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)

One week after treatment with intravenously administered immune globulin and aspirin, a child with Kawasaki disease had persistent fever and an increase in coronary artery diameter to greater than 3 mm. Two additional doses of immune globulin were given intravenously. Rapid hemolysis occurred, followed by disseminated intravascular coagulation and serum sickness. Clinicians should be aware that immune globulin preparations contain antibodies to blood-type antigens that may cause significant hemolysis and disseminated intravascular coagulation.
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PMID:Immune hemolysis, disseminated intravascular coagulation, and serum sickness after large doses of immune globulin given intravenously for Kawasaki disease. 159 53

Thrombomodulin (TM) is a constituent glycoprotein of endothelial cell membrane, and soluble TM is present also in plasma and urine. It was revealed by experiments using cultured HUVEC in vitro that TM is released from endothelial cell membrane not with monensin, thrombin, fibroblast growth factor, interleukin-1 or endotoxin, but with H2O2 or endotoxin-treated granulocytes. And the release was suppressed by the coexistence of gabexate mesilate or superoxide dismutase. It was suggested that soluble TM was released from endothelial cell membrane by its injury and digested to multiple molecular forms by endogenous and granulocytic protease(s). TM level in circulation is increased in cases of SLE, MCLS, diabetic angiopathy. It was increased in cases of overt DIC and decreased to the normal level when the patient was recovered from DIC. TM level in circulation was also increased in cases of decompensated liver cirrhosis and markedly in cases of renal insufficiency. It was concluded that plasma TM is a parameter reflecting endothelial injury due to inflammation or metabolic disorders of vascular system. But the interpretation of increased plasma TM was difficult when renal insufficiency was complicated.
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PMID:[Soluble thrombomodulin: a specific parameter of endothelial injury]. 185 Dec 35

Septicemia encountered at Kawasaki Municipal Hospital between 1985 and 1986 were studied clinically. Forty six patients had monomicrobial and 5 has polymicrobial infections, respectively. Out of these 46 patients with septicemia, 17 were due to Escherichia coli, 7 were due to Klebsiella pneumoniae and 4 were due to Staphylococcus aureus. Ten patients had hepatobiliary, 7 had hematological, 7 had malignant diseases as underlying diseases, respectively. Out of 10 patients complicated with septic shock, 7 died. Twenty three patients were community acquired infections. The age of most of the patients were over 50. The mortality rate of more than 65-year-old patients were higher than that of other patients. Our of 5 patients with septicemia due to polymicrobial infection, only 1 patient with erythroleukemia died. Fifty patients were treated mainly with beta-lactam antibiotics such as piperacillin or cefmetazole alone or in combination with aminoglycosides and so on. Three patients with infective endocarditis were encountered during this period. Two were due to alpha-streptococcus and 1 was due to Enterococcus. A 41-year-old patient with mitral valve insufficiency and metastatic gastric carcinoma to the bone marrow were complicated with disseminated intravascular coagulation. This patient, however, was successfully treated with a daily dose of 24 mega units of benzylpenicillin, and was given gabexate mesilate, concomitantly.
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PMID:[Clinical studies on septicemia and infective endocarditis encountered between 1985-1986]. 250 8

Thrombocytosis is always noted in patients with Kawasaki disease (KD). Here we present a case of KD with an unusual finding of thrombocytopenia. A 3 months old female baby was admitted to our hospital presenting with the classical symptoms and signs of KD. However, initially she also had thrombocytopenia and disseminated intravascular coagulation. She was treated successfully with a single high dose of intravenous immunoglobulin. (2 gm/kg). Thrombocytosis was found on the 10th day of illness, and treatment with low dose aspirin was administered for 3 months. No coronary aneurysm was found on cardiac echography. She was found to be well on a follow-up of 8 months.
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PMID:Kawasaki disease presenting with disseminated intravascular coagulation: report of one case. 808 58

The authors report on a 2-year-old boy with atypical Kawasaki disease (KD) and thrombocytopenia who developed 3 coronary artery aneurysms. The mechanism of thrombocytopenia in KD seems to be consumption coagulopathy. Review of the 30 reported cases of KD and thrombocytopenia revealed that this combination is more common in girls and in young age groups, and is associated with an increased risk of coronary artery aneurysm and myocardial infarction.
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PMID:Thrombocytopenia in Kawasaki disease: a risk factor for the development of coronary artery aneurysms. 1457 29

We report a case of Yersinia pseudotuberculosis (Y. ptbc) infection complicated by disseminated intravascular coagulation (DIC) that presented as Kawasaki disease (KD). A 9-year-old girl had been well until two days before, when she developed a fever, exanthem, and abdominal pain. An erythematous macular rash was observed in the perineum, and she had a strawberry tongue. The patient was admitted to Kawasaki Medical School Hospital because the macular rash spread over her entire body, and edema of her hands and conjunctivitis subsequently developed. Echo cardiography showed dilation of the left coronary artery. Thrombocytopenia and an elevated total fibrin degeneration product level were noted on the third hospital day, and the prothronmbin and partial-thromboplastin times were prolonged. Her clinical presentation was typical of KD and DIC. A stool culture and a blood culture were negative. Serologic tests were positive for antibodies to Y. ptbc. The antibody titer against Y. ptbc-derived mitogen was not elevated after her recovery. Y. ptbc infection should be considered in an older child whose clinical findings fulfill the criteria for KD complicated by DIC.
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PMID:[Yersinia pseudotuberculosis type 4a infection meeting the diagnostic criteria for Kawasaki disease complicated by disseminated intravascular coagulation]. 1636 61

Disseminated intravascular coagulation is a rare complication of Kawasaki disease and appears in <0.1% of Kawasaki disease patients. We report a case of refractory Kawasaki disease complicated with disseminated intravascular coagulation and giant coronary aneurysm. A 5-month-old boy presented with Kawasaki disease with coagulopathy. Although the coagulopathy improved after fresh-frozen plasma and antithrombin-III administration, the fever persisted despite two rounds of intravenous immunoglobulin, along with intravenous methylprednisolone pulse therapy and infliximab administration. Despite all efforts to treatment, the patient had giant coronary aneurysms and died suddenly.
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PMID:Extremely refractory Kawasaki disease with disseminated intravascular coagulation. 2826 46

The COVID-19 pandemic is an unprecedented healthcare emergency causing mortality and illness across the world. Although primarily affecting the lungs, the SARS-CoV-2 virus also affects the cardiovascular system. In addition to cardiac effects, e.g. myocarditis, arrhythmias, and myocardial damage, the vasculature is affected in COVID-19, both directly by the SARS-CoV-2 virus, and indirectly as a result of a systemic inflammatory cytokine storm. This includes the role of the vascular endothelium in the recruitment of inflammatory leucocytes where they contribute to tissue damage and cytokine release, which are key drivers of acute respiratory distress syndrome (ARDS), in disseminated intravascular coagulation, and cardiovascular complications in COVID-19. There is also evidence linking endothelial cells (ECs) to SARS-CoV-2 infection including: (i) the expression and function of its receptor angiotensin-converting enzyme 2 (ACE2) in the vasculature; (ii) the prevalence of a Kawasaki disease-like syndrome (vasculitis) in COVID-19; and (iii) evidence of EC infection with SARS-CoV-2 in patients with fatal COVID-19. Here, the Working Group on Atherosclerosis and Vascular Biology together with the Council of Basic Cardiovascular Science of the European Society of Cardiology provide a Position Statement on the importance of the endothelium in the underlying pathophysiology behind the clinical presentation in COVID-19 and identify key questions for future research to address. We propose that endothelial biomarkers and tests of function (e.g. flow-mediated dilatation) should be evaluated for their usefulness in the risk stratification of COVID-19 patients. A better understanding of the effects of SARS-CoV-2 on endothelial biology in both the micro- and macrovasculature is required, and endothelial function testing should be considered in the follow-up of convalescent COVID-19 patients for early detection of long-term cardiovascular complications.
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PMID:Endothelial dysfunction in COVID-19: a position paper of the ESC Working Group for Atherosclerosis and Vascular Biology, and the ESC Council of Basic Cardiovascular Science. 3275 Jan 8

Coronavirus disease 2019 (COVID-19) is a prominent pandemic disease that emerged in China and hurriedly stretched worldwide. There are many reports on COVID-19 associated with the amplified incidence of thrombotic events. In this review, we focused on COVID-19 coupled with the coagulopathy contributes to severe outcome inclusive of comorbidities such as venous thromboembolism, stroke, diabetes, lung, heart attack, AKI, and liver injury. Initially, the COVID-19 patient associated coagulation disorders show an elevated level of the D-dimer, fibrinogen, and less lymphocyte count such as lymphopenia. COVID-19 associated with the Kawasaki disease has acute vasculitis in childhood which further affects the vessels found all over the body. COVID-19 linked with the thrombotic microangiopathy triggers the multiple vasculitis along with the arterioles thrombosis, medium, large venous and arterial vessels mediates the disseminated intravascular coagulation (DIC). SARS-Co-V-2 patients have reduced primary platelet production, increased destruction of the platelet, decreased circulating platelet leads to the condition of increased thrombocytopenia which contributes to the coagulation disorder. Endothelial dysfunction plays an important role in the coagulation disorders via increased generation of the thrombin and stops fibrinolysis further leads to hypercoagulopathy. Along with that endothelial dysfunction activates the complement system pathways and contributes to the acute and chronic inflammation via cytokine storm with the production of the cytokines and chemokines, coagulation in different organs such as lung, brain, liver, heart, kidney and further leads to multi-organ failure.
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PMID:SARS-CoV-2 and coagulation disorders in different organs. 3294 15

In atherosclerosis patients, vascular endothelial dysfunction is commonly observed alongside damage of the vascular endothelial glycocalyx, an extracellular matrix bound to and encapsulating the endothelial cells lining the blood vessel wall. Although atherosclerotic risk factors have been reported in severe patients with coronavirus disease 2019 (COVID-19), the exact mechanisms are unclear. The mortality associated with the COVID-19 outbreak is increased by comorbidities, including hypertension, diabetes, obesity, chronic obstructive pulmonary disease (COPD), and cardiovascular disease. Besides, older individuals and smokers have significantly worse outcomes. Interestingly, these comorbidities and risk factors are consistent with the pathophysiology that causes vascular endothelial glycocalyx damage. Moreover, vascular glycocalyx dysfunction causes microvascular leakage, which results in interstitial pulmonary abnormal shadows (multiple patchy shadows with a ground glass inter-pneumonic appearance). This is frequently followed by severe acute respiratory distress syndrome (ARDS), closely related to coagulo-fibrinolytic changes contributing to disseminated intravascular coagulation (DIC) and Kawasaki disease shock syndrome, as well as inducing activation of the coagulation cascade, leading to thromboembolism and multiple organ failure. Notably, SARS-CoV-2, the causative virus of COVID-19, binds to ACE2, which is abundantly present not only in human epithelia of the lung and the small intestine, but also in vascular endothelial cells and arterial smooth muscle cells. Moreover, COVID-19 can induce severe septic shock, and sepsis can easily lead to systemic degradation of the vascular endothelial glycocalyx. In the current review, we propose new concepts and therapeutic goals for COVID-19-related vascular endothelial glycocalyx damage, based on previous vascular endothelial medicine research.
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PMID:Endothelial glycocalyx damage as a systemic inflammatory microvascular endotheliopathy in COVID-19. 3303 65


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