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)

Coagulopathy, or non-mechanical hemorrhage, complicated the operative course of 17 of 33 (51.5%) patients suffering severe liver trauma. The highest incidence of non-mechanical hemorrhage (66.7%) occurred in patients undergoing anatomic lobectomy. Serial hemostatic parameters were assessed and thrombocytopenia was the most striking abnormality in patients with non-mechanical hemorrhage. The degree of thrombocytopenia was directly correlated with the number of blood transfusions administered. The mean operative blood transfusion requirement was significantly greater in patients with non-mechanical hemorrhage, 25.1 +/- 2.87 (S.E.M.) units, than in those without, 12.2 +/- 1.83 units (p < 0.001). The bulk of this transfusion was given before the onset of clinically overt coagulopathy. Massive transfusion of stored blood was felt to be the most important factor in causing non-mechanical hemorrhage. Convincing evidence for disseminated intravascular coagulation was lacking, and abnormal fibrinolysis was infrequent and mild when observed. Although uneventful in most, in six patients non-mechanical hemorrhage resulted in excessive blood transfusion, unnecessary operation or death. Infusions of platelet concentrate, fresh frozen plasma, and fresh blood were used to successfully treat most cases of non-mechanical hemorrhage. In all cases, these components were not started until non-mechanical hemorrhage was clinically apparent. The value of prophylactic use of blood components is stressed. Because of troublesome side effects associated with the use of prothrombin complex concentrates, these agents are contraindicated in patients with severe liver injury. After receiving concentrates, one patient developed severe hypotension leading to ventricular fibrillation, two developed transient thrombocytopenia and two others demonstrated multiple pulmonary microthrombi at autopsy, a finding not observed in autopsied patients not receiving the concentrates.
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PMID:Non-mechanical hemorrhage in severe liver injury. 64 75

On the basis of three case histories we discuss the menstrual toxic shock syndrome (TSS), characterised by multi-organ involvement, fever, exanthema and shock. The symptoms are provoked by a toxin (TSST-1), a product of certain St. aureus strains. Rapid recognition is important in order to prevent complications such as the adult respiratory distress syndrome, disseminated intravascular coagulation or ventricular fibrillation. It appears that a tampon can lower the magnesium concentration in the vagina by a process of ion exchange, thus creating an environment that favours the production of TSST-1 by St. aureus. This knowledge may lead to preventive measures in the production of tampons in the future.
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PMID:[Tampon disease, still not past tense]. 156 Aug 69

Thirty-nine patients with untreated acute promyelocytic leukemia (APL) were randomly allocated to receive rubidazone (zorubicin) 200 mg/m2/d, days 1 to 4 plus cytarabine (Ara C) 200 mg/m2/d, days 1 to 7 (arm A, 21 patients), or amsacrine (Amsa) 150 mg/m2/d, days 1 to 4 plus Ara C 200 mg/m2/d, days 1 to 7 (arm B, 18 patients). Prophylaxis of disseminated intravascular coagulation was made by platelet transfusions and heparin. In case of leukemic resistance, patients received a second course with 2 days of rubidazone (arm A) or Amsa (arm B) and 3 days of Ara C. Patients who achieved complete remission (CR) received three consolidation courses with the two drugs used for induction and maintenance therapy for 3 years. Two patients in arm A and one in arm B were allografted in first CR. Initial characteristics were similar in both arms. In arm A, 18 patients (86%) reached CR, two had hypoplastic death, and one had leukemic resistance after two courses. In arm B, 12 patients (66%) achieved CR, two had early death (CNS bleeding, one case; ventricular fibrillation, one case), and four had resistant leukemia after two courses. The difference in CR rate between the two arms was not significant. In arm A, disease-free survival (DFS) showed a plateau at 54.3% after 34 months (95% confidence interval [CI], 32.1% to 74.9%), with eight CRs longer than 34 months. In arm B, DFS was significantly shorter (P less than .03), showing a plateau at 16.7% after 38 months (95% confidence interval, 4.7% to 44.6%), and only two prolonged CRs were seen. The difference in DFS remained significant after censoring allografted patients and patients who died in CR (one in arm A, two in arm B). Our results suggest that Amsa-Ara C combinations may be inferior to anthracycline-Ara C combinations in the treatment of APL, because they seem to provide shorter DFS and, possibly, a higher incidence of initial leukemic resistance. However, studies with larger numbers of patients are required.
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PMID:A randomized trial of amsacrine and rubidazone in 39 patients with acute promyelocytic leukemia. 172 18

A 53-year-old man with a prior history of myocardial infarcts and small cell lung cancer presented with lower limb ischemia. Laboratory tests revealed acute consumption coagulopathy and echocardiography showed massive intracavitary thrombi in the right atrium and both ventricles. Despite the administration of heparin, the patient died 3 weeks later of ventricular fibrillation. Autopsy demonstrated no relapse of lung cancer but large old myocardial infarcts.
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PMID:Intracardiac thrombosis associated with an acute consumption coagulopathy. 381 55

A patient with severe hypothermia (core temperature of 22.2 C) and ventricular fibrillation had manual cardiopulmonary resuscitation for 3 1/2 hours while various rewarming technics raised her temperature to a level permitting successful electrical cardioversion. Laboratory testing revealed disseminated intravascular coagulation and several endocrinologic abnormalities. The need for prolonged, aggressive resuscitative measures and the possible role of corticosteroids in the management of profound hypothermia are discussed.
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PMID:Profound hypothermia: value of prolonged cardiopulmonary resuscitation. 722 65

A 34-year old woman, with a 3 yr history of severe seropositive rheumatoid arthritis (RA) with lupus anticoagulant and anticardiolipin antibodies, developed a massive anterior myocardial infarction and ischemia of the lower extremities, with disseminated intravascular coagulation resulting from extensive tissue damage. Seven days after admission, she died of severe heart failure complicated by ventricular fibrillation. To our knowledge, this is the first documented case of fatal acute antiphospholipid syndrome in RA.
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PMID:Catastrophic antiphospholipid syndrome with fatal acute course in rheumatoid arthritis. 747 89

We studied the post-resuscitation syndrome in 42 healthy dogs after normothermic ventricular fibrillation cardiac arrest (no blood flow) of 7.5, 10, or 12.5 min duration, reversed by standard external cardiopulmonary resuscitation (CPR) (< or = 10 min) and followed by controlled ventilation to 20 h and intensive care to 72 h. We reported previously, in the same dogs, no difference in resuscitability, mortality, or neurologic outcome between the three insult groups. There was no pulmonary dysfunction, but post-arrest cardiovascular failure, of greater severity in the 12.5 min arrest group. This report concerns renal, hematologic, hepatic and bacteriologic changes. Renal function recovered within 1 h after arrest, without permanent dysfunction. Clotting derangements at 1-24 h postarrest reflect transient disseminated intravascular coagulation with hypocoagulability, more severe after longer arrests, which resolved by 24 h after arrest. Hepatic dysfunction was transient but more severe in the animals that did not recover consciousness and correlated with neurologic dysfunction, but not with brain histologic damage. Bacteremia was present in all animals postarrest. We conclude that in the previously healthy organism after cardiac arrest of 7.5-12.5 min no flow, visceral and hematologic changes, although transient, can retard neurologic recovery.
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PMID:Visceral, hematologic and bacteriologic changes and neurologic outcome after cardiac arrest in dogs. The visceral post-resuscitation syndrome. 849 1

The novel coronavirus disease (COVID-19) outbreak, caused by SARS-CoV-2, represents the greatest medical challenge in decades. We provide a comprehensive review of the clinical course of COVID-19, its comorbidities, and mechanistic considerations for future therapies. While COVID-19 primarily affects the lungs, causing interstitial pneumonitis and severe acute respiratory distress syndrome (ARDS), it also affects multiple organs, particularly the cardiovascular system. Risk of severe infection and mortality increase with advancing age and male sex. Mortality is increased by comorbidities: cardiovascular disease, hypertension, diabetes, chronic pulmonary disease, and cancer. The most common complications include arrhythmia (atrial fibrillation, ventricular tachyarrhythmia, and ventricular fibrillation), cardiac injury [elevated highly sensitive troponin I (hs-cTnI) and creatine kinase (CK) levels], fulminant myocarditis, heart failure, pulmonary embolism, and disseminated intravascular coagulation (DIC). Mechanistically, SARS-CoV-2, following proteolytic cleavage of its S protein by a serine protease, binds to the transmembrane angiotensin-converting enzyme 2 (ACE2) -a homologue of ACE-to enter type 2 pneumocytes, macrophages, perivascular pericytes, and cardiomyocytes. This may lead to myocardial dysfunction and damage, endothelial dysfunction, microvascular dysfunction, plaque instability, and myocardial infarction (MI). While ACE2 is essential for viral invasion, there is no evidence that ACE inhibitors or angiotensin receptor blockers (ARBs) worsen prognosis. Hence, patients should not discontinue their use. Moreover, renin-angiotensin-aldosterone system (RAAS) inhibitors might be beneficial in COVID-19. Initial immune and inflammatory responses induce a severe cytokine storm [interleukin (IL)-6, IL-7, IL-22, IL-17, etc.] during the rapid progression phase of COVID-19. Early evaluation and continued monitoring of cardiac damage (cTnI and NT-proBNP) and coagulation (D-dimer) after hospitalization may identify patients with cardiac injury and predict COVID-19 complications. Preventive measures (social distancing and social isolation) also increase cardiovascular risk. Cardiovascular considerations of therapies currently used, including remdesivir, chloroquine, hydroxychloroquine, tocilizumab, ribavirin, interferons, and lopinavir/ritonavir, as well as experimental therapies, such as human recombinant ACE2 (rhACE2), are discussed.
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PMID:COVID-19 and the cardiovascular system: implications for risk assessment, diagnosis, and treatment options. 3235 35