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)

The effects of soman poisoning on hematological (counts of red blood cells (RBC), white blood cells (WBC), and platelets and measurement of hematocrit) and coagulation parameters (prothrombin time, activated partial thromboplastin time, thrombin time and concentrations of fibrinogen, factor V, factor VII, and factor XI) and serum biochemistry (concentration of albumin, protein, calcium, cholesterol, triglycerides, blood urea nitrogen (BUN), magnesium, and creatinine and activities of alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, cholinesterase, creatinine phosphokinase (CPK), hydroxybutyrate dehydrogenase, and amylase) were determined at 1, 2, 4, 24, and 48 hours after poisoning of rabbits. There were significant (p less than 0.05) decreases in the RBC counts in all treatment groups that were measured initially at 4 hours and were reflected by parallel decreases in the hematocrit values. These changes were probably due to an increase in the hemolysis of the RBC rather than a decrease in the production of RBC. There were minor changes in the coagulation parameters. Generally, the fibrinogen content increased. The activated partial thromboplastin time decreased significantly (p less than 0.05) 24 and 48 hours after soman (50 micrograms/kg) poisoning. Blood cholinesterase values were significantly reduced in all treatment groups at all time periods. The CPK activity was increased after 4 and 24 hours in the 20 and 50 micrograms/kg soman groups. There were minor changes in the other biochemistry values, but none that showed a dose-response relationship; thus, they were considered to be of limited significance with regard to the toxic manifestations of soman exposure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of soman poisoning on hematology and coagulation parameters and serum biochemistry in rabbits. 212 98

Effects of dietary aflatoxin (AF) and T-2 toxin, singly and in combination, were evaluated in growing crossbred (Yorkshire x Landrace x Hampshire) pigs. The experimental design consisted of 4 treatment groups of 6 barrows each fed diets containing 0 mg of AF and T-2/kg of feed (controls; group 1), 2.5 mg of AF/kg of feed (group 2), 10 mg of T-2/kg of feed (group 3), or 2.5 mg of AF plus 10 mg of T-2/kg of feed (AF + T-2; group 4) ad libitum for 28 days (7 to 11 weeks of age). Production performance, and serum biochemical, and hematologic evaluations were made weekly. Body weight and body weight gain were depressed by all toxin treatments, but the effect of AF and T-2 toxin in combination was less than additive. Liver and kidney weights, as a percentage of body weight, were increased by AF treatment, and heart weight, as a percentage of body weight, was increased by T-2 treatment. Treatment with T-2 toxin induced necrotizing contact dermatitis on the snout, buccal commissures, and prepuce. Consumption of AF resulted in increased serum activities of alkaline phosphatase, aspartate transaminase, cholinesterase, and gamma-glutamyltransferase, and decreased serum concentrations of urea nitrogen, cholesterol, albumin, total protein, calcium, potassium, magnesium, and phosphorus. Consumption of T-2 toxin resulted in increased serum triglyceride concentration and decreased serum iron concentration. Treatment with AF induced lower serum unsaturated iron-binding capacity and high RBC count, PCV, hemoglobin concentration, WBC count, and prothrombin time.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of treatment of growing swine with aflatoxin and T-2 toxin. 224 Jul 92

To evaluate the impact cirrhosis has on survival the records of 40 cirrhotic trauma victims from the registries of two Level 1 trauma centers were reviewed and probability of survival calculated using the TRISS methodology. Mechanism of injury, anatomic location, involvement of single or multiple sites, presence of ascites, elevations in serum glutamic oxaloacetic transaminase (SGOT), alkaline phosphatase, serum bilirubin, prothrombin time (PT), and hypoalbuminemia were tabulated for each patient. Contingency tables were created for injury and hepatic parameters, as related to survival, and subjected to chi square analysis. Loglinear analysis was performed on all significant parameters to evaluate the independent effects of injury characteristics and hepatic insufficiency on survival. Predicted survival was 93%; observed survival was 70% (Z = -6.92; p less than 0.001). Cause of death was multiple-system organ failure (9) and closed head injury (3). Admission markers of poor outcome included one or more of the following: ascites, elevated PT or bilirubin, history of motor vehicle accident, multiple trauma, or blunt abdominal trauma requiring laparotomy. Loglinear analysis revealed that the presence of ascites, elevated PT, or bilirubin, further diminished the rate of survival for any individual injury characteristic. We concluded that survival among cirrhotic trauma victims was significantly lower than predicted. In addition the presence of hepatic insufficiency further diminishes survival, regardless of the injury sustained.
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PMID:Cirrhosis in the trauma victim. Effect on mortality rates. 230 96

Six patients were studied to evaluate the efficacy and safety of plasma exchange (PE) in the treatment of primary biliary cirrhosis (PBC). All patients were affected by PBC at stage III-IV and presented symptoms refractory to pharmacologic therapy. Patients underwent PE for a mean period of 40 weeks (range 10-88). A mean of 33 liters (range 17-64) of plasma per patients was removed. Patients reported less fatigue (4/6), pruritus (5/5), nausea (3/3), Sjogren's syndrome (2/6), and painful neuropathy (2/3). A reduction of xanthomata was noted in one of the three affected patients. Definitive improvement was seen in the patient with Raynaud's phenomenon. A significant reduction was noted for serum cholesterol and gammaglobulins. ALT, AST, gamma-GT, alkaline phosphatase, bilirubin, prothrombin activity, AMA titers were not affected by PE. All patients suffered some mild adverse effects during PE. Two patients (IV stage) developed late edema and ascites after 34 and 44 weeks of treatment. We conclude that PE can be considered effective chronic treatment for advanced symptomatic PBC refractory to pharmacological therapy.
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PMID:Effects of plasma exchange (PE) in primary biliary cirrhosis (PBC). A pilot study. 231 37

Tissue cholestasis is a histologic feature in some patients with alcoholic liver disease, but its significance is unknown. We studied prospectively the clinical, laboratory, and histologic findings of 306 chronic male alcoholics in whom liver tissue was available. Tissue cholestasis permitted identification of two groups: group I, absent or mild cholestasis (239 patients), and group II, moderate to severe cholestasis (67 patients). Statistical evaluation was performed by Student's t test and regression analyses. In patients with tissue cholestasis, 97% had elevated serum cholylglycine levels, while only 61% had significant jaundice (serum bilirubin greater than 5 mg/dl). In patients without tissue cholestasis, 66% had elevated serum cholylglycine and 13.5% jaundice. Highly significant statistical correlations (P less than 0.0001) were found between cholestasis and malnutrition, prothrombin time, AST, alkaline phosphatase, bilirubin, Maddrey's discriminant function, serum cholylglycine level, albumin, and histologic severity score. In group I, 54% survived 60 months versus 22% in group II (P less than 0.0001). Highly significant statistical correlations (P less than 0.0001) were noted between serum cholylglycine levels and the parameters enumerated earlier, but not with survival. We conclude that tissue cholestasis is a highly significant prognostic indicator of outcome in alcoholic hepatitis and is more consistently associated with bile salt retention than jaundice.
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PMID:Prognostic significance of cholestatic alcoholic hepatitis. VA Cooperative Study Group #119. 236 44

The time change of laboratory variables in cirrhosis was studied by analysis of data from 488 patients with cirrhosis included in a controlled clinical trial of long-term prednisone vs. placebo. In the placebo group, a marked regression towards normal was seen within 3 months of entry into the trial (increase in serum albumin, acetylcholinesterase, cholesterol, hemoglobin and decrease in erythrocyte sedimentation rate). The subsequent course did not show a clear pattern, except for a slight increase in serum bilirubin and decrease in albumin. When studied in relation to the time of death in patients dying from a "hepatic" cause, marked increase in bilirubin and decrease in prothrombin index, albumin and cholesterol were seen in the year prior to death with little change before that time. In the prednisone group, a more marked decrease in bilirubin, SGOT, alkaline phosphatase, gamma-globulin, sulfobromophthalein retention, erythrocyte sedimentation rate and increase in leukocytes, prothrombin index and cholesterol were seen during the first 3 months. In relation to time of death from a "hepatic" cause, similar changes were seen as in the placebo group except that alkaline phosphatase increased and cholesterol did not decrease. A beneficial effect of prednisone on survival, as expressed by a previously developed therapeutic index, was associated with decrease in SGOT, alkaline phosphatase and gamma-globulin within the first 3 months. An increase in SGOT during prednisone seemed to be associated with harmful effects of therapy.
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PMID:Changes of laboratory variables with time in cirrhosis: prognostic and therapeutic significance. 241 49

Hydrated sodium calcium aluminosilicate (HSCAS), an anticaking agent for mixed feed, was added to the diets of growing barrows and was evaluated for its potential to ameliorate the clinical signs of aflatoxicosis. The experimental design consisted of 6 treatments of 5 barrows each at concentrations of 0 g of HSCAS and 0 g of aflatoxin (AF)/kg of feed (control), 5 g of HSCAS/kg of feed (0.5%), 20 g of HSCAS/kg of feed (2.0%), 3 mg of AF/kg of feed, 5 g of HSCAS (0.5%) plus 3 mg of AF/kg of feed, or 20 g of HSCAS (2.0%) plus 3 mg of AF/kg of feed. Barrows were maintained in indoor concrete-floored pens, with feed and water available ad libitum for 28 days (from the age of 7 to 11 weeks). Barrows were observed twice daily and were weighed weekly, and blood samples were obtained weekly for hematologic and serum biochemical measurements. At the termination of the study, barrows were euthanatized and necropsied. Body weight gains were diminished significantly (P less than 0.05) by consumption of 3 mg of AF/kg of feed, whereas body weight gain in barrows consuming diets containing HSCAS or HSCAS plus AF did not differ from that in control barrows. Serum enzymatic activities of alkaline phosphatase and gamma-glutamyl transferase and prothrombin time were increased in barrows consuming 3 mg of AF/kg of feed, but not in those consuming HSCAS or HSCAS plus AF.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prevention of aflatoxicosis by addition of hydrated sodium calcium aluminosilicate to the diets of growing barrows. 256 91

Interleukin-2 (IL-2)-based immunotherapy is associated with profound reversible cholestasis and hyperbilirubinemia. We performed a nonrandomized retrospective and prospective analysis to determine the incidence, characteristics, clinical course, and nature of the IL-2-induced liver dysfunction in patients with cancer. Patients received IL-2 at a dose of 20,000 to 100,000 units (U)/kg thrice daily for up to 5 days. Fifty-one patients on adjuvant treatment protocols received a mean of 10.18 +/- 2.38 IL-2 doses and 11.67 +/- 4.16 doses were delivered to 210 patients with advanced disease during this period. Retrospective analysis of all patients receiving this therapy revealed increases in the following liver function tests expressed as median, 25th percentile, and 75th percentile (range): bilirubin (mg/dL) 4.5, 2.6, 6.5 (.4 to 38.5); alkaline phosphatase (U/L) 256, 179, 378 (56-1680); SGOT (U/L) 80, 52, 117 (18 to 483); SGPT (U/L) 91, 64, 132 (20-540); prothrombin time 13.4, 12.8, 14.5 (10.8 to 35.4); and albumin (g/dL) values decreased (trough) slightly 3.0, 2.8, 3.2 (2.3 to 3.8). Multiple regression analysis revealed several factors that were significantly associated with the increase in bilirubin when jointly considered (model P2 less than or equal to .001) including total IL-2 dosage, increase in creatinine, alkaline phosphatase, weight, and SGOT. Similar increases were noted in a prospectively evaluated group of 10 patients. A return to normal levels of bilirubin was noted within 5.6 days of stopping IL-2. Fasting serum cholylglycine increased from a mean of 32.3 +/- 1.6 to a peak of 1556.0 +/- 625.0 mg/mL. Although conventional ultrasound examinations were unrevealing, tissue ultrasound examinations revealed a mean scatterer spacing (MSS) increase compared to baseline of .10 +/- .04 (P less than .02) suggesting hepatic edema or an infiltrative process. Further, computerized hepatobiliary nuclear medicine scans revealed a delay in uptake (2.2 +/- 0.5 fold greater) and excretion (8.0 +/- 5.9 fold greater) of technetium-99m labeled disofenin. These findings support the development of profound reversible cholestasis as the primary basis for the elevated bilirubin in patients undergoing IL-2 treatment and may have implications for understanding the jaundice observed in some patients postoperatively as well as that associated with sepsis and other inflammatory disorders. Specifically, the release of IL-2 or the induction of other factors similarly induced by IL-2 may be responsible for these findings. Tissue ultrasound and computerized hepatobiliary scans provide additional noninvasive assessments of liver function and physiology.
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PMID:Interleukin-2 induces profound reversible cholestasis: a detailed analysis in treated cancer patients. 258 24

Serum levels of F protein, a 44 kD cytoplasmic protein mainly found in hepatocytes, became elevated during episodes of graft dysfunction following orthotopic liver transplantation. In a study of 27 liver transplant recipients, the rise in F protein did not precede rises in the other conventional biochemical indices of hepatic dysfunction. Serum F protein concentration significantly correlated with serum levels of aspartate aminotransferase, gamma-glutamyltransferase, alkaline phosphatase, and bilirubin (all P less than 0.001) and also with the prothrombin time (P = 0.048). Despite its high concentration in liver cells, this marker does not provide any additional benefit in the diagnosis of graft dysfunction or in monitoring liver allograft function following transplantation.
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PMID:Serum F protein estimation in liver allograft recipients with graft dysfunction. 259 89

Recently, the association of granulocytic fragments on blood smear with leukoerythroblastosis in sepsis has been identified in nine patients. Granulocytic fragments were identified by both light and electron microscopy as well as cytochemistry. Leukoerythroblastosis is a poorly defined, uncommon syndrome with leukocytosis, left shift, and nucleated red blood cells (nRBCs) disproportionate to the degree of anemia, which may be associated with leukemia or neoplasia in the bone marrow, acute infection, hemolysis, myelofibrosis, or miscellaneous causes. Here a subgroup with high white blood cells (WBC) and acute infection was studied. The corrected WBC for nine patients was 40 x 10(9) per L with 33 nRBC per 100 WBC; serum C3 and C4 levels before and after the development of leukoerythroblastosis were 0.6 +/- 2 g per L; 0.18 +/- 0.04 g per L pre-leukoerythroblastosis and 0.7 +/- 0.46 g per L; 0.30 +/- 0.27 g per L post-leukoerythroblastosis, respectively, in four patients. The platelet count, prothrombin time (PT), and activated partial prothrombin time (aPTT) were 133 x 10(9) per L, 24.4 sec., and 53.5 sec., respectively, for nine patients. Multiphasic chemistries at the time of leukoerythroblastosis were measured in five patients; abnormal values included calcium of 2.0 +/- 0.4 mmol per L, creatinine of 336 +/- 130 mumol per L, total protein of 45 +/- 17 g per L, albumin of 27 +/- 11 g per L, total bilirubin of 421 +/- 362 mumol per L, uric acid of 499 +/- 264 mumol per L, triglycerides of 4.9 +/- 3.7 mmol per L, and alkaline phosphatase of 3.5 +/- 1.0 mu kat per L.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Biochemical values, complement levels, and hemostatic data in septic leukoerythroblastosis. 260 78


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