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

Viral hepatitis (VH) was diagnosed in 65% of patients with infectious endocarditis (IE) abusing intravenous narcotic drugs. VH caused recurrent course of IE in 8% examinees. The virusological tests of the blood for HBs-antigen or antibodies to viral hepatitis C were positive in 39 patients (group 1) and negative in 21 patients (group 2). VHB, VHC, VHB + VHC were diagnosed in 15, 57 and 28% patients, respectively. An acute course of IE was observed in 72% patients from group 1 and 76% patients from group 2, respectively, subacute course--in 20 and 24%, respectively, recurrent in 8% and 0%, respectively. IE patients with VH often had thrombohemorrhagic complications. DIC syndrome was detected in 25 and 4% patients, hemophthisis--in 33 and 28%, nephritis--in 71 and 48% patients, acute cerebral ischemia--in 7 and 4%, acute myocardial infarction--in 71 and 4%, hypocoagulation--in 53 and 8%, hypercoagulation--in 29 and 50% patients from group 1 and 2, respectively.
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PMID:[Clinical characteristics of endocarditis running with viral hepatitis in intravenous drug abusers]. 1189 18

Heme oxygenase-1 (HO-1) is a stress-induced enzyme that catalyses the oxidation of heme to biliverdin. The primary deficiency of this enzyme has been shown in HO-1 knockout mice, and is characterized by intrauterine death and chronic inflammation. The first case of human HO-1 deficiency was reported in 1999. Human HO-1 deficiency has been observed to involve the endothelial cells more severely, resulting in hemolysis and disseminated intravascular coagulation. We report another case of human HO-1 deficiency in a young girl with congenital asplenia, who presented with severe hemolysis, inflammation, nephritis, which was refractory to therapy with corticosteroids, cyclophosphamide, and rituximab.
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PMID:Human heme oxygenase-1 deficiency presenting with hemolysis, nephritis, and asplenia. 2108 18

Renal complications of influenza A virus infections are uncommon but can contribute to a deterioration in the patient's condition, which include acute kidney injury (AKI) in critically ill patients, rhabdomyolysis, hemolytic uremic syndrome (HUS), acute glomerulonephritis (AGN), disseminated intravascular coagulation (DIC), Goodpasture's syndrome, and acute tubulointerstitial nephritis (TIN). The clinical characteristics of AKI in critically ill patients with pandemic influenza A(H1N1) 2009 virus (A(H1N1)pdm09) infection are similar to uninfected patients. Underlying conditions associated with AKI include older age, diabetes mellitus, obesity, pregnancy, history of asthma, and chronic kidney disease. Histologic examination of the kidneys from patients with A(H1N1)pdm09 infection who died include acute tubular necrosis (ATN), myoglobin pigment, and DIC. A(H1N1)pdm09 is present in the kidneys of some patients. The clinical characteristics of patients with rhabdomyolysis associated with influenza A include younger age and the frequent occurrence of muscle symptoms. AKI occurs in approximately one third of patients with rhabdomyolysis due to influenza A. HUS is associated with A(H1N1)pdm09 as follows: Streptococcus pneumoniae-associated HUS following A(H1N1)pdm09 infection, HUS triggered by A(H1N1)pdm09 in patients with genetic complement dysregulation, and HUS associated with A(H1N1)pdm09 without known underlying disorder. AGN, Goodpasture's syndrome, and acute TIN are extremely rare complications of influenza A virus infection. Although the pathogenesis underlying renal injuries due to influenza A virus has not been delineated, some hypotheses have been advanced, including ATN due to renal hypoperfusion or rhabdomyolysis, glomerular microthrombosis due to DIC, direct viral injury to the kidney, and an altered immune system with systemic mononuclear cell activation following influenza A virus infections.
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PMID:Renal complications of seasonal and pandemic influenza A virus infections. 2306 28


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