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)

Phenylhydrazine (PHZ) is a hemolytic agent which has been used in the treatment of polycythemia vera. Recent studies performed in our laboratory have indicated that the PHZ-induced anemia is immuno-hemolytic in etiology, and a prolonged bleeding time was present in some of the rats chronically treated with PHZ. The nature of this bleeding tendency was explored in the present experiment. PHZ was administered to rats once a week for a six week period. During this time, the animals were monitored for prothrombin time (PT), activated partial thromboplastin time (APTT), fibrinogen concentration, and individual coagulation factor levels as well as routine plasma chemistries and blood cell counts. In addition, radioimmunoassays (RIA) for prostacyclin, a platelet aggregation inhibitor, and prostaglandin (PG) E2 were performed. PHZ-treated animals displayed a significant elevation in both PT and APTT when compared with saline injected controls, although plasma fibrinogen levels were not appreciably altered. Further tests revealed a PHZ-induced decrease in prothrombin and factor V levels. In addition, a significant increase in plasma serum glutamate oxaloacetate transaminase (SGOT), lactate dehydrogenase (LDH), and alkaline phosphatase levels was observed as well as a diminution in cholesterol and triglycerides following PHZ administration. PHZ treatment also induced an elevation in prostacyclin levels and transient thrombocytopenia. These findings indicate that several factors may contribute to the prolonged bleeding time in PHZ-treated rats including a drug induced thrombocytopenia possibly associated with enhanced synthesis of autologous immunoglobulin G (IgG) against the senescent red cell antigen, and diminished synthesis of vitamin K-dependent coagulation factors which may be mediated by reduced vitamin K uptake by the hypo-cholesterolemic subjects.
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PMID:Hemostatic alterations associated with phenylhydrazine-induced anemia in the rat. 262 15

In two 19-year-old girls with Wilson's disease the condition took a fulminant course, including a poor general state, marked haemolysis and ascites. In the first patient the diagnosis was histologically confirmed only after three weeks, and onset of treatment with penicillamine was therefore delayed. With this medication the concentrations of alkaline phosphatase, cholinesterase and total bilirubin returned to normal, but again became abnormal after about seven weeks. Despite substitution of clotting factors thromboplastin time remained reduced. She died 82 days after the onset of symptoms. In the second patient, treatment with penicillamine was started at once, without waiting for histological confirmation. All laboratory values became normal and remained so. It is concluded from these observations that liver transplantation is indicated if the abnormal values for cholinesterase, thromboplastin time and bilirubin do not remain normal after six weeks and if the initial suppression of alkaline phosphatase continues or occurs again.
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PMID:[Indications for liver transplantation in Wilson's disease with a fulminant course]. 265 82

Gram-negative septicemia/endotoxemia remains a serious clinical disorder that is often complicated by disseminated intravascular coagulation (DIC). Plasma antithrombin-III (AT-III) levels usually decrease during gram-negative septicemia/endotoxemia, and even moderate decreases in this major inhibitor of the coagulation system are associated with serious DIC. We demonstrated in an earlier study that prophylactic treatment of rats with 250 U/kg of AT-III followed by endotoxin challenge markedly attenuates DIC, indices of organ damage, and metabolic dysfunction. The present study was to determine whether treatment with 250 U/kg AT-III 1 hr after endotoxin challenge would be similarly efficacious. Rats treated with 250 U/kg of AT-III inactivated by human sputum elastase (ATX) served as protein controls. Blood samples for analysis were obtained 4 hr after AT-III or ATX treatment (5 hr after endotoxin challenge). Rats in the ATX treatment group exhibited abnormalities characteristic of endotoxemia, i.e., decreased fibrinogen levels and platelet counts, increases in prothrombin time and activated partial thromboplastin time, elevated serum glutamic oxaloacetic transaminase (SGOT) and alkaline phosphatase (AKP), and hypoglycemia. Treatment with AT-III markedly and significantly (P less than .05) attenuated all of these abnormalities, although survival was not increased. This study strongly suggests that supplementation of plasma AT-III is efficacious after the development of sepsis, although not as efficacious as prophylactic treatment.
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PMID:Antithrombin-III treatment limits disseminated intravascular coagulation in endotoxemia. 273 21

Case records of 177 patients admitted with Hodgkin's disease were reviewed to assess the frequency and significance of coagulation abnormalities. Prolongation of the prothrombin time, activated partial thromboplastin time, or thrombin time occurred in 56 patients, 32 percent of all evaluable cases. The most frequent clotting abnormalities involved the prothrombin time, which was increased in 43 patients (24 percent). Prothrombin time prolongation correlated with bulky or advanced disease as defined by stage (p = 0.001), constitutional symptoms (p less than 0.0001), massive mediastinal involvement (p = 0.02), and elevated alkaline phosphatase levels (p less than 0.0001). Abnormal coagulation test results followed the course of disease, normalizing with tumor regression and reappearing during relapse. Despite the surprising incidence of abnormal coagulation results, bleeding complications were reported in only two cases. Patients undergoing invasive procedures in the presence of clotting abnormalities fared no worse than those in whom procedures were cancelled. There is no evidence that complete staging evaluation should be comprised because of these abnormal test values. Extensive hematologic testing revealed no single mechanism to explain the coagulation factor disorders found in Hodgkin's disease.
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PMID:Abnormal coagulation results in patients with Hodgkin's disease. 316 Feb 35

Bromovinyldeoxyuridine (BVDU), a substituted pyrimidine analog with antiviral activity, was given orally to beagle dogs (6/sex/dosage) at dosages of 0, 5, 12, and 30 mg/kg/day for 52 weeks. Complete physical examinations, including ECG recordings and rectal temperature measurements, and clinical laboratory determinations were performed every 13 weeks. At the end of the dosing period, 4 dogs/sex/dosage were sacrificed and complete gross and microscopic examinations performed. The remaining 2 dogs/sex/dosage were sacrificed following a 13-week recovery period. BVDU had no effect on feed consumption, respiration, body temperature, or heart rate. At 30 mg/kg, males gained less weight than controls. At 12 mg/kg (males) and 30 mg/kg (both sexes) there were slight, but statistically significant decreases in mean corpuscular volume, but no changes in red blood cell (RBC) count, hematocrit, or hemoglobin, and no evidence of reticulocytosis. In males dosed at 30 mg/kg, during the last 6 months of dosing, partial thromboplastin times, serum alanine aminotransferase, and alkaline phosphatase increased, and cholesterol decreased. Histologically, bile ductule hyperplasia and gall bladder epithelial hyperplasia were present at 12 and 30 mg/kg in both sexes at the end of both the dosing and recovery periods. At 30 mg/kg, bone marrow hypocellularity and testicular germ cell atrophy were also present in males. Thus, the liver and gall bladder are the major target organs of chronically administered BVDU in dogs. BVDU causes degenerative and proliferative hepatobiliary damage, and secondarily causes changes in clinical chemical parameters. At higher dosages, there are hypoplastic and degenerative changes in the bone marrow and testes.
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PMID:The chronic toxicity of bromovinyldeoxyuridine in beagle dogs. 320 11

Zinc is essential to numerous metabolic processes in the organism, multiform symptoms being found especially in deficiencies. In addition to nutritional factors, diseases such as cirrhosis of the liver. Crohn's disease and chronic renal diseases are relevant in this context. In the present work, serum zinc levels were investigated in 109 patients with various chronic liver diseases. The lowest serum zinc concentrations were seen in patients with decompensated hepatic cirrhosis with coma. Patients with decompensated alcoholic cirrhosis had lower zinc levels as subjects with nonalcoholic cirrhosis. None of the groups exhibited a significant change in serum zinc levels during the treatment period. Laboratory data (such as transaminases, thromboplastin time, alkaline phosphatase, total proteins) did not correlate with the serum zinc concentrations. The concentration of plasma ammonia, however, appeared to be inversely related to the serum zinc levels. Thus, patients with coma had maximum ammonia and minimum zinc levels.
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PMID:Clinical studies on zinc in chronic liver diseases. 321 83

Intraabdominal pseudotumor of the plasma cell granuloma type in a 19-year-old man is reported. The patient presented with fever and weight loss lasting months, and the laboratory findings revealed high sedimentation rate, hypochromic, microcytic anemia, thrombocytosis, elevated alkaline phosphatase, decreased thromboplastin time and polyclonal hypergammaglobulinemia. When the plasma cell granuloma was removed, all laboratory findings returned to normal within 3 months and the patient remained asymptomatic during the two-year follow-up.
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PMID:[Abdominal inflammatory pseudotumor (plasma cell granuloma) with anemia and hypergammaglobulinemia]. 370 10

T-2 toxin was given as a single intravascular dose at either 0.6 or 4.8 mg/kg to different groups of 50-kg female swine. Blood samples were taken at hourly intervals for determination of concentrations or activities of the following substances in serum or plasma: creatinine, blood urea nitrogen, inorganic phosphorus, total calcium, ultrafilterable calcium, magnesium, sodium, potassium, chloride, total protein, albumin, cholesterol, glucose, alkaline phosphatase, aspartate aminotransferase, and total bilirubin. Coagulation analyses included prothrombin time, partial thromboplastin time, activated coagulation time, and fibrin degradation products. Red blood cell, white blood cell, and platelet counts, hemoglobin concentrations, and hematocrits were determined from whole blood samples. An initial leukocytosis was followed by a leukopenia. The numbers of red cells, the hemoglobin concentration, and the hematocrit were increased. Nucleated red blood cells were seen in the blood smears. The serum concentration of bound calcium decreased, while phosphorus, magnesium, and potassium increased. Clinical screening tests detected no evidence of a coagulopathy in swine given T-2 toxin intravascularly.
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PMID:Experimental T-2 toxicosis in swine. II. Effect of intravascular T-2 toxin on serum enzymes and biochemistry, blood coagulation, and hematology. 406 62

Blood coagulation changes induced by sequential oral contraceptive (OC) therapy were studied. 112 healthy women volunteers were monitored over a 2-year period while on a regimen of sequential OC therapy (50 mcg ethinyl estradiol daily from Day 5 through 14 and 50 mcg ethinyl estradiol plus 1 mg morethindrone acetate on Day 15 through 25). The treated group showed marked increases toward hypercoagulability in the Hicks and Pitney thromboplastin generation time screening test at 3 and 9 months, Factor 5 at 9 months, Factor 8 at 3 and 9 months, and fibrinogen at 3 months. Decreases from base lines were seen in antiplasmins at 24 months and in alkaline phosphatase at all intervals (3, 9, and 24 months). It was suggested that the decrease in serum antiplasmin indicates a compensatory tesponse in the fibrinolytic system to the hyperactivity of the coagulation system.
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PMID:Progestational agents and blood coagulation. V. Changes induced by sequential oral contraceptive therapy. 427 88

A patient is presented with a postpartum hepatic artery thrombosis in association with presumed fibromuscular hyperplasia. Massive hepatic infarction developed characterized clinically by fever, coma, ascites, ileus, jaundice, and renal failure; and biochemically by markedly elevated SGOT and SGPT, alkaline phosphatase, total bilirubin levels, and decreased thromboplastin time. The diagnosis was made in vivo by computed tomography (CT). Angiography revealed thrombotic occlusion of the hepatic artery in association with presumed fibromuscular hyperplasia. Laparoscopy and biopsy confirmed the diagnosis.
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PMID:In vivo diagnosis of massive hepatic infarction by computed tomography. 646 35


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