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)

To determine whether or not kinin activation in the blood during severe infection with gram-negative bacteria may be related to hemodynamic abnormalities encountered, blood prekallikrein, kallikrein inhibitor and kinin values in 2l surgical patients with sepsis were compared with those in normotensive and hypotensive states. Because of reduced prekallikrein synthesis in patients with hepatic insufficiency, the normotensive and hypotensive groups were each subdivided according to the presence or absence of liver dysfunction, as indicated by elevated blood bilirubin, serum glutamic-oxalacetic transaminase or alkaline phosphatase levels. The mortality was zero in group 1, normotensive normal liver function; 80 per cent in group 2, hypotensive-normal liver function; 20 per cent in group 3, normotensive liver dysfunction, and 67 per cent in group 4, hypotensive liver dysfunction. Ultimately, the majority of deaths were due to respiratory failure. Although the blood prekallikrein level, was below normal in all groups and was significantly less in all patients with liver dysfunction, it was reduced proportionately in hypotensive patients to less than 30 per cent of the values noted in the two normotensive groups. This finding suggests prekallikrein consumption in the hypotensive groups to be the result of the process of activating kallikrein and bradykinin. This concept is supported by finding elevated kinin values, above 3 nanograms per milliliter of plasma, in only 28 per cent of those in group 1 and 12 per cent of those in group 3, while in the hypotensive patients, groups 2 and 4, the kinin level was elevated in 60 and 66 per cent, respectively.
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PMID:Kinin activation in the blood of patients with sepsis. 95 70

In 17 anaesthetized dogs effects on blood pressure, respiration and biochemical changes in blood, i.e. serum glutamic oxaloacetic transaminase (SGOT), alkaline phosphatase (Alk.Pase), and urea, after intravenous administration of pyridine at various dose levels of 88 to 880 mg/kg body weight (LD5 to LD50) are reported. Commonly observed toxicity signs and symptoms are due to action of pyridine on the nervous system. There is no direct evidence of lowering of blood pressure. Lowering of blood pressure is noticed only at lethal doses and is accompanied by marked tachycardia. Death is due to respiratory failure. The significant biochemical changes are increase in SGOT and blood urea (p less than 0.01) and decrease in serum Alk,Pase (p less than 0.01).
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PMID:Toxicological effects of intravenous administration of pyridine in anaesthetized dogs. 115 21

In a prospective study of community-acquired pneumonias, 30 patients were diagnosed with Legionnaires' disease in 15 months. Clinical, laboratory and radiologic features of these patients are reviewed and compared with those who have pneumococcal pneumonia. Alcoholism, history of smoking, previous antimicrobial therapy, gastrointestinal and neurologic manifestations, elevations of serum transaminases, alkaline phosphatase and creatinine levels were more frequent in pneumonia due to Legionella pneumophila than in pneumococcal pneumonia. The presence of respiratory failure and radiologic progression were common findings that suggested L pneumophila as the etiologic agent of a community-acquired pneumonia. Development of respiratory failure was associated with involvement of several lobes and isolation of L pneumophila in any specimen. In 21 of 30 patients with Legionnaires' disease, L pneumophila was isolated from respiratory specimens. Overall mortality was 10 percent, but it increased to 27 percent in patients not treated with erythromycin initially.
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PMID:Legionella pneumophila. A cause of severe community-acquired pneumonia. 191 47

Multiple organ system failure is a major cause of mortality in the adult respiratory distress syndrome (ARDS). We serially evaluated parameters of multiple organ function in 24 patients during the first week after the diagnosis of ARDS and related them to outcome. The adult respiratory distress syndrome was associated with sepsis (n = 16), postoperation (n = 7), and trauma (n = 1). Fourteen of the 24 patients (58 percent) died. Although there were no significant differences in the indices of pulmonary or renal dysfunction between survivors and nonsurvivors, evidence of hepatic dysfunction was different in the two groups. On the day we identified ARDS, serum bilirubin was 1.2 mg/dl +/- 0.9 mg/dl in patients who survived, and was 2.3 mg/dl +/- 2.8 mg/dl (chi +/- SD) in those who died. Initial serum glutamic oxalacetic transaminase (SGOT) and alkaline phosphatase levels were lower in survivors than in those who died (71 +/- 44 IU/L vs 399 +/- 807 IU/L, and 121 +/- 53 IU/L vs 269 +/- 243 IU/L, respectively). These abnormalities persisted during the first week of respiratory failure, with significant differences in serum bilirubin and alkaline phosphatase between survivors and nonsurvivors (p less than 0.01). The degree of pulmonary and renal dysfunction was similar in both groups. These data suggest that liver function may be a major determinant of survival in patients with the adult respiratory distress syndrome.
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PMID:Hepatic dysfunction in the adult respiratory distress syndrome. 292 17

A 26-year-old male with renal allograft, who received immunosuppressive treatment with azathioprine, presented marked elevations of serum biliary tract enzymes, such as gamma-glutamyl transpeptidase (5,609 units/l) and alkaline phosphatase (60.5 Bessey-Lowry units), 14 months after transplantation. Two months later the patient became icteric; he died of respiratory failure 19 months after the renal allograft. Postmortem examination revealed intrahepatic cholestasis with minimal inflammatory cell infiltration, indicating drug hepatotoxicity.
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PMID:Nonicteric liver damage with a gamma-glutamyl transpeptidase level of 5,609 units/l in a renal-transplant recipient receiving azathioprine. 615 83

A new familial disorder, inherited as an autosomal dominant trait and characterized by dual features of neurologic degeneration and skeletal disorganization, is reported. The neurologic disease is a degenerative process of lower motor neurons and develops in middle age with progressive muscle weakness and ends in respiratory failure and premature death. Clinical examination, electromyography, and muscle biopsy with histochemical stains are diagnostic. The skeletal disorganization resembles Paget's disease of bone. It is characterized by polyostotic radiographic abnormalities, elevated serum alkaline phosphatase of bone origin, abnormal radioisotopic bone scan, elevated hydroxyprolinuria, and bone histology.
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PMID:A new familial disorder of combined lower motor neuron degeneration and skeletal disorganization. 718 74

One hundred twelve client-owned dogs with blastomycosis were treated with itraconazole, 5 or 10 mg/kg/d. The first group of 70 dogs treated in 1987 and 1988 received 10 mg/kg/d (group 1), and the second group of 42 dogs treated after October 1988 received 5 mg/kg/d (group 2). Even though the groups were treated at different times, the dogs were similar in age and gender distribution, number of sites involved, and percent and severity of pulmonary involvement. The proportion of dogs cured with a 60-day course of itraconazole was similar for both groups (53.6% versus 54.3%) and for a second historical control group treated with amphotericin B (57%); the recurrence rate was also similar, 20%, 21.4%, and 20%, respectively. Dogs treated with itraconazole had similar mortality rates (25.7% at 5 mg/kg/d; 25% at 10 mg/kg/day) to those treated with amphotericin B (23%). Seventeen of the 23 dogs that died (74%), did so during the first week of treatment; these early deaths were usually attributed to respiratory failure. The only site of infection that was significantly associated with failure (death or recurrence) was the brain. There was a marked difference in survival times between dogs without lung disease or with mild lung disease compared with dogs with moderate or severe lung disease. Serum itraconazole concentrations reached steady state by 14 days of treatment. Dogs receiving 5 mg/kg/d of itraconazole (group 2) had mean serum concentrations of 3.55 +/- 2.81 mg/mL (range, 0.67 to 10.8 micrograms/mL), whereas dogs receiving 10 micrograms/kg/d (group 1) had mean concentrations of 13.46 +/- 8.49 micrograms/mL (range, 1.8 to 28 micrograms/mL) (P < or = .001). There was no association between cure and serum itraconazole concentrations. Dogs in group 1 had significantly more adverse effects than dogs in group 2 (P = .046). Anorexia was the most common adverse effect, occurring in 14.9% of dogs in group 1. Only 8% of dogs in group 2 had adverse effects. Serum concentrations of itraconazole were positively correlated with serum alkaline phosphatase and alanine aminotransferase activities. Our findings indicate that itraconazole administered at a dose of 5 mg/kg/d is the drug of choice for blastomycosis in dogs.
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PMID:Treatment of blastomycosis with itraconazole in 112 dogs. 894 68

Hypophosphatasia is associated with a defect of the tissue-non-specific alkaline phosphatase gene. We performed a mutational analysis in a surviving patient diagnosed at birth as having hypophosphatasia, on the basis of a low level of serum alkaline phosphatase (ALP) activity and characteristic radiographical findings. She had two sisters, one of whom died of respiratory failure complicated by perinatal hypophosphatasia; the other seemed healthy, with a relatively low activity level of ALP. The patient's parents also had low ALP activity. Sequence analysis of the tissue-nonspecific alkaline phosphatase gene was performed, using genomic DNA and total RNA from the skin fibroblasts of the patient and the peripheral mononuclear cells of her parents. The conversion of Phe to Leu at codon 310 (F310L) and Gly to Arg at 439 (G439R) were identified in the patient. Interestingly, the reconstructive experiments demonstrated that the F310L mutant exhibited an ALP activity level 65% of the normal level, whereas the mutant G439R had no activity. Moreover, the digestion by StuI, after a PCR using complementary DNA extracted from fibroblasts of the patient and lymphocytes of her father, revealed a relatively low messenger RNA level of F310L. These findings suggest that the neonatal case of hypophosphatasia was associated with compound mutations, one of which caused the loss of ALP activity and the other of which caused a slight reduction of the ALP activity, with a relatively low level of messenger RNA.
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PMID:Identification of novel missense mutations (Phe310Leu and Gly439Arg) in a neonatal case of hypophosphatasia. 895 59

We report factors associated with severe manifestations of histoplasmosis (such as shock, respiratory failure, and death) in patients with AIDS during an outbreak. Severe disease was present in 28 of 155 patients (17.9%). The following factors were associated with severe disease: black race (odds ratio [OR], 2.8; 95% confidence interval [CI], 1.2-6.2); hemoglobin level <9.5 g/dL (OR, 2.7; 95% CI, 1.2-6.4), partial thromboplastin time >45 s (OR, 3.1; 95% CI, 1.1-9.3); alkaline phosphatase level >2.5 times normal (OR, 3.4; 95% CI, 1.3-8.7); aspartate aminotransferase level >2.5 times normal (OR, 4.2; 95% CI, 1.7-10.0); bilirubin level concentration >1.5 mg/dL (OR, 9.2; 95% CI, 2.5-34.3); creatinine concentration >2.1 mg/dL (OR, 8.3; 95% CI, 2.2-31.9); and albumin concentration <3.5 g/dL (OR, 4.6; 95% CI, 1.3-16.4). Zidovudine use was associated with decreased risk of severe disease (OR, 0.3; 95% CI, 0.1-0.7). Multivariate analysis showed that a creatinine value >2.1 mg/dL (OR, 9.5; 95% CI, 1.7-52) and an albumin value <3.5 g/dL (OR, 4.8; 95% CI, 1.0-22) were associated with an increased risk of severe disease, and zidovudine therapy remained associated with a decreased risk (OR, 0.2; 95% CI, 0.1-0.6). Findings associated with severe histoplasmosis should be recognized early and the cases managed aggressively.
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PMID:Factors associated with severe manifestations of histoplasmosis in AIDS. 1085 63

A 77-year-old man with pneumonia associated with acute myeloid leukemia was introduced to the hepatology unit at our hospital for hyperbilirubinemia. He had been suffering from a high fever because of pneumonia. He was icteric and his serum concentrations of total and direct bilirubin were 13.1 and 7.9 mg/dl, respectively. However, the other standard biochemical examinations for hepatic function, such as serum concentrations of aspartate aminotransferase, alanine aminotransferase, gamma-glutamyl transpeptidase and alkaline phosphatase were normal except for lactate dehydrogenase. Lactate dehydrogenase isoenzyme analysis revealed that the high concentration was derived from leukemia cells. Ultrasonography of the abdomen revealed no abnormality in the liver or biliary tract. Administration of antibiotics for pneumonia decreased the serum bilirubin concentration, however, he died because of respiratory failure caused by the progression of pneumonia at 33 days after the admission. It was suggested that a disturbance in the bilirubin metabolism without hepatocyte necrosis or mechanical cholestasis might be involved in the pathogenesis of hyperbilirubinemia in patients with infectious diseases.
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PMID:Unusual hyperbilirubinemia associated with bacterial pneumonia and acute myeloid leukemia. 1280 38


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