Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021831 (enteropathy)
 4,403 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Disseminated intravascular coagulation (DIC) was diagnosed as a secondary disease in 6 horses. Four horses had localized and/or systemic sepsis, one horse had disseminated neoplasia, and one had idiopathic ulcerative enteropathy. The diagnosis of DIC was based on the finding of at least 3 of 4 abnormalities: thrombocytopenia, prolonged prothrombin time, prolonged activated partial thromboplastin time, and a high concentration of fibrinolytic degradation products. The most common clinical signs other than those attributable to the primary disease process were abnormal hemorrhage (4 hours) and venous thrombosis (4 horses). All horses eventually died or were euthanatized because of the severity of the primary disease.
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PMID:Disseminated intravascular coagulation in six horses. 664 11

A 7 months old infant with transient hypoproteinemia and hypoprothrombinemia is described. The hypoproteinemia is attributed to protein losing enteropathy, and transient Menetrier's disease is suggested as a possible cause for the protein loss. Assuming that this baby was not vitamin K deficient, and knowing that the mononuclear weight of prothrombin is lower than that of albumin, the hypoprothrombinemia might be due to prothrombin loss into the gut together with albumin
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PMID:Transient hypoproteinemia and hypoprothrombinemia in an infant. 722 95

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

A patient with chronic idiopathic thrombocytopenia and fatal strongyloides hyperinfection syndrome following prolonged corticosteroid therapy is briefly described. Diagnosis was difficult to perform due to absence of eosinophilia and diarrhea at presentation, as well as to the negativity of multiple stool specimens examined by direct microscopy of saline smear, formol-ether concentration techniques, and Baermann's test. The striking hypoalbuminemia in the setting of the normal results of liver function tests and prothrombin time was assumed to be due to enteropathy. Therefore, an upper endoscopy was undertaken, revealing Strongyloides stercoralis (SS) larvae in the biopsy specimens of the gastric and duodenal mucosa. The SS larvae were also demonstrated in the multiple specimens of the concentrated sputum. Despite thiabendazol treatment, death ensued. On autopsy, SS larvae were recovered in the gastrointestinal tract and lungs. The importance of early diagnosis and of ruling out strongyloidosis prior to administration of corticosteroids are discussed, as well as the pathogenetic aspects of strongyloidosis in the patient under corticosteroids.
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PMID:Fatal strongyloidosis following corticosteroid therapy in a patient with chronic idiopathic thrombocytopenia. 1043 74

The potential mechanism underlying the rapid response to vitamin K replacement in acquired deficiency states is incompletely understood. To examine vitamin K metabolism, a 10-year-old boy with autoimmune enteropathy on oral vitamin K supplementation, who presented with profuse nosebleeds and calf tenderness, was evaluated. Laboratory analyses were consistent with severe vitamin K deficiency: vitamin K dependent protein (VKDP) levels < 5%, normal vitamin K epoxide level and depressed total prothrombin antigen (carboxylated and undercarboxyated forms). Intramuscular vitamin K (10 mg) was administered. Nine hours following therapy, VKDP levels corrected completely. Total prothrombin antigen increased indicating new prothrombin synthesis. However, the increase in the prothrombin-clotting assay far exceeded the increase in total prothrombin, supporting storage of undercarboxylated prothrombin in vitamin K deficiency states, with carboxylation and secretion after vitamin K replacement. Although this mechanism is known to occur in rodents, it has not been reported in humans. Our findings suggest a new potential mechanism of prothrombin metabolism in humans.
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PMID:Severe acquired vitamin K deficiency: a hypothesis for rapid response to therapy. 1087 Aug 12