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)

Pneumocystis carinii pneumonia (PCP) is a major opportunistic infection in acquired immunodeficiency syndrome (AIDS) and is treated with co-trimoxazole, pentamidine and others. The severe adverse reactions, including bone marrow suppression, by these therapeutic agents often preclude their continued use. A 14-year-old male HIV-positive hemophilia A patient, who was complicated by disseminated intravascular coagulation syndrome (DIC) following acute pancreatitis during treatment for PCP, was treated with proteinase inhibitors and anticoagulant agents. He was improved and discharged. As pentamidine may cause pancreatitis and develop DIC, it is important that pancreatic enzymes should be carefully followed when this agent administrated. In this case, granulocyte colony-stimulating factor and erythropoietin were effective for the bone marrow suppression, suggesting that importance of these agents for the prophylaxis of other secondary infections during the treatment.
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PMID:[HIV-1 seropositive hemophilia A complicated by disseminated intravascular coagulation syndrome and acute pancreatitis during treatment of Pneumocystis carinii pneumonia]. 143 51

We have studied the potential thrombogenicity of two different heat-treated prothrombin complex concentrates (PCC) in patients with Haemophilia B. Seven patients were studied on nine separate occasions. Four of the patients had chronic hepatitis C (HCV) associated liver disease and three were HIV-antibody positive. The PCCs were Profilnine (Alpha Therapeutics, Thetford, UK) and 9A (Bio-Products Laboratory, Elstree, UK) and the dose administered ranged from 35 to 60 U/kg. Blood samples were taken on ten separate occasions; twice before the infusion and at 15, 40, 60, 75 and 120 min and 4, 8 and 24 h after the infusion of PCC. Investigations included prothrombin time, kaolin cephalin clotting time, thrombin time, fibrin(ogen) degradation products, factor VIII, factor IX, antithrombin III and fibrinopeptide A (FPA). Fibrinopeptide A rises were seen following two of six infusions of 9A and one of three infusions of Profilnine. On all three occasions the rise in FPA was transient, returning to baseline levels within 120 min. Plasma beta-thromboglobulin (BTG) was assayed in three patients and in one patient, the rise in FPA was followed by an increase in BTG. No other changes were observed and there were no clinical features of disseminated intravascular coagulation. Our results indicate that even with normal clinical doses of PCC, intravascular thrombin generation can occur in patients with Haemophilia B. However, this effect is inconsistent both with respect to PCC batch and patient, but may occur in the absence of HIV infection and HCV liver disease.
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PMID:Potential thrombogenicity of heat-treated prothrombin complex concentrates in Haemophilia B. 178 33

The central nervous system was examined in 135 adult AIDS patients who died between August 1982 and December 1990. Twenty two brains showed non-diagnostic changes including microglial nodules, discrete myelin pallor with reactive astrocytosis, mineralization of blood vessels and granular ependymitis. In 105 brains with specific changes, toxoplasmosis was the most frequent finding (55 cases) manifested by multifocal necrotic lesions or diffuse pseudo-encephalitic process. Other opportunists included cytomegalovirus (21 case), progressive multifocal leukoencephalopathy (1 cases), cryptococcosis (6 cases), mycobacterium avium intracellulaire (2 cases), varicella-zoster virus (2 cases), aspergillosis (1 case) and multiple bacterial microabscesses (1 case). Multinucleated giant cells were found in 52 cases. In 40 cases, they were widely disseminated throughout the brain and in 39 cases, they were associated with diffuse or multifocal white matter changes. Fifteen cases had a cerebral lymphoma, 9 hepatic encephalopathy, 1 centropontine myelinolysis and 1 focal pontine leukoencephalopathy. Three cases had a cerebral haemorrhage due to disseminated intravascular coagulation, antithrombin therapy and amyloid angiopathy. Spinal changes in 13 cases included vacuolar myelopathy (7 cases), HIV myelitis (1 case) and ganglio-radiculitis (1 cases), cytomegalovirus myelo-radiculitis (1 case) secondary spread from a lymphoma (1 case) and spinal infarcts due to disseminated intravascular coagulation (1 case). These lesions were frequently atypical and various combinations of all these pathologies were encountered in the same brain, sometimes in the same area and occasionally in the same cell. Chronological variations in the incidence of some complications could be related to changes in treatment.
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PMID:[Neuropathologic study of 135 adult cases of acquired immunodeficiency syndrome (AIDS)]. 195 58

The risks and adverse reactions of fresh frozen plasma (FFP) and coagulation components have changed considerably in the last few years because of the spread of HIV on the one hand, and the advances in preparation and sterilisation of the coagulation components on the other hand. Therefore, the indication for FFP and the various coagulation components deserves permanent consideration. FFP is still the therapeutical means of choice for the treatment of acquired (complex) plasmatic coagulation disorders, even though the (still) small risk of virus transmission in Middle Europe has to be taken into account. Coagulation components are primarily indicated in congenital (isolated) plasmatic coagulation disorders. Only in gross or very acute acquired coagulation disorders are coagulation components needed in addition to FFP. The same regimen is recommended for the use of antithrombin III (AT III) concentrates. In cases of acquired antithrombin deficiency, antithrombin III substitution is indicated only when the anticoagulation by heparin alone or in combination with FFP is insufficient or when the heparin dose required might cause an unacceptable bleeding risk, e.g. in simultaneous thrombocytopenia. Then AT III becomes an important therapeutic agent, especially in DIC. In addition, information regarding a rational and economic substitution of FFP and coagulation components is given, and other substitutes are mentioned which could possibly be used with less risk. Finally, the necessity of accurate diagnosing is emphasized. Close cooperation between the physicians in the clinics and in the department of transfusion medicine/hemostaseology reduces unnecessary and inadequate application of coagulation components. This also means an improvement in the patient's therapy.
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PMID:[Perioperative blood coagulation therapy and diagnosis]. 219 26

The risks and adverse reactions of fresh frozen plasma (FFP) and coagulation components have changed considerably in the last few years because of the spread of HIV on the one hand, and advances in the preparation and sterilization of coagulation components on the other. Therefore, the indication for FFP and the various coagulation components deserves constant consideration; this is the intention of this paper. FFP is still the therapeutic choice for the treatment of acquired (complex) plasmatic coagulation disorders, even though the (still) small risk of virus transmission in Middle Europe has to be taken into account. Coagulation components are primarily indicated in congenital (isolated) plasmatic coagulation disorders. Only in gross or very acute acquired coagulation disorders are coagulation components needed in addition to FFP. The same regimen is recommended for the use of antithrombin III (AT III) concentrates. In cases of acquired antithrombin deficiency, antithrombin III substitution is indicated only when the anticoagulation by heparin alone or in combination with FFP is insufficient or when the heparin doses required might entail an unexceptable bleeding risk, e.g. in simultaneous thrombocytopenia. Then AT III becomes an important therapeutic factor, especially in DIC. In addition, information regarding a rational and economic substitution of FFP and coagulation components is given, and other substitutes are mentioned which could possibly be used with less risk. Finally, the necessity for an adequate diagnostic procedure is emphasized. Close cooperation between the physicians in the clinics and in the department of transfusion medicine/hemostaseology reduces unnecessary and inadequate application of coagulation components. This also means an improvement of the patient's therapy.
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PMID:[The status of blood coagulation preparations within the scope of modern hemotherapy in surgical patients]. 248 30

We studied the prevalence, clinical spectrum and epidemiologic features of thrombocytopenia among 442 (333 male, 109 female) HIV infected patients. Thrombocytopenia was defined as a platelet count < 100,000/mmc and severe if platelet count was < or = 30,000/mmc. Intravenous drug abusers were 83% (369/442). At the first clinical evaluation according to Walter-Reed (WR) classification, 90% (396/442) of patients were in stage 1-5 and 10% (45/442) in stage 6. Severe thrombocytopenia (platelet count < or = 30,000/mmc) was present in 24% (11/45) of the entire thrombocytopenic population. Forty percent (18/45) of the thrombocytopenic patients were positive to: HBV (6), HCV (7), HBV+HCV (5). Mild bleeding was present in 16% (7/45) of the patients but one case, with severe thrombocytopenia, died of intracranial hemorrhage. Major hemorrhagic sequelae with even fatal events are possible, especially when a low platelet count is associated with other hemostatic abnormalities (e.g. haemophilia, liver disease, disseminated intravascular coagulation). Zidovudine therapy (range 500-1250 mg/day) is effective in normalizing the platelet count (platelets > 100,000/mmc) only in 29% (9/31) of the patients.
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PMID:Thrombocytopenia in HIV infected patients. Prevalence and clinical spectrum. 775 81

Disseminated intravascular coagulation (DIC) is uncommon in acquired immunodeficiency syndrome (AIDS), despite the high incidence of infectious diseases. We describe an HIV-infected patient presenting with disseminated cryptococcosis, who had clear-cut laboratory evidence of progressively worsening DIC (thrombocytopenia, prolonged prothrombin time and partial thromboplastin time, hypofibrinogenemia, increased fibrin(ogen) degradation products and D-Dimer, reduced antithrombin III), although the clinical signs of the disease were rather scarce. The patient died despite intense treatment, which included heparin and fresh frozen plasma, and DIC was confirmed histologically. It is suggested that, in a patient with AIDS presenting with an opportunistic infection, laboratory signs of DIC should be carefully checked to early recognize this complication and promptly initiate the required therapy.
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PMID:Disseminated intravascular coagulation associated with disseminated cryptococcosis in a patient with acquired immunodeficiency syndrome. 836 14

Hemostasis is a result of interactions between fibrillar structures in the damaged vessel wall, soluble components in plasma, and cellular elements in blood represented mainly by platelets and platelet-derived material. During formation of a platelet plug at the damaged vessel wall, factors IXa and VIIIa form the "tenase" complex, leading to activation of factor X on the surface of activated platelets. Subsequently, factors Xa and Va form the "prothrombinase" complex, which catalyzes the formation of thrombin from prothrombin, leading to fibrin formation. An enhanced expression of negatively charged phosphatidylserine in the outer membrane leaflet resulting from a breakdown of the phospholipid asymmetry is essential for the formation of the procoagulant surface. An ATP-driven and inward-acting aminophospholipid "translocase" and a "floppase" counterbalancing this have been postulated to maintain the dynamic state of phospholipid asymmetry. A phospholipid-nonspecific "scramblase," believed to be responsible for the fast breakdown of the asymmetry during cell activation, has recently been isolated from erythrocytes, cloned, and characterized. An intracellular calcium-binding segment and one or more thioesterified fatty acids are probably of importance for calcium-induced activation of this transporter protein. Cytosolic calcium ions also activate the calcium-dependent protease calpain associated with shedding of microvesicles from the transformed platelet membrane. These are shed with a procoagulant surface and with surface-exposed P-selectin from the alpha-granules. Theoretically, therefore, microvesicles can be involved in both coagulation and inflammation. Scott syndrome is probably caused by a defect in the activation of an otherwise normal scramblase, resulting in a relatively severe bleeding tendency. In Stormorken syndrome, the patients demonstrate a spontaneous surface expression of aminophospholipids. Activated platelets and the presence of procoagulant microvesicles have been demonstrated in several clinical conditions, such as thrombotic and idiopathic thrombocytopenia, disseminated intravascular coagulation, and HIV-1 infection, and have been found to be associated with fibrin in thrombosis. Procoagulant microvesicles may also be formed from other cells as a result of apoptosis.
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PMID:Procoagulant expression in platelets and defects leading to clinical disorders. 1059 59

We describe a 2 year-old non-immunocompromised girl with disseminated histoplasmosis who presented with a 2-month history of fever and bloody diarrhoea. On presentation, she was severely wasted and anaemic. There were gross hepatosplenomegaly and multiple lymphadenopathy. A septic screen was negative. A subsequent stool culture isolated Salmonella enteriditis. Serial Widal-Weil Felix (WWF) titres showed serological response after 2 weeks of Ceftriaxone. However, she continued to have spiking fever, bloody diarrhoea and weight loss. She developed pancytopaenia and disseminated intravascular coagulation. A bone marrow aspirate and trephine, and lymph node biopsy showed the presence of Histoplasma capsulatum, confirmed by Gomori-Methenamine Silver staining. She responded to intravenous amphotericin B followed by fluconazole (intravenous then oral) for 6 months after discharge. Human Immunodeficiency Virus screening tests were negative. Complement and immunoglobulin levels were normal. T and B enumeration tests showed gross leucopaenia with very low T cell function with defective phagocytic function. A repeat T and B cell enumeration test and phagocytic function tests done 3 months later were normal.
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PMID:Disseminated histoplasmosis in a non-immunocompromised child. 1097 16

40 patients with infective endocarditis (IE) abusing intravenous drugs (heroin, opium surrogates) and 9 IE patients predisposed to heart diseases were examined by Duke diagnostic criteria. IE in drug abusers is characterized by acute course of the disease with affection of the intact valves of the right heart (97.5%) and septicemia provoked by high-virulent microflora (Staph. aureus in 65%). Drug abusers showed the following principal clinical syndromes of IE: thromboembolic (65%); septic with formation of acute DIC syndrome (75%), development of pyodestructive foci in the organs and polyorganic insufficiency (23.3%); acute circulatory insufficiency (37.5%); secondary nephropathy (100%). In IE abusers with predisposition to heart diseases IE ran subacutely in the presence of bacteriemia caused by low-virulent microflora (Strept. viridans in 11%) or in the absence of microbial growth in blood seeding (78%). High IE lethality in drug abusers (40%) is explained both by severe complications and concomitant diseases (viral hepatitis B and C, HIV infection, etc.).
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PMID:[The course of infectious endocarditis in IV drug abusers and in subjects predisposed to heart diseases]. 1158 79


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