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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serious hepatotoxicity is uncommon with the proper therapeutic use of non-narcotic analgesics but experience with new non-steroidal anti-inflammatory drugs (NSAIDs) is limited. Drugs such as ibufenac, fenclofenac and benoxaprofen were withdrawn from the market because of hepatotoxicity, and liver damage has been reported on occasion with virtually all non-narcotic analgesics. However, a clear pattern of toxicity with characteristic clinical, biochemical and histopathological abnormalities has emerged with relatively few. With the exception of acute hepatic necrosis following overdosage of paracetamol, little is known of the mechanisms of liver injury induced by non-narcotic analgesics. Involvement of the liver in a generalised drug reaction does not imply specific hepatotoxicity. About 50% of patients given aspirin regularly in anti-inflammatory doses develop mild, dose-dependent reversible liver damage as shown by elevation of the plasma aminotransferase activity. Liver damage is more severe in a small minority and it may rarely be complicated by disseminated intravascular coagulation and encephalopathy with a fatal outcome. There have also been isolated reports of chronic active hepatitis associated with the use of salicylates. Salicylate hepatitis has been reported most often in young females with connective tissue diseases. Many patients with Reye's syndrome have been given aspirin during the prodromal phase, and this serious condition closely resembles subacute salicylate intoxication in children. Salicylate probably has a causal or contributory role in Reye's syndrome, but many refuse to accept this and the issue is the subject of heated debate. Paracetamol in overdosage causes acute hepatic necrosis, and liver damage has been attributed to its therapeutic use. However, most reports have involved chronic alcoholics who took excessive doses and in these patients the clinical, biochemical and pathological findings were typical of paracetamol overdosage. Many authors have failed to make the distinction between therapeutic use and a therapeutic dose. In other cases liver damage could have been caused by exposure to other agents, viral infection or naturally occurring liver disease. If these cases are excluded, there are very few reports of liver damage associated with the proper therapeutic use of paracetamol. In some cases, the picture resembled chronic active hepatitis but no causal relationship has been established between this condition and paracetamol use. Paracetamol does not cause deterioration in liver function in patients with chronic liver disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of non-narcotic analgesics on the liver. 355 80

Endothelial injury is important in the pathogenesis of thrombosis, atherosclerosis, disseminated intravascular coagulation, and vasculitis. The ability of several common human viruses to infect cultures of endothelial cells obtained from human umbilical veins or bovine thoracic aorta was demonstrated. Indicators of infection included cytopathology, viral growth curves, and antigen detection by immunofluorescence. Herpes simplex virus type 1, adenovirus type 7, measles virus, and parainfluenza virus type 3 infected both human venous and bovine aorta endothelium. Mumps virus, poliovirus type 1, and echovirus type 9 grew only in human venous cells; coxsackievirus B4 infected only bovine arterial cultures; and cytomegalovirus, influenza A/Victoria/75 (H3N2) virus, and respiratory syncytial virus failed to grow in either cell culture. During replication some viruses caused acute lytic changes; some produced chronic, less destructive alterations; and other induced no apparent cytopathology. The results suggest that viral replication within endothelium may be important in the pathogenesis of viral disease of initiation of vessel-wall injury.
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PMID:Virus infection of endothelial cells. 626 Aug 74

A patient had disseminated herpes simplex, type 1, virus infection manifested by fulminant hepatitis and disseminated intravascular coagulation. The diagnosis was established by isolation of the virus from throat, urine, and buffy coat and confirmed at autopsy by the visualization of typical inclusions, demonstration of herpesvirus particles by electron microscopy, and specific immunoperoxidase staining. Therapy with vidarabine did not alter the fatal course. On the basis of clinical features and serologic results, the case represented a disseminated primary infection with herpes simplex, rather than reactivation of an endogenous infection, following renal transplantation.
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PMID:Primary disseminated herpes simplex infection with fulminant hepatitis following renal transplantation. 702 79

There are occasional reports in medical literature of peripheral gangrene and subsequent extremity amputation following systemic infection. Although the authors of these case reports speculated that the gangrene was due to septic embolization, pathologic study of the amputated tissue failed to reveal evidence of septic emboli. In reviewing reports of amputation following scarlet fever, varicella, pneumococcemia, and appendicitis, we found cases with clinical, hematologic, and pathologic evidence of disseminated intravascular coagulation (DIC). We describe 2 patients who required extremity amputation following an acute, systemic infection: transmetatarsal and Lisfranc amputation following meningococcal meningitis and bilateral below-knee amputation following pneumococcal meningitis. Both of these patients had clinical, hematologic, and pathologic evidence of DIC. Following amputation, both of these patients had significant problems with skin healing and prosthetic fitting. The presence of an acute systemic bacterial or viral infection, coagulation abnormalities and pathologic tissue indicative of DIC, and skin lesions of the extremities progressing to dry gangrene and ultimately requiring bilateral amputation are the key clinical features of this syndrome. We conclude that DIC is a major pathophysiologic mechanism responsible for peripheral gangrene following systemic infection.
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PMID:Extremity amputation: disseminated intravascular coagulation syndrome. 736 47

Coagulation is explored in 129 children infected by dengue virus and presenting either banal symptoms, or an hemorrhagic fever. Results are given, and commented according to the disease's clinical staging. A disseminated intravascular coagulation symdrome is brought out in all the cases, but with less or more intensity, though it belongs to dengue virus infection. Etio-pathogenic mechanism is then discussed.
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PMID:[Hemorrhagic dengue fever: evidence of consumption coagulopathy (author's transl)]. 738 88

A 60-year-old woman who was previously in good health presented with a sore throat, fever, and a flu-like syndrome. Treated initially with acetaminophen and fluids for a presumed viral infection, she had a syncopal episode 4 days later, was admitted to the hospital, and died 3 hours after admission. Laboratory test results suggested sepsis with disseminated intravascular coagulation (DIC), whereas blood cultures grew group A beta-hemolytic streptococci. A postmortem diagnosis of streptococcal toxic shock syndrome was established. It was of particular interest that the pulmonary microcirculation was filled with thrombi that contained numerous gram-positive cocci. Although death from sepsis with DIC is not uncommon, septic pulmonary thrombosis has not been previously described. We speculate that this paradox may reflect unique properties of the virulent strains of Streptococcus pyogenes that are associated with streptococcal toxic shock syndrome.
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PMID:Septic pulmonary thrombosis in streptococcal toxic shock syndrome. 755 52

It has been noticed that hyperamylasemia occurs after hepatic resection. Between July 1973 and April 1991, hyperamylasemia was observed in 57 (42%) of 136 patients with hepatocellular carcinoma and 13 (32%) of 41 patients with metastatic liver cancer. The incidence was not correlated with extent of resection, blood loss, hypoxemia, disseminated intravascular coagulation, liver cirrhosis, or hepatitis B virus infection. There were three patterns: salivary-type dominant hyperamylasemia (type I), pancreatic-type dominant hyperamylasemia (type II), and a mixture of types I and II (type III). The point at issue is whether types II and III indicate postoperative pancreatitis. Although the pathogenesis remains unclear, surgeons should be alert to this complication and take reasonable measures with regard to the types of hyperamylasemia.
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PMID:Hyperamylasemia after hepatic resection. 768 77

Pichinde virus infection of inbred guinea-pigs is a model for arenaviral infections in humans. Infected animals experience reduced levels of multiple coagulation factors caused by either consumption coagulopathy or impaired factor synthesis. A radioimmunoassay (RIA) of guinea-pig fibrinopeptide A (gFPA) has been developed to measure the degree of thrombin action in vivo. gFPA was synthesized via the solid-phase method and conjugated to bovine serum albumin (BSA). A double antibody RIA was established employing goat anti-rabbit IgG to precipitate the primary complex composed of either 125I-5-Tyr-gFPA or 125I-12-Tyr-gFPA and rabbit anti-gFPA-BSA. The cross-reaching material was removed by mixing the plasma with 3 vol of ethanol. The supernatant was filtered through a hollow fibre apparatus by centrifugation. Plasma gFPA immunoreactivities of outbred guinea-pigs averaged 6.56 ng/ml. The gFPA-RIA was validated by determining the quantity of gFPA released from thrombin-degraded fibrinogen. A transient elevation of gFPA levels was detected in Pichinde-infected animals by the gFPA-RIA using 125I-12-Tyr-gFPA as a tracer. The pathogenic mechanism by which the increased gFPA levels may lead to the lethality of Pichinde virus infection remains to be elucidated. It is possible that the coagulopathy triggers changes in immune and inflammatory pathways that induces high cytokine concentrations, with deleterious effects on organs such as the heart and lungs.
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PMID:Haemostatic derangements associated with arenavirus infection in the guinea-pig: radioimmunoassay of fibrinopeptide A to assess thrombin action in infected animals. 838 97

We retrospectively studied 42 patients hospitalized for Stevens-Johnson syndrome at the Veterans General Hospital-Taipei between 1979 and 1991. Twenty-seven patients were males and 15 females; the ages ranged from 7 months to 82 years old with a mean age 50. The most common precipitating factor was drugs among which diphenylhydantion was the leading offender followed by nonsteroidal anti-inflammatory agents and allopurinol. Sixteen cases might be etiologically associated with infection, including 13 with upper respiratory infection, one with acute hepatitis B, one with pulmonary tuberculosis, and one with fever of unknown origin that was suspected to be viral infection. Although mycoplasma infection was thought in the literature to be a common etiologic factor of Stevens-Johnson syndrome, it was scarcely found in our study. Four patients were not treated with systemic steroids but still recovered uneventfully. Systemic steroid as a whole was not proved to be necessary, but early large-dose steroid therapy might abbreviate the course of the disease. The mortality rate was 11.9% which differs unremarkably from the reported rate (5-15%). Two patients died of pneumonia with sepsis, one of hemorrhagic shock (bleeding of adenocarcinoma of stomach), one of aspiration pneumonia, and one of sepsis with disseminated intravascular coagulation, upper gastrointestinal bleeding, and hyperglycemic hyperosmolar nonketotic coma.
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PMID:[Stevens-Johnson syndrome: a review of 42 cases]. 849 Jul 98

Experimental infection of three indigenous breeds of sheep in Nigeria, namely the West African Dwarf (WAD), Yankasa and Ouda resulted in fatal disease with the Zinga Rift Valley Fever virus. Infected sheep of the three breeds responded by pyrexia within 24 h of infection, that lasted 6 to 7 days, but peaked between day 2 and 4 post-infection. Viraemia coincided with pyrexia and peaked (10(9) PFU/ml) 3 days p.i. in Yankasa and WAD sheep, but with highest titre (10(7.5) PFU/ml) in Ouda sheep. Zinga Rift Valley Fever virus infection of sheep was characterised by hyperactivity, watery and mucoid nasal discharges, projectiles and bloody diarrhoea, external haemorrhage and clinical manifestations of nervous disorders. Viraemia was followed by low level of antibody development in all the infected sheep. Haemotological changes included a sharp fall in the PCV, Hb concentration and total RBC count during the course of the disease. These changes were most severe in the Yankasa, followed by WAD and Ouda breeds. There were thrombocytopaenia, prolongation of prothrombin and clotting times in all the infected sheep. There was also progressive leucopaenia associated with lymphopaenia. The total protein and albumin levels were depressed, but the globulin level rose from day 5 p.i. The changes in the serum biochemical constituents included sharp and progressive increase in the level of alanine aminotransferase and aspartate aminotransferase. The sodium level decreased gradually while that of potassium was initially stable but later increased until the infected animals died. There was a significant increase in the level of blood urea nitrogen from day 3 p.i. that continued until the infected animals died. Gross and microscopic examinations of the carcasses of the infected sheep showed significant lesions in many organs, including disseminated intravascular coagulation.
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PMID:Experimental infection of three Nigerian breeds of sheep with the Zinga strain of the Rift Valley Fever virus. 888 13


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