Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Multiorgan thrombotic disorders have been described in a variety of conditions including systemic lupus erythematosus. Among these are the 'catastrophic' antiphospholipid syndrome, disseminated intravascular coagulation and the thrombotic thrombocytopenic purpura-haemolytic uraemic syndrome. In this review we briefly analyse some specific clinical and haematological characteristics of these conditions and attempt to uncover common links between them.
Lupus 1992 Aug
PMID:Multiorgan thrombotic disorders in systemic lupus erythematosus: a common link? 130 83

Changes of blood coagulation in 32 cases of SLE were investigated. Abnormalities frequently found were elevation of blood fibrinogen, FDP, V111R: Ag levels, prolonged or shortened KPTT time, and depressed AT-III value. Half of the patients with SLE showed laboratory changes compatible with the diagnostic criteria of DIC, but acute DIC was encountered clinically only in 2 cases hypercoagulation state or hypercoagulation with lower fibrinolysis, however were frequently seen. Lupus anticoagulant were detected in 6 patients and deep vein thrombosis of lower extremity in 1 patient. Examination of blood coagulation in patients with SLE was, therefore, of clinical importance.
 ...
PMID:[Blood coagulation changes in systemic lupus erythematosus]. 212 40

We describe a patient with previous venous thrombosis while using oral contraceptives and recurrent pregnancy loss, who presented with massive hepatic infarction in the last trimester of the fourth gestation. Thrombocytopenia, the lupus anticoagulant (LA) and the anticardiolipin antibody (aCL) were detected and a diagnosis of a 'primary' antiphospholipid syndrome (APS) was made. The clinical and histological manifestations and the differential diagnosis, especially with DIC and pre-eclampsia, are discussed.
Lupus 1993 Aug
PMID:Hepatic infarction in a pregnant patient with the 'primary' antiphospholipid syndrome. 826 78

Thirty one patients with antiphospholipid antibodies who developed multi-organ failure ("Catastrophic Antiphospholipid Syndrome") are reviewed. Thirteen suffered from a 'Primary' antiphospholipid syndrome, 13 from defined SLE, 4 from 'lupus-like' disease and one from rheumatoid arthritis. In more than one third precipitating factors were evident (e.g. infections, major/minor surgical procedures, oral contraceptives). Death occurred in 60% of patients from a variety of causes (myocardial failure, ARDS, CNS causes or, often a combination). Disseminated Intravascular Coagulation was present in 8 of 31 patients. Plasmapheresis appeared to be useful in several who had not responded to conventional therapy (e.g. IV heparin, steroids, immunosuppression).
Lupus 1996 Oct
PMID:The catastrophic antiphospholipid syndrome 1996: acute multi-organ failure associated with antiphospholipid antibodies: a review of 31 patients. 890 72

Colitis in systemic lupus erythematosus (SLE) poses a diagnostic challenge as clinical, radiological and laboratory findings are often non-specific. Fulminant amoebic colitis is a rare cause of death in SLE. Early diagnosis coupled with timely surgery can reduce the mortality. The demonstration of haematophagous trophozoites in the stool is diagnostic but insensitive. Early endoscopy with adequate specimen collection is an important part of the diagnosis. Serology is both sensitive and specific but can take up to 2-4 weeks for seroconversion making it less useful in a disease that takes a rapid downhill course if treated inappropriately. We report a fatal case of colitis in a patient with SLE due to invasive amoebiasis which was complicated by Salmonella bacteraemia, disseminated intravascular coagulation, acute oliguric renal failure and adult respiratory syndrome. We also reviewed the literature on the clinical features and diagnosis of fulminant amoebic colitis. Amoebic colitis, although rare, should be considered in the differential diagnosis of lupus patients with colitis.
Lupus 1997
PMID:Fatal amoebic colitis in a patient with SLE: a case report and review of the literature. 930 65

Endothelial cells form a multifunctional cell lining that covers all of the inner surface of blood vessels and regulates several important physiological and pathological reactions. These include inflammation/immune reaction, blood vessel tonus, hemostasis/thrombosis, angiogenesis and so on. Thus, abnormalities of endothelial function may play crucial roles in the development of angitis syndrome, thrombosis/embolism, bleeding disseminated intravascular coagulation (DIC), and neovascularization in some pathological states including tumor growth and diabetic retinopathy. Research on endothelial cells now forms a new frontier termed 'Endotheliology'. Recent advances of the functional and structural aspects of endothelial cells are reviewed here mainly from the viewpoint of endothelial regulation of coagulation and the fibrinolytic system. First we show that the natural endothelial membrane protein thrombomodulin is localized not only on apical endothelial surface but also in caveolae. Since it has been reported that such factors involved in coagulation/fibrinolysis as tissue factor, tissue factor pathway inhibitor (TFPI), thrombin receptor and urokinase receptor are also localized in the caveolae, this membrane structure may act as a special component to regulate coagulation/fibrinolysis on the endothelial membrane surface. Next we demonstrate the signaling pathway of the thrombin receptor. Thrombin cleaves the N-terminus of the receptor as a substrate, exposing a new N-terminus. This newly exposed N-terminus acts as a ligand and activates platelets, endothelial cells and vascular smooth-muscle cells. We have identified that the signal from the thrombin receptor activates NF-kappaB through the activation of protein C kinase, tyrosine kinase and MAP kinase, and results in proliferation of the cells. We have also shown that the receptor is over-expressed on platelets from diabetes patients.
Lupus 1998
PMID:Biology of endothelium. 981 71

A review of 50 patients who manifest features of the catastrophic antiphospholipid syndrome (CAPS) is presented. The clinical features comprise mainly organ involvement as opposed to large-vessel venous or arterial occlusions as is seen in patients with 'simple' antiphospholipid syndrome (APS), which makes the pathogenesis of this unusually rare complication perhaps somewhat different from that of patients with the APS. The mortality of the condition is 50%, most patients dying as a result of a combination of cardiac and respiratory failure. Fifteen patients (28%) suffered from disseminated intravascular coagulation (DIC) as well, which may have contributed to the multiorgan thrombotic microangiopathy characteristic of the CAPS. Although most patients were treated with high-dose i.v. steroids, heparin, cyclophosphamide and other modalities of therapy (such as i.v. globulin), plasmapheresis (advocated for TTP, a similar microangiopathic condition) seemed to offer some benefit (68% recovery). The systemic inflammatory response syndrome (SIRS) was responsible for some of the clinical manifestations such as adult respiratory distress syndrome (ARDS) seen in 15 patients. Pathogenesis of the CAPS seems dependent on a 'two-hit' or even 'three-hit' hypothesis in patients already suffering from a hypercoagulable state. Precipitating factors include infections, trauma (surgical), drug administration and warfarin withdrawal. A recent view that the multiple thrombotic lesions themselves may contribute to further thrombosis ('thrombotic storm') is also discussed.
Lupus 1998
PMID:The catastrophic antiphospholipid syndrome, 1998. A review of the clinical features, possible pathogenesis and treatment. 981 75

Thrombomodulin (TM), a high affinity thrombin receptor present on endothelial cell membrane, plays an important role as a natural anticoagulant. It acts as a cofactor of thrombin-catalyzed activation of protein C, and inhibits the procoagulant functions of thrombin. TM is also located in other cells (keratinocytes, osteoblasts, macrophages,...) where it might be involved in cell differentiation or in inflammation. In the presence of cytokines, activated neutrophils and macrophages, endothelial TM is cleaved enzymatically, releasing soluble fragments which circulate in the blood and are eliminated in urine. Plasma TM level (pTM) can be measured using a two-site enzyme-linked immunosorbent assay (ELISA). pTM level is regarded as a molecular marker reflecting injury of endothelial cells. It is often increased in case of diffuse endothelial damage as in disseminated intravascular coagulation, diabetic microangiopathy, Plasmodium falciparum and rickettsial infections. pTM is also a predictive marker of hypertensive complications in pregnancy. In several systemic inflammatory diseases, pTM levels are correlated to the activity of the disease.
Lupus 1998
PMID:Thrombomodulin: an overview and potential implications in vascular disorders. 981 88

The recurrence of widespread and diverse vascular lesions is a hallmark of systemic lupus erythematosus (SLE). Inflammatory and thrombotic mechanisms almost invariably associated with circulating antiphospholipid antibodies play a role in the pathogenesis of SLE-related vascular disease. Both mechanisms can coexist in the same patient. Vasculitis is most commonly induced by the local deposition of immune complexes. However, some SLE patients have an inflammatory complement-mediated vascular injury in the absence of immune complex deposition. We report on a fatal case of disseminated intravascular coagulation (DIC) in a young woman with active SLE. Hemorrhagic lesions due to localized intravascular coagulation (Shwartzman phenomenon) preceded disseminated intravascular coagulation accompanied by disseminated cardiac necrosis. Immune complex 'independent' and other mechanisms of vascular injury and states of hypercoagulability will be discussed.
Lupus 2002
PMID:Shwartzman phenomenon in a patient with active systemic lupus erythematosus preceding fatal disseminated intravascular coagulation. 1204 82

Colitis in patients with systemic lupus erythematosus (SLE) is quite rare. It can be caused by intestinal vasculitis, mesenteric vascular thrombosis, concomitant inflammatory bowel disease or infectious colitis. It is important to make an accurate and early diagnosis as the treatments for each condition differ and a delayed diagnosis can result in life-threatening complications. However, non-specific gastrointestinal symptoms make a timely diagnosis challenging. Amoebic colitis is a rare condition in patients with SLE. Here we present a case of fulminant amoebic colitis in a patient with SLE which was initially misdiagnosed as ischemic colitis due to intestinal vasculitis. Her colitis was complicated with multiple intestinal perforations, disseminated intravascular coagulation and acute respiratory distress syndrome; but in the end, the patient was successfully treated with metronidazole and paromomycin.
Lupus 2012 Oct
PMID:Fulminant amoebic colitis mimicking intestinal vasculitis in a patient with systemic lupus erythematosus. 2257 Mar 37


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