Signs of congestive heart failure were observed in some rats while in others moderate kidney lesions. No histopathological lesions were detected by light microscopy in heart, liver, spleen and bone marrow. For the rats given 2 mg/kg + PH body weight gain, microscopic observations and blood chemistry data (total protein, albumin, alkaline phosphatase, alanine aminotransferase, total bilirubin, creatinine and urea) were comparable to the PH controls. No significant differences in survival were registered between partially hepatectomized and sham-operated rats. The results indicate that Epi-A may be given preoperatively to liver resection without inducing long-term effects on vital organs.
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PMID:Long-term toxicity of preoperative 4'-epidoxorubicin (Epi-adriamycin) in partially hepatectomized rats. 193 80

The significance of alkaline phosphatase (AP) elevation with otherwise normal transaminase and bilirubin values remains unclear. We evaluated the clinical outcome of hospitalized patients with an "isolated" AP elevation. Eighty-seven inpatients with isolated AP elevation were identified during February 1984 and followed for 1 year. Forty-five of 87 patients had normalization of AP during the follow-up period, usually within 1-3 months. The most common diagnoses in this group were congestive heart failure in nine, benign bone disease in six, and treatable malignancy in three patients. Twelve patients had no apparent explanation for the transient rise of AP. Persistent AP elevations were noted in 42 patients--14 of whom had terminal malignancies. Clinically obvious life-threatening diagnoses were made in 24 of the patients with persistent AP elevation. The etiology of AP elevation remained enigmatic in seven patients: two died, four are stable during 1 1/2-3 years of follow-up, and one patient was found to have metastatic carcinoma 17 months later. If the initial AP was greater than 1 1/2 times normal, there was a higher likelihood of persistent elevation (68% vs. 41%, p less than 0.05). Isolated elevations of AP in inpatients may be associated with a variety of medical illnesses and often normalize within months. If the AP elevation is persistent, there is usually a clinically obvious diagnosis. A reasonable approach to such patients is a careful history, physical exam, and routine lab studies to detect obvious diagnoses, followed by repeat enzyme determination at 1-3 months.
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PMID:"Isolated" elevation of alkaline phosphatase: significance in hospitalized patients. 239 49

To characterize the incidence and severity of liver function abnormalities in patients with congestive heart failure, we analyzed systemic hemodynamics and biochemical profiles in 133 patients with stable chronic congestive heart failure, secondary to a dilated cardiomyopathy. The patients were divided into three groups, based on the severity of the reduction in cardiac index (CI). The mean values of all liver function tests in groups 1 (n = 43; CI greater than or equal to 2.0 L/min/m2) and 2 (n = 48; CI greater than 1.5 and less than 2.0 L/min/m2) were essentially normal, except for minimally elevated alkaline phosphatase levels and slightly decreased albumin levels in both groups, and slight increases in levels of gamma-glutamyl transpeptidase and total bilirubin in group 2. In contrast, group 3 patients (n = 42; CI less than or equal to 1.5 L/min/m2) had the most severe heart failure, as assessed by the lowest CI and highest cardiac filling pressures, and significantly higher levels of aspartate aminotransferase (65 +/- 82 U/L), alanine aminotransferase (77 +/- 102 U/L), lactate dehydrogenase (282 +/- 91 U/L), and total bilirubin (29 +/- 14 mumol/L [1.7 +/- 0.8 mg/dL]). The percentage of patients in group 3 with these abnormalities ranged between 27% and 80%. Although linear regression analysis showed that the elevations in right atrial and pulmonary wedge pressures, and the decreases in CI, were significantly correlated with liver function abnormalities, the correlation coefficients were small. Thus, liver function abnormalities remain common in patients with congestive heart failure but are generally small in magnitude and not associated with clinically apparent hepatic disease. It is likely that reduced forward flow and passive backward congestion are both contributing factors in the pathogenesis of these biochemical abnormalities, although nonhemodynamic factors may also be important.
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PMID:Liver function abnormalities in chronic heart failure. Influence of systemic hemodynamics. 360 80

Whole body hyperthermia was induced in older, tumour-bearing dogs using a radiant heat device. Dogs were anaesthetized (thiopental), paralysed (atracurium), and mechanically ventilated (100 per cent O2) during the heating procedure. Heart rate, systolic/diastolic, and mean arterial blood pressure, and arterial blood gases were monitored throughout the procedure. Serum biochemical parameters, complete blood count, and coagulation profiles were evaluated before, during, and after whole body hyperthermia. Significant increases (p less than 0.05) were noted in heart rate, systolic pressure, diastolic pressure, and mean arterial pressure during the treatment period. A significant decrease in arterial oxygen partial pressure due to unknown causes occurred during the treatment period. Clinical evidence of cardiac decompensation was not manifested in any dog following whole body hyperthermia. Total white blood cell count, neutrophil count, alkaline phosphatase, and creatinine kinase were significantly (p less than 0.05) increased 24 h following whole body hyperthermia. These elevations returned to normal within 1 week of treatment in all dogs. Changes in coagulation profiles 24 h following the procedure were not clinically significant. Adequate pretreatment evaluation of cardiovascular, metabolic, and haemostatic function in tumour-bearing dogs is necessary to identify candidates for treatment with systemic hyperthermia. Otherwise healthy, tumour-bearing dogs withstand the physiological stress of whole body hyperthermia without significant acute or persistent toxicity and represent a valuable model for whole body hyperthermia research.
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PMID:Cardiovascular and metabolic response of tumour-bearing dogs to whole body hyperthermia. 369 85

The case histories of 1200 patients admitted to our hospital over a 20 month period were reviewed to determine the degree, frequency and cause of dissociated cholestasis as a biological syndrome. Patients were divided into two groups: group I with 80 cases, included all patients whose gamma-GT levels were more than 30 mU/ml and serum-bilirubin less than 1.2 mg/ml, with alkaline phosphatase levels between 90-180 mU/ml. Group II included those with alkaline phosphatase levels higher than 180 mU/ml (57 cases). All over incidence of dissociated cholestasis was 13.82%. Main causes in group I were infectious diseases, mainly pneumonias and urinary infections and congestive cardiac failure. In group II, neoplasias such as Hodgkin's disease and epithelial metastases and obstructions of the biliary tract such as vesicular or choledocal litiasis were the main causes. Transaminase levels underwent variable increases according to the different entities, without there being any difference between the two groups. The physiopathology as well as the anatomopathological aspects which could originate the syndrome are discussed.
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PMID:[Clinical significance of dissociated cholestasis as a biological syndrome (author's transl)]. 611 5

Hyperthyroidism was diagnosed in 131 cats during a 3 1/2-year period. The cats ranged in age from 6 to 20 years; there was no breed or sex predilection. The most frequent clinical signs included weight loss, polyphagia, increased activity, polydipsia, polyuria, and vomiting. Common serum biochemical abnormalities included high values for alkaline phosphatase activity (75%), lactate dehydrogenase activity (66%), aspartate transaminase activity (66%), and alanine transaminase activity (54%). Electrocardiographic changes included tachycardia (greater than or equal to 240 beats/min) and increased R-wave amplitude in lead II (greater than or equal to 0.9 mV) in 66% and 29% of the 131 cats, respectively. Thoracic radiography in 82 cats revealed cardiomegaly in 40 (49%) of these cats; 16 cats with congestive heart failure also had pulmonary edema or pleural effusion. In 5 cats with markedly increased fecal volume, mean 48-hour fecal fat content was significantly greater than normal, with daily fat excretion 2 to 15 times the upper limit of normal. Base-line serum thyroxine concentrations were increased above normal range in all cats, whereas triiodothyronine concentrations were increased in 127 (97%) of the 131 cats. In 11 cats tested, mean thyroxine concentration did not increase significantly after thyroid-stimulating hormone administration. Mean 24-hour percentage of thyroid radioiodine uptake in 32 hyperthyroid cats was significantly higher (39.1%) than normal (9.2%). Thyroid scans, performed on 126 cats, showed enlargement and increased radionuclide accumulation in 1 thyroid lobe in 36 (29%) and both lobes in 90 (71%) of the cats.
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PMID:Feline hyperthyroidism: pretreatment clinical and laboratory evaluation of 131 cases. 687 10

Although hypercalcemia is a well-known complication of malignant diseases, hypocalcemia seems to be a rather rare one. A 34-yr-old woman with advanced breast cancer who presented hypocalcemia is described. She had generalized multiple osteolytic bone metastases which were progressive in spite of chemo-endocrine and radiation therapy. She was admitted because of severe bone pain and dyspnea caused by bilateral pleural effusion. Laboratory examination on admission showed that the serum calcium was 9.6 mg/dl, serum total protein 5.9 g/dl, serum inorganic phosphorus 4.6 mg/dl, and serum alkaline phosphatase 29.6 King-Armstrong units. The serum calcium gradually fell to 7.0 mg/dl on the 45th hospital day when the serum total protein was 6.8 g/dl and she complained of paresthesia in the extremities. On the 58th day, severe tachycardia and hypotension developed and she died of congestive heart failure on the 67th hospital day. At that time the serum calcium was 5.4 mg/dl. During her hospital course, the plasma parathyroid hormone levels were examined repeatedly and were 0.4, 0.6, 0.6 and 0.7 ng/ml (normal; less than 0.5 ng/ml). Autopsy revealed that cancer invaded the space between the thyroid and the trachea and no parathyroid glands could be found even in the mediastinum. Microscopically the parathyroid glands were replaced completely by the cancer cells. These observations indicate that metastasis of breast cancer to the parathyroid glands caused relative hypoparathyroidism, resulting in hypocalcemia. In addition, congestive heart failure which was refractory to digitalis and diuretics might have been caused by impaired contractility of the myocardium associated with hypocalcemia.
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PMID:A case of advanced breast cancer associated with hypocalcemia. 688 61

Plasma aldosterone levels were measured in 50 patients with confirmed liver metastases from various histologically proved primary tumors. None of these patients had electrolyte abnormalities or history of benign liver disease, congestive heart failure, hypertension, or renal disease. Patients with edema, ascites, or both had significantly greater elevation of plasma aldosterone levels compared to nonedematous patients; these patients also demonstrated a substantial degree of hepatic dysfunction as evidenced by lower serum albumin levels and higher bilirubin and alkaline phosphatase levels. This study provides a rational basis for the use of the specific aldosterone inhibitor spironolactone in the treatment of patients with advanced metastatic liver disease and edematous states.
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PMID:Hyperaldosteronism associated with liver metastases. 738 77


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