Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.69 (APC)
 16,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Protein C content and plasminogen activity were measured in plasma from 100 horses with signs of colic. Data were analyzed by grouping horses 4 ways. Each horse was allotted to 1 of 2 outcome groups (survivors and nonsurvivors), 1 of 3 broad-category diagnosis groups (inflammatory disorders, strangulating obstructions, and all other gastrointestinal disorders), and 1 of 2 clinical management groups (medical and surgical). In a fourth grouping, all horses (although numbers of horses included in each subgroup were small) were assigned either to specific diagnostic groups that had high expectation for activated hemostasis (intestinal ischemia, endotoxemia, jugular thrombosis, peritoneal adhesions, and laminitis) or to a control group, in which active hemostasis was unlikely. Within 2 to 24 hours after admission, nonsurvivors developed lower protein C content than did survivors. Protein C content and plasminogen activity became low during hospitalization in horses with strangulating obstructions and in horses having surgery. The results from the grouping by specific diagnosis must be considered pilot data because the numbers of horses in each subgroup were small. Although not statistically significant, trends were noticed in protein C and plasminogen: (1) horses with intestinal ischemia and endotoxemia developed low protein C content and plasminogen activity, (2) protein C content became low in horses that developed peritoneal adhesions or laminitis, and (3) plasminogen activity became low in horses that developed jugular thrombosis. Low protein C content or low plasminogen activity, or both, may be useful as predictors for outcome and for these specific complications of equine colic.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Use of newly developed assays for protein C and plasminogen in horses with signs of colic. 201 48

Components of the coagulation and fibrinolytic cascades, prothrombin and activated partial thromboplastin times, endotoxin activity, and albumin concentration were measured in blood and peritoneal fluid from 20 healthy horses and from 153 horses with acute gastrointestinal tract diseases at admission. Overall, 77% (117/153) of affected horses survived to discharge from the hospital, and 85% (82/97) of horses discharged were reported to be normal 9 to 14 months later. Significant differences in hemostatic factors were more common in peritoneal fluid than in blood. Tissue plasminogen activator, plasminogen, protein C, antithrombin III, and alpha 2-antiplasmin activities and concentrations of fibrinogen and fibrin degradation products were significantly (P < 0.05) greater in peritoneal fluid from horses with colic, and, with the exception of fibrinogen concentration, were associated with detection of endotoxin. Higher values for these variables, except tissue plasminogen activator activity, were significantly (P < 0.05) associated with survival. Plasminogen, antithrombin III, and alpha 2-antiplasmin activities were significantly (P < 0.05) greater in peritoneal fluid from horses with inflammatory or strangulating lesions, compared with those in horses with simple colic. Plasminogen-activator inhibitor type 1 activity, fibrin degradation products concentration, and prothrombin time were significantly (P < 0.05) greater in the blood of horses with colic. Survival was inversely associated with significantly (P < 0.05) greater intravascular concentrations of fibrin degradation products and fibrinogen and prothrombin time. This study revealed marked contrasts between peritoneal and intravascular coagulation and fibrinolysis in horses with colic, indicating that inferences regarding the peritoneal environment, particularly with respect to fibrinolytic capacity, should not be made on the basis of factors measured in blood.
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PMID:Intravascular and peritoneal coagulation and fibrinolysis in horses with acute gastrointestinal tract diseases. 759 47

Eight tests of hemostasis were measured in 233 horses with colic. Blood samples were obtained at admission and for 4 consecutive days of hospitalization. Data were analyzed retrospectively by outcome, by broad-category diagnosis group, by small intestinal disorder, and by smaller categories for comparing specific diseases. Nonsurviving horses and horses with the most severe forms of intestinal ischemia had changes interpreted as hypercoagulative, the intensity of which was increased on the first and second mornings (sample times 2 and 3) after admission, when most significant differences for results of specific tests were detected. Nonsurvivors had decreased antithrombin III activity and prolonged prothrombin and activated partial thromboplastin times; those with strangulating obstructions also had decreased protein C and plasminogen activities. During hospitalization and with survival, these changes tended to reverse. In most horses, regardless of diagnosis or outcome, concentration of fibrin degradation products and fibrinogen, and alpha 2-antiplasmin activity increased over time. Whether these changes reflected specific effects of colic or of the acute-phase response was not determined. In comparisons of small intestinal disorders (proximal enteritis, strangulations, and impactions), diagnostically distinguishing features were not found. Likewise, in comparisons of specific diseases (small vs large intestinal impaction, proximal enteritis vs colitis, small vs large intestinal obstruction), diagnostically distinguishing features were not found.
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PMID:Analysis of hemostasis in horses with colic. 840 38

The case presented raised our scientific curiosity and it is worthy of being brought in front of the medical audience because of several reasons presented below. Presently, there are 3 hereditary syndromes that have a demonstrated etiological relationship with the colorectal cancer: Familiar Adenomatous Polyposis (FAP syndrome), HNPCC syndrome (Hereditary Nonpoliposis Colorectal Cancer) and MAP syndrome.Discovered only in 2002, the MAP syndrome (MYH associated polyposis) is the first hereditary syndrome that has autosomal recessive transmission. The APC gene can be mutated in several ways during the colonic oncogenesis: congenital in the FAP syndrome, somatic in sporadic colorectal cancers and secondary to the MYH gene inactivation in MAP syndrome. MAP phenotype is similar to the FAP phenotype because of the somatic mutations to the APC gene. Colonic polyposis is lower than FAP syndrome and appeared later, in the 40's and 50's. Colorectal cancers are frequent and discovered in the same moment as the colonic polyposis. Patients are diagnosed mostly in cancer stages. Colonoscopy shows polyps disseminated around the entire colic frame. Treatment in these cases is total rectocolectomy with ileoanal anastomosis. When working in a general emergency surgery clinic, physicians are often faced with colorectal cancers in different evolutive stages, and mostly they are faced with their complications.
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PMID:Map syndrome (MYH Associated Polyposis) colorectal cancer, etiopathological connections. 2150 84