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)

Vitamin E pretreatment significantly prevented E. coli-induced Disseminated Intravascular Coagulation (DIC) in rats (1). DIC, a reduction in fibrinogen and a falling platelet count and diffuse haemorrhage are part of the clinical features of Haemorrhagic Shock Encephalopathy Syndrome (HSES), recognised as a disease entity in the 1980s (2). At the SIDS Conference 1974 Reisinger described the effect of Escherichia coli (E. coli) endotoxin on the rabbit (3). An early effect was a reduction in fibrinogen and a falling platelet count, resulting in the release of relatively large amounts of the neuro-transmitter serotonin, stored in platelets (3, 4). Fibrinogen inhibited the release of serotonin from platelets (24). Serotonin is released from platelets during platelet aggregation (14). Platelet aggregation is inhibited by vitamin E (1). Serotonin is a neuro-transmitter associated with deep sleep, respiratory movements and cardiovascular collapse (3). Death at a later stage involved vascular permeability, edema and haemorrhage. After fibrin-platelet clots had formed DIC was present in lungs, kidneys and other organs (3). Medical researchers in Australia linked almost half of SIDS victims with a poisonous strain of intestinal E. coli bacteria (5). Dietary selenium in the intestinal villous tip is considered a daily modulator of cytochrome P450-dependent metabolism of drugs and toxins absorbed by intestinal mucosa (6). Villous atrophy occurs in HSES (2).
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PMID:Sudden infant death syndrome (SIDS) and the immune response. 146 Nov 72

Disseminated intravascular coagulation (DIC) and other clotting abnormalities are common in sick newborn infants who have a variety of conditions. To document evidence of DIC at autopsy, immunoperoxidase staining of fibrin-related antigens (FRA) was used to detect intravascular microthrombi in liver, kidney, and lung from 127 newborns. Patients were selected from seven major disease groups: hyaline membrane disease/bronchopulmonary dysplasia, infection, meconium aspiration, necrotizing enterocolitis, congenital heart disease, other congenital anomalies, and extreme prematurity. Staining for FRA in intravascular microthrombi was seen in 40% of cases studied. The liver showed the highest frequency of intravascular microthrombi, located predominantly in the sinusoids. Unlike the adult kidney, the newborn kidney seldom had evidence of intravascular coagulation. Extravascular staining of FRA was observed in the renal distal tubular epithelium in 48 cases, many of which also had evidence of intravascular FRA staining. No significant differences in FRA staining patterns were seen among the disease groups except for cases of extreme prematurity in which all tissues showed minimal staining. Control tissues from SIDS patients also showed minimal FRA staining. Hepatic sinusoidal staining was the only tissue finding that correlated with thrombocytopenia, a clinical indicator of DIC. Despite the use of this immunohistochemical staining method, discrepancies between the clinical and autopsy diagnosis of DIC remain.
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PMID:Immunohistochemical diagnosis of disseminated intravascular coagulation in newborns. 170 Apr 4

The cause of death in a 45-day-old male infant who was found apneic at home and died 21 hours later was disseminated intravascular coagulation (DIC). The patient was admitted to a hospital in a state of cardio-respiratory arrest. The initial diagnosis was interrupted sudden infant death syndrome. The patient remained apneic, and recurrent discharge of bloody stool was the dominant clinical findings. He died without spontaneous respiration being restored. The autopsy revealed hemorrhages in the lungs and the ventricular septum and the free wall of the left ventricle of the heart. Microscopically, fibrin thrombi were noted in the large intestine and heart. The DIC was probably triggered by a widespread endothelial injury caused by severe hypoxia and acidosis originating from the apnea and cardiac arrest lasting longer than 30 min.
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PMID:A case of disseminated intravascular coagulation probably arising from sudden infant death syndrome. 954 58

It has been well documented that experimental hypomagnesemia in rodents evokes, as an early consequence, an inflammatory response. This also leads to the activation of cells producing reactive species of oxygen and, as a result, to the oxidative damage of tissues. Several studies have shown that lungs might be a specific target of Mg deficiency. Here, we report that 3 weeks of Mg deficiency in mice resulted in inflammatory processes in the lungs, including interstitial and perivascular pneumonia, manifested by the infiltration of leukocytes, plasmocytes and histiocytes, as well as the phenomenon of disseminated intravascular coagulation (DIC). These phenomena were accompanied by changes in gene expression assessed by cDNA array. In this study we identified 26 genes significantly changed by Mg deficiency, mostly involved in the anti-oxidative response, regulation of cell cycle and growth, apoptosis as well as cell-cell and cell-matrix interactions. We conclude that these changes are related to the phenomena of inflammatory and oxidative processes and consecutive remodeling occurring in the tissues as a result of Mg deficiency. This may have implications for at least several lung pathologies, including allergies, asthma, SIDS (Sudden Infant Death Syndrome) or facilitate formation of lung metastases.
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PMID:Changes in gene expression in the lungs of Mg-deficient mice are related to an inflammatory process. 1572 1