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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The significance and frequency of fibrin thrombi (FT), the pathological hallmark of disseminated intravascular coagulation (DIC), in ischemic intestine were analyzed in a retrospective study of the infarcted bowel of patients with occlusive mesenteric ischemia (OMI) and nonocclusive mesenteric ischemia (NOMI). Representative intestinal sections were studied from 10 patients with NOMI of the small and/or large bowel and 12 patients, with OMI of varied etiology. Three patients with inflammatory bowel disease and 1 patient with DIC and bowel necrosis were also studied. Routine hematoxylin and eosin stains for fibrin were prepared for each specimen. The number of FT was quantitated. FT were identified in each of the 10 cases of NOMI; however in only 2 were they prominent. FT were identified in 6 of the 12 cases of OMI and in 4 of these 6 they were a prominent feature. Rare FT were present in the cases of inflammatory bowel disease and did not correlate with the inflammatory process. No FT were present in the intestinal sections of the DIC case. FT are a nonspecific feature of necrosis and can be identified in both occlusive and nonocclusive ischemic bowel disease. Their presence in the intestine of NOMI therefore cannot be used to implicate DIC as the primary cause of this entity.
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PMID:Disseminated intravascular coagulation in nonocclusive mesenteric ischemia: the lack of specificity of fibrin thrombi in intestinal infarction. 99 77

The plasma kallikrein-kinin system is activated in Gram-negative sepsis and typhoid fever, two diseases in which bacterial products have been shown to initiate inflammation. Because a single intraperitoneal injection of bacterial cell wall peptidoglycan-polysaccharide polymers from group A steptococci (PG-APS) into a Lewis rat produces a syndrome of relapsing polyarthritis and anemia, we investigated changes in the role of the kallikrein-kinin system in this model of inflammation. Coagulation studies after injection of PG-APS revealed an immediate and persistent decrease in prekallikrein levels. High-molecular-weight kininogen levels decreased significantly during the acute phase and correlated with the severity of arthritis. Factor XI levels were decreased only during the acute phase. Antithrombin III levels remained unchanged, indicating that neither decreased hepatic synthesis nor disseminated intravascular coagulation caused the decreased plasma contact factors. Plasma T-kininogen (an acute phase protein) was significantly elevated during the chronic phase. PG-APS failed to activate the contact system in vitro. Thus the kallikrein-kinin system plays an important role in this experimental model of inflammation, suggesting that activation of this system may play a role in the pathogenesis of inflammatory bowel disease and rheumatoid arthritis in which bacterial products might be etiologically important.
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PMID:Role of kallikrein-kinin system in pathogenesis of bacterial cell wall-induced inflammation. 199 42

I discussed indications for surgical intervention in cases of ulcerative colitis and Crohn's disease, based on the results of our experience at both Tohoku University Hospital and Sendai National Hospital as well as the data of collective studies carried out by the Investigation and Research Committee for Inflammatory Bowel Disease organized by the Japanese Ministry of Health and Welfare. Particularly, I stressed usefulness of a 5-day intensive intravenous regimen which was developed by Truelove and Jewell in 1974, as the best method for determining if urgent surgery is indicated in cases of acute severe or fulminant types of ulcerative colitis. Emergency surgery is required in severe cases where symptoms do not disappear or are not improved with the application of this regimen. Thus, ulcerative colitis can be safely controlled by medical management unless we misjudge the timing for surgical intervention. In addition, we mentioned hypercoagulability as a factor in both diseases. Particularly, 2 severe cases of ulcerative colitis at Sendai National Hospital were accompanied with disseminated intravascular coagulation syndrome (DIC) and one of these patients died after emergency surgery. Investigation of blood coagulation offers very important information concerning severity, prognosis and the advisability of surgical intervention. When marked hypercoagulability and intravascular coagulation syndrome are present, the therapeutic program must include anticoagulant therapy and surgical intervention.
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PMID:[Indications for surgery from the point of view of an internist]. 408 66

We have reported previously the association between hyposplenism and inflammatory bowel disease. Our study has now been extended to a total of 65 patients with ulcerative colitis and 42 with Crohn's disease so that the incidence of hyposplenism could be more accurately determined. Hyposplenism rarely complicated distal ulcerative colitis, but was found in 15 of 37 patients with total colonic disease. Hyposplenism occurred in 11 out of 31 patients with Crohn's disease of the colon, but in none of 11 individuals with isolated ileal disease. In order to determine whether hyposplenism has any prognostic implications, the peri-operative course of 12 hyposplenic individuals who underwent colectomy was compared with that of 12 controls who required surgery and who had normal splenic function. Four of the hyposplenic subjects became severely shocked after operation and developed disseminated intravascular coagulation. In contrast, the post-operative course in the control patients was uneventful.
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PMID:Further experience of hyposplenism in inflammatory bowel disease. 734 71

Culture for bacteria and assays for endotoxin were performed on specimens of mesenteric and peripheral venous blood from eight patients with ulcerative colitis who underwent surgery for severe uncontrolled disease. No significant bacteraemia occurred in either portal or systemic blood. Systemic endotoxaemia developed in three patients during surgery but occurred before bowel mobilisation only in the one patient whose colitis was complicated by hyposplenism. Mesenteric endotoxaemia occurred in only three patients before bowel mobilisation, but was detected during surgery in two of the three patients who developed systemic endotoxaemia. We conclude that, contrary to earlier reports, portal bacteraemia must be infrequent in ulcerative colitis. Systemic endotoxaemia does, however, occur in a significant proportion of cases during colectomy. Although in the patients studied this led to no clinical problems, it is likely to have been the precipitating factor for the syndrome of disseminated intravascular coagulation (DIC) that we have previously observed after colectomy in some of our patients with hyposplenism secondary to inflammatory bowel disease.
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PMID:Bacteriological and endotoxin studies in cases of ulcerative colitis submitted to surgery. 743 4

A hypercoagulable condition and poor perfusion to distal extremities might occur during equine endotoxaemic or septic shock, which could cause thrombosis of limb arteries. In our review, thrombosis occurred in neonatal foals in association with gram-negative bacteraemia. In 3 older foals and adults, thrombosis was associated with inflammatory bowel disease, diarrhoea and toxaemia. All patients had been treated with broad-spectrum antibiotics, nonsteroidal antiinflammatory drugs and i.v. crystalloid solutions. Two horses received i.v. hyperimmune plasma. A generalised coagulopathy was not suspected prior to clinical signs of distal limb necrosis, although thrombocytopenia occurred in 4 of the 5 cases at the time of, or shortly before, thrombosis. Thrombocytopenia, possibly due to platelets adherence to exposed subendothelial collagen, which induces contact activation of the intrinsic coagulation pathway, has been described in endotoxaemic horses and foals with gastrointestinal infectious or inflammatory diseases and disseminated intravascular coagulation. Activation of procoagulants by endotoxins, decreased blood flow to the limbs and endothelial damage, may have been responsible for a hypercoagulable condition leading to thrombosis in these 5 cases. The 3 enterocolitis patients may have had increased risk of thrombosis because of loss of antithrombin III, haemoconcentration and acidosis.
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PMID:Acute thrombosis of limb arteries in horses with sepsis: five cases (1988-1998). 1119 2

We report a 30-year-old woman with pleuropericarditis, cardiac tamponade, and disseminated intravascular coagulation complicating active ulcerative colitis (UC). Other autoimmune diseases were not present. She responded to pulsed steroid therapy and anticoagulant with resolution of the complication and UC. We reviewed the literature and found 27 cases of pleuropericarditis associated with idiopathic inflammatory bowel disease (IBD). It has been reported that pleuropericarditis associated with IBD responds well to nonsteroidal antiinflammatory drugs, as well as steroids. The causes of cardiac involvement in IBD remain unclear, but the pleuropericarditis must be recognized as a potential extraintestinal manifestation of IBD.
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PMID:Pleuropericarditis and disseminated intravascular coagulation in ulcerative colitis. 1124 57

The plasma kallikrein-kinin system (KKS) participates in the pathogenesis of inflammatory reactions involved in cellular injury, coagulation, fibrinolysis, kinin formation, complement activation, cytokine secretion and release of proteases. It has been shown that KKS activation in the systemic inflammatory response syndrome results in decrease of its component plasma proteins. Similar changes have been documented in diabetes, sepsis, children with vasculitis, allograft rejection, disseminated intravascular coagulation, patients with recurrent pregnancy losses, hereditary angioedema, adult respiratory distress syndrome and coronary artery disease. Direct involvement of the KKS in the pathogenesis of experimental acute arthritis and acute and chronic enterocolitis has been documented by previous studies from our laboratory using experimental animal models. It has been found that in HK deficient Lewis rats, experimental IBD was much less severe. We showed a genetic difference in kininogen structure between resistant Buffalo and susceptible Lewis rats, which results in accelerated cleavage of HK and it is responsible for the susceptibility to the inflammatory process in the Lewis rats. It has been demostrated that therapy with a specific plasma kallikrein inhibitor (P8720) modulated the experimental enterocolitis, arthritis and systemic inflammation. Furthermore, it has been shown that a bradykinin 2 receptor (B2R) antagonist attenuates the inflammatory changes in the same animal model. We have showed that a monoclonal antibody targeting HK decreases angiogenesis and arrests tumor growth in a syngeneic animal model. In summary, these results indicate that the plasma KKS plays a central role in the pathogenesis of chronic intestinal inflammation, arthritis and angiogenesis.
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PMID:[High molecular weight kininogen in inflammation and angiogenesis: a review of its properties and therapeutic applications]. 1670 6

The case of a 20-year-old Japanese man, diagnosed as having autosomal recessive chronic granulomatous disease (CGD), who was being treated with corticosteroids for intractable unclassified colitis, is described. He died from multiple organ failure following disseminated intravascular coagulation secondary to disseminated varicella-zoster virus (VZV) infection. He was diagnosed as an index case of CGD when 2 years old, was inoculated against VZV at the age of 5 years and had had an unremarkable course for 19 years. He was admitted to hospital because of a third episode of recurrent bloody diarrhoea. Clinical remission for each episode was achieved by intravenous corticosteroid therapy. Unclassified colitis associated with CGD was diagnosed based on a colonic biopsy demonstrating characteristic macrophages with lipofuscin deposits. From a treatment viewpoint, idiopathic inflammatory bowel disease (IBD) should be differentiated from secondary IBD occurring in CGD, in which immunosuppressive drugs including corticosteroids, still the mainstay of IBD treatment, should be avoided.
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PMID:Intractable colitis associated with chronic granulomatous disease. 1776 93

Alterations in expression of protein C (PC) pathway components have been identified in patients with active inflammatory disease states. While the PC pathway plays a pivotal role in regulating coagulation and fibrinolysis, activated PC (aPC) also exhibits cytoprotective properties. For example, PC-deficient mice challenged in septic/endotoxemic models exhibit phenotypes that include hypotension, disseminated intravascular coagulation, elevated inflammatory mediators, neutrophil adhesion to the microvascular endothelium, and loss of protective endothelial and epithelial cell barriers. Further, inflammatory bowel disease has been correlated with diminished endothelial PC receptor and thrombomodulin levels in the intestinal mucosa. Downregulated expression of the cofactor, protein S, as well as PC, is also associated with ischemic stroke. Studies to elucidate further the structural elements that differentiate the various functions of PC will serve to identify novel therapeutic approaches toward regulating these and other diseases.
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PMID:The protein C pathway and pathologic processes. 1963 Jul 87


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