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)

Clinical studies in the treatment of 54 children suffering from DHF with a combination of dipyridamole and ASA as an adjuvant of our standard therapy consisted of fluid, electrolytes, blood, plasma and plasma expanders were evaluated. Heparin was administered in cases of DIC. It appeared that dipyridamole and ASA did not change the mortality significantly, but it prevented the progress of the severity of the disease from grade I and II to grade III and IV.
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PMID:Dipyridamole in the treatment of dengue haemorrhagic fever. 51 1

Decreases in platelet count, fibrinogen concentration, factor VIII, antithrombin III and alpha 2-antiplasmin activities, increase in FDP-D fraction, and pleural effusion were observed transiently at early fever stage of DHF at grade II, indicating DHF patients had manifestations of the acute type of DIC with increased permeability of vascular wall.
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PMID:DHF characterized by acute type DIC with increased vascular permeability. 244 85

Forty children, aged 1/2-14 years, with serologically proven dengue haemorrhagic fever were daily studied for hemostatic tests. There were 4, 20 and 16 cases of grade I, II III respectively. Hemostatic derangements in DHF is a multifactorial mechanism. Vasculopathy, thrombocytopenia, platelet dysfunction were found in most cases. Mild to moderate degree of prothrombin complex deficiency was observed in 15% and 50% of grade II and grade III respectively while laboratory evidence of consumptive coagulopathy was noted in 30% of shock cases and 10% of non-shock cases. Hypofibrinogenemia and increased PTT are commonly seen in grade III reflect the presence of stimulation of intrinsic coagulation pathway probably from immunologic reaction. Frank DIC is very rarely observed. FDP is slightly increased but not as high as in classical DIC. Further study on the role of platelet-endothelial interaction should be elucidated including the efficient management to stop bleeding in severe shock cases.
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PMID:Hemostatic derangement in dengue haemorrhagic fever. 343 65

A retrospective study on 18 cases of DHF presented with jaundice and neurological signs which were considered unusual manifestation of DHF reveals that the causes or contributing factors are multifactorial. Most commonly found associated conditions were prolonged shock with metabolic acidosis and severe DIC that lead to hypoxia/ischaemia and resulted in both hepatic and brain dysfunction. Gross haemorrhage in the brain was noted in 6 of the 10 fatal cases while brain oedema was noted in 3 cases. Electrolyte disturbance such as hyponatremia could be another cause of brain oedema. It is certain from this study that there is no pathological evidence of encephalitis. Hepatic dysfunction found in associated with jaundice and encephalopathy is possibly caused by toxic substances, drugs and/or associated with underlying liver conditions. Reye's or Reye's-like syndrome was postulated in one case.
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PMID:Dengue haemorrhagic fever with unusual manifestations. 343 70

Abstract. Abnormal hemostasis in dengue hemorrhagic fever includes:- 1. Vasculopathy which occurs during the early febrile to pre-shock and shock phase. The evidences support are: 1.1 Increased anaphylatoxin, released by complement activation causing leakage of intravascular fluid in to serous space. 1.2 Positive tourniquet test, some of which occur preceeding thrombocytopenia in the acute phase of DHF. 1.3 Excessive increased in PGI2 which is the most potent vasodilator and platelet aggregation inhibitor. 2. Platelets: 2.1 Thrombocytopenia due to 2.1.1 The bone marrow hypocellularity with increased in all forms of megakaryocytes but the vacuolated and disintegrated ones. 2.1.2 Destruction by the liver and spleen. 2.1.3 Immune-mediated injury as demonstration of dengue antibody complexes on the platelet surface. 2.1.4 The in vitro spontaneous aggregation to vascular endothelial cell pre-infected by dengue virus inducing platelet aggregation, causing lysis and platelet destruction. 2.2 Dysfunction shown by 2.2.1 Increased release of betathromboglobulin (BTG), PF4 and PGI2. 2.2.2 In vitro hypoaggregation stimulated by ADP and defect in ADP-releasing ability. 3. Coagulopathy including: 3.1 Prothrombin complex deficiency due to liver damage. 3.2 Consumptive coagulopathy due to the activation by mononuclear phagocytes, PF3 released from platelet aggregation. DIC is seen in prolonged shock cases of DSS.
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PMID:Abnormal hemostasis in dengue hemorrhagic fever. 788 14

Dengue is an arthropod-borne viral disease whose frequency has increased steadily in the Americas over the past 25 years. The type of dengue that carries the highest mortality is the clinical variant known as dengue hemorrhagic fever/dengue shock syndrome (DHF/DSS). Even though no vaccine or drug against the disease is available, successful management consists of preventing serious illness through patient follow-up and monitoring danger signals so as to be able to initiate aggressive intravenous rehydration and prevent shock or treat it early and successfully. These measures are also useful in preventing other complications, such as massive hemorrhage, disseminated intravascular coagulation, multiple organ failure, and respiratory failure due to non-cardiogenic pulmonary edema. Primary health care (PHC) settings and the community are ideal spaces for this type of preventive management based on health education and active case detection. It involves training all medical and nursing staff, students, and community health workers, as well as reorganizing health care in PHC units and hospitals and redistributing available resources during a dengue epidemic.
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PMID:[Preventing deaths from dengue: a space and challenge for primary health care]. 1701 26

A 46 year old woman who presented with severe multiorgans involvement including liver brain, cardio-pulmonary failure, gastrointestinal bleeding, progressive cytopenia, DIC and hemophagocytic syndrome during the convalescent phase of Dengue type II has been successfully treated primarily with pulse methyl prednisolone and high dose intravenous immunoglobulin G. The authors believe that HPCS are not infrequently seen with high mortality and recommended early diagnosis and treatment with the regimen. This is the first complete report of hemophagocytic syndrome in adult dengue hemorrhagic fever in Thailand. The literature of HPCS in DHF was reviewed and discussed.
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PMID:Hemophagocytic syndrome in Dengue hemorrhagic fever with severe multiorgan complications. 1838 53