Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alterations in coagulation factors have been reported during acute pancreatitis. Therefore the relationship of coagulation measurements to complications of pancreatitis was evaluated prospectively in 35 patients in whom 130 serial coagulation profiles were performed, consisting of fibrinogen, platelet count (PC), fibrinogen-fibrin-related-antigen (FR-antigen), prothrombin time (PT), partial thromboplastin time, thrombin time, euglobulin clot lysis, and Factors II, V and VII-X levels. During attacks of acute pancreatitis, over-all mean initial fibrinogen and PC of 268 mg. per 100 ml. and 214,000 per cubic millimiter rose significantly (p less than 0.005) to peaks of 362 mg. per 100 ml. and 477,800 per cubic millimeter by day 6 to 10. Mean initial FR-antigen of 4.8 microgram per milliliter rose to peak 7.4 microgram per milliliter on day 5. In 21 patients with mild pancreatitis, mean highest fibrinogen, PC, FR-antigen, and PT were 329 mg. per 100 ml., 361,500 per cubic millimeter, 5.3 microng per milliliter and 14.1 seconds. These values were significantly higher (p less than 0.05 to 0.01) in patients with severe pancreatitis, being 422 mg. per 100 ml. 528,000 per cubic millimeter, 13.7 microng per milliliter, and 15.5 seconds, respectively. Evaluation of the relationship of coagulation measurements to early clinical features showd that mean initial fibrinogen levels were significantly higher (p less than 0.05 to 0.01) in patients with initial amylase greater than 1,000 Somogyi units percent, serum glutamic oxaloacetic transaminase (SGOT) greater than 250 S.F.U. percent, and initial 72 hour PAO2 less than 75 mm. Hg. Early hypoxemia also correlated (p less than 0.05) with elevated initial FR-antigen levels. Impaired early renal function correlated (p less than 0.01) with elevated initial PC only. Early hypocalcemia did not correlate with coagulation measurements. These findings demonstrate that marked changes in coagulation parameters occur during acute pancreatitis and are related to over-all morbidity. Correlation of early coagulation measurements with amylase levels and with respiratory, renal, and hepatic dysfunction suggests that enzyme-related intravascular coagulation may be implicated in the pathogenesis of these complications of pancreatitis.
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PMID:The relationship of coagulation factors to clinical complications of acute pancreatitis. 85 Aug 68

Two cases of thrombocytopenia due to a low molecular weight heparin (Fraxiparine) are reported. The first case was a 35-year-old alcoholic man with acute mild pancreatitis. After having been treated with Fraxiparine for 12 days to prevent venous thrombosis, routine laboratory studies revealed a thrombocytopenia (49 G.l-1). At the same time, a minor haemorrhage occurred in the nasogastric tube. Prothrombin time, partial thromboplastin time, fibrin degradation products and D-dimers remained normal. There were no soluble fibrin monomers. Fraxiparine was discontinued. The thrombocyte count continued to decrease (12 G.l-1) up to the thirteenth day, it raised 3 days later to 110 G.l-1, and returned to normal after 9 days more (395 G.l-1). The second patient was a 58-year-old man given prophylactic Fraxiparine between the 5th and 16th days after admission for a severe asthma attack. Here again, after 12 days of treatment, the thrombocyte count decreased to 74 G.l-1. There were no other abnormalities, neither clinically nor in laboratory findings. Heparin administration was discontinued and the thrombocytopenia had resolved 3 days later. In both patients, the diagnosis of thrombocytopenia elicited by low molecular weight heparin was confirmed by finding, in vitro, a platelet aggregating factor in the presence of Fraxiparine. The literature concerning this topic is reviewed and discussed.
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PMID:[Thrombocytopenia induced by low molecular weight heparin]. 133 4

The detection of TATC may inform about the presence of thrombin generation and, and hence of a pre-thrombotic status. An ELISA test (Enzygnst TAT) has been developed here in order to evaluate the predictive role played by TATC, and it was applied on 182 patients who distributed in 14 with cirrhosis of the liver, 11 with sepsis, 17 with chronic arterial insufficiency, 55 with neoplasms, 9 with thrombosis, 15 in postoperative period, 15 with pneumonia, 16 with disseminated intravascular coagulation (DIC), 14 with multiple injuries and 16 with pancreatitis. TATC levels were significantly increased in all groups with regard to the control group. Patients with thrombosis, sepsis, multiple injuries, DIC and in the postoperative period showed especially high TATC figures. No correlation between TATC and fibrinogen, platelet count, activated partial thromboplastin time or prothrombin complex assay was found in the post-operative patient-group. It was concluded that TATC are a good indicator of hypercoagulability.
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PMID:[Detection of thrombin-antithrombin complexes in hypercoagulability conditions. Analysis of 182 cases]. 229 Nov 47

The recognition of the postoperative thrombopenia is important because thrombopenia give an hemorrhage risk and modify the tolerance to preventive anticoagulant treatments. Some thrombopenias can be iatrogenic: thrombopenias by transfusion of a large volume of preserved blood, or by hemodilution, but require a substitution, therapy are easily diagnosed. Post-transfusional thrombopenias require an antibody analysis (especially for antiPLA1). The search for drugs interactions is often complex; heparin induced thrombopenia constitutes a severe but fortunately a rare complication of the heparin therapy. Other thrombopenias are related to operative complications this is the case of consumption-coagulopathies due to infections, the release of thromboplastin from tissues, hepatic cirrhosis, pancreatitis, etc. The evaluation of hemostasis verifies clinical hypotheses and guides the treatment. Thrombopenias can be due to various disorders revealed or occurring during an operation. Although the concurrences are rare, they do not always preclude the possibility of finding a collagen disease (connectivitis), a thrombocytogenetic thrombotic purpura, and especially an idiopathic thrombopenic purpura. In any case, diagnosis is easier if the preoperative platelet levels are known. Thus, platelet counts should be included in pre and postoperative evaluations.
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PMID:[Biological diagnosis of postoperative thrombopenia]. 409 Dec 94

A patient who had received multiple transfusions for complications of acute hemorrhagic pancreatitis developed a potent factor V anticoagulant with bleeding due to defective hemostasis. Despite its potency, the anticoagulant disappeared within 15 days of its first manifestation. A second patient with adenocarcinoma of the colon developed an anticoagulant to factor V postoperatively after a single blood transfusion. The anticoagulants appeared to react stoichiometrically with factor V in normal plasma in vitro. They had the physicochemical properties of immunoglobulins, and their activity was neutralized by antihuman immunoglobulin antiserum. One anticoagulant appeared to be slightly more active against homologous than against autologous factor V, but it also inhibited heterologous factor V. Both anticoagulants progressively inactivated intrinsic prothrombin activator formed from normal reagents in the incubation mixture of the thromboplastin generation test, thus confirming that factor V is required for the effective action of the intrinsic prothrombin activator. Since the anticoagulants were immunoglobulins whose activity was consumed in their reaction with factor V, consumption of anticoagulant activity was used to detect factor V antigenic material in test materials. Human serum without factor V clotting activity was found to consume anticoagulant activity, i.e., to contain inactive factor V antigenic material. Plasma from two patients with hereditary factor V deficiency (parahemophilia) failed to consume significant anticoagulant activity. Thus, the lack of factor V activity in these patients represents a deficiency of factor V molecules rather than the synthesis of a defective molecule with impaired clotting activity.
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PMID:Factor V anticoagulants: clinical, biochemical, and immunological observations. 419 89

Coagulation abnormalities induced by pancreatitis were studied in 36 dogs. The 12 dogs in group I underwent a duodenotomy alone. The six dogs in groups II, III, IV, and V had pancreatitis induced by bile injection (1 cc/kg) into the pancreatic duct. Twenty minutes after bile-induced pancreatitis, group III was given 1.0 mg/kg aprotinin (trasylol), group IV was given 10 mg/kg S-2441, a new synthetic protease inhibitor, and group V was given 0.5 mg/kg alpha 2-antitrypsin by intravenous infusion over 10 min. Blood was drawn for amylase, protime (PT), partial thromboplastin time (PTT), fibrinogen, and platelets, in addition to markers of hypercoagulation, fibrinopeptide A, and antithrombin III, and markers of fibrinolysis, B beta 15-42 immunoreactive peptide (IP), and alpha 2-antiplasmin at baseline, 1/2, 1, 3, 6, 24, 48, and 72 hr after duodenotomy or bile injection. There was no significant difference in PT, platelets, antithrombin III, and fibrinopeptide A among the five groups. With the induction of pancreatitis (group II), serum amylase was significantly elevated but fibrinogen only became elevated at 24 hr and PTT at 48 hr. The increase in B beta 15-42 IP seen 30 min after induction of pancreatitis and the decrease in alpha 2-antiplasmin were blunted by aprotinin, alpha 1-antitrypsin, and S-2441, but inhibition of the rise in amylase and B beta 15-42 IP only reached significance with S-2441 (P less than 0.05). Pancreatitis-induced fibrinolysis was inhibited by S-2441 suggesting that synthetic protease inhibitors may play a therapeutic role in pancreatitis.
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PMID:Comparative study of protease inhibitors on coagulation abnormalities in canine pancreatitis. 620 58

Coagulation abnormalities associated with severe pancreatitis were studied in 24 dogs. Group I consists of six control subjects who had duodenotomy alone. Group II consists of six dogs with pancreatitis induced by bile injection ( lcm3 /kg) into the pancreatic duct. The six dogs in Group III and the six in Group IV were given aprotinin (trasylol) 1.0 mg/kg and S-2441 (10mg/kg), a new synthetic protease inhibitor, respectively. These were given over 10 minutes by intravenous infusion, 20 minutes after bile induced pancreatitis. Blood was drawn for amylase, prothrombin time (PT), partial thromboplastin time (PTT), fibrinogen, and platelets, in addition to markers for hypercoagulation, fibrinopeptide A, antithrombin III, and markers for fibrinolysis, B beta 15-42 immunoreactive peptides and alpha 2 antiplasmin at baseline, 30 minutes, 1 hour, 3 hours, 6 hours, and daily for 3 days after injection of bile or duodenotomy. There was no significant difference in PT, platelets, antithrombin III, and fibrinopeptide A among the four groups. Fibrinogen levels and PTT were minimally elevated in animals with bile induced pancreatitis, but these changes reached significance only at 24 hours and 48 hours, respectively (P less than 0.05). Immunoreactive B beta 15-42 became elevated at 30 minutes indicating fibrinolysis in animals with pancreatitis, and these changes were significant compared with Group I control subjects (P less than 0.05) throughout the study. Levels of alpha 2 antiplasmin were decreased in Group II animals with pancreatitis, which also suggests fibrinolysis. Amylase was elevated in Group II animals with pancreatitis (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of protease inhibitors on coagulation abnormalities in acute canine pancreatitis. 620 48

The coagulation changes observed in acute pancreatitis were studied clinically and those changes observed in acute experimental pancreatitis were compared with those after the intravenous infusion of pancreatic juice and ascitic fluid exudate obtained from bile-induced pancreatitis in dogs. The coagulation changes observed in six among 37 patients with acute pancreatitis and half of them died. Those changes observed clinically were either hypercoagulability or hypocoagulability. The coagulation changes after trypsin-induced acute experimental pancreatitis, elastase and autologous bile showed an indication of consumption coagulopathy. The effect upon blood coagulation after the intravenous injection of pancreatic juice included decreased platelet counts and plasma fibrinogen levels, prolonged partial thromboplastin and prothrombin time. The intravenous injection of pancreatic exudate produced greater changes than did those of an equal amounts of pancreatic juice. There was a shortening of E.L.T. and a marked increase in F.D.P. pancreatic exudate which accumulated during acute pancreatitis may contains a toxic substance or substances which contribute to the consumption of coagulation factors.
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PMID:[Disseminated intravenous coagulation in acute necrotizing pancreatitis]. 667 61

Acute necrotizing (hemorrhagic) pancreatitis was induced in 12 dogs by infusing oleic acid into their pancreatic ducts. There were decreases in blood pH, complement, antithrombin III, blood platelets, 24- and 48-hour plasminogen, and 24-hour haptoglobin and modest decreases in serum albumin. There were increases in fibrinogen, 48- to 120-hour haptoglobin, and 96-hour and 120-hour plasminogen and prolongations of prothrombin and activated partial thromboplastin times. The latter 2 changes together with decreases in antithrombin III, platelet numbers, and complement were indicative of consumption coagulopathy. A clinically innocuous but statistically significant decrease in serum total and ionized calcium despite significant acidosis was noted. This indicates that serum total and ionized calcium is helpful in making the diagnosis of acute necrotizing pancreatitis. Methemalbuminemia of 6 mg/dl at 24 hours and 7 mg/dl at 48 hours indicates that methemalbuminemia is a valuable diagnostic and prognostic finding in association with acute necrotizing pancreatitis.
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PMID:Biochemical and coagulation changes in a canine model of acute necrotizing pancreatitis. 725 99

An analysis was made of 41 cases of disseminated intravascular coagulation in dogs, with the objective of evaluating routine and nonroutine laboratory tests used in making the diagnosis. The dogs were grouped on the basis of underlying disease, which included neoplasia (39%), pancreatitis (30%), chronic active hepatitis (15%), heat stroke (12%), and sepsis (4%). Of the diagnostic tests evaluated, those for determination of activated partial thromboplastin time, antithrombin III activity, prothrombin time, and the platelet count were the most valuable. Of the clotting factors, factor V activity was decreased more frequently than the activity of factor VIII:C (factor VIII: procoagulant). The factor VIII:C activity was in conflict with prevailing dogma that reflects depression of this factor in disseminated intravascular coagulation. Factor VIII:C activity was decreased in only 29% of dogs studied. Activation of the fibrinolytic system was manifested by decreased plasminogen activity in 49% of the dogs studied. Sixty-one percent of the dogs had increased amounts of fibrin (ogen) degradation products.
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PMID:Disseminated intravascular coagulation: antithrombin, plasminogen, and coagulation abnormalities in 41 dogs. 726 67


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