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)

Platelet abnormalities associated with hepatobiliary diseases include increased (thrombocytosis) and decreased (thrombocytopenia) numbers of platelets as well as abnormalities in function (thrombocytopathy or thrombasthenia). Hepatic diseases that are accompanied by platelet abnormalities include hepatitis, cirrhosis, portal hypertension, and neoplastic disorders both benign and malignant. The objective of this work is to examine the platelet abnormalities that occur with a variety of hepatobiliary disorders. Thrombocytosis is seen as a reactive entity following splenectomy. Thrombocytopenia is associated with hypersplenism, dysproteinemias and liver disease related disseminated intravascular coagulation (DIC). Qualitative platelet abnormalities are found in hepatic failure, liver diseases associated with high or low levels of lipid, and with medications given for a variety of hepatocellular diseases. Clinically common and significant platelet abnormalities associated with liver disease are thrombocytopenia secondary to portal hypertension and the thrombasthenias following metabolic changes and/or therapeutic interventions of liver disease.
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PMID:Platelet abnormalities in hepatobiliary diseases. 218 3

A 25-year-old man, known to have chronic myeloid leukaemia for four years, acutely developed a fever of 39.5 degrees and severe pain in the shoulder and hip joints. There was no evidence of joint disease. Treatment with indomethacin briefly improved the symptoms, but within 72 hours the patient developed a fulminant illness with high fever and clinical as well as biochemical signs of a severe consumption coagulopathy. Herpetiform efflorescences appeared over the head and trunk shortly before death. At autopsy there was histological and immunohistochemical evidence of a varicella infection with hepatitis, oesophageal involvement and severe internal organ bleedings. In immune-compromised patients with atypical prodromal symptoms a varicella infection must be considered so that causal treatment with acyclovir and hyperimmune-globulin can be begun in time.
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PMID:[Atypical joint symptoms as initial symptoms of varicella infection in chronic myeloid leukemia]. 222 57

In the present study, the first case of ruptured hepatoma followed by disseminated intravascular coagulation is reported. An elastase-like enzyme which possessed elastolytic and caseinolytic activities was confirmed from patient plasma. On the other hand, no elastase activity was detected in the plasma of patients with hepatitis, liver cirrhosis or hepatoma without disseminated intravascular coagulation. The patient plasma did not possess H-D-Val-Leu-Lys-p-nitroanilide hydrochloride, succinyl-L-alanyl-L-alanyl-p-nitroanilide, and pyro-Glu-Pro-Val-p-nitroanilide amidolytic activities. However, when chromatographed on Sephadex G-200, the presence of low-molecular weight plasminogen was confirmed. Its molecular weight was approximately 52,000. A slight decrease of alpha 2-plasmin inhibitor was noted, but no decrease of alpha 2-macroglobulin was detected.
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PMID:A case of ruptured hepatoma followed by elastase-induced disseminated intravascular coagulation. 241 97

Hantaviruses, the causative agents of HFRS, have become more widely recognized. Epidemiologic evidence indicates that these pathogens are distributed worldwide. People who come into close contact with infected rodents in urban, rural and laboratory environments are at particular risk. Transmission to man occurs mainly via the respiratory tract. The epidemiology of the hantaviruses is intimately linked to the ecology of their principal vertebrate hosts. Four distinct viruses are now recognized within the hantavirus genus and that number is likely to increase to six very soon; however, further investigations are necessary. Much more work is still needed before we fully understand the wide spectrum of clinical signs and symptoms of HFRS as well as the pathogenicity of the different viruses in the hantavirus genus of the Bunyaviridae family. HFRS is difficult to diagnose on clinical grounds alone and serological evidence is often needed. A fourfold rise in IgG antibody titer in a 1-week interval, and the presence of the IgM type of antibodies against hantaviruses are good evidence for an acute hantavirus infection. Physicians should be alert for HFRS each time they deal with patients with acute febrile flu-like illness, renal failure of unknown origin and sometimes hepatic dysfunction. Especially the mild form of HFRS is difficult to diagnose. Acute onset, headache, fever, increased serum creatinine, proteinuria and polyuria are signs and symptoms compatible with a mild form of HFRS. Differential diagnosis should be considered for the following diseases in the endemic areas of HFRS: acute renal failure, hemorrhagic scarlet fever, acute abdomen, leptospirosis, scrub typhus, murine typhus, spotted fevers, non-A, non-B hepatitis, Colorado tick fever, septicemia, dengue, heartstroke and DIC. Treatment of HFRS is mainly supportive. Recently, however, treatment of HFRS patients with ribavirin in China and Korea, within 7 days after onset of fever, resulted in a reduced mortality as well as shortened course of illness.
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PMID:Hemorrhagic fever with renal syndrome. 257 14

A study is presented of 159 patients with cholestatic forms of viral hepatitis and 82 patients with viral hepatitis showing no cholestasis. The disorders of the coagulation activity were found to be nonhomogeneous and depended on the clinical variant of viral hepatitis, the period and severity of the disease, premorbid background and ways of infection. It is emphasized that development of the syndrome of disseminated intravascular coagulation is characteristic of the most severe forms of hepatitis against the background of prolonged and maximal bile stasis as well as in viral hepatitis B. Use of heparine, contrical and antihemorrhagic drugs when indicated prevents or controls the DIC syndrome.
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PMID:[The hemostatic system and DIC syndrome in cholestatic forms of viral hepatitis]. 260 5

The case of a young shepherd with Brucella melitensis aortic valve endocarditis is presented. His illness ran an afebrile course and was also complicated by disseminated intravascular coagulation (DIC), nephritis, hepatitis and peritonitis, all of which responded well to supportive measures and a combination of tetracycline, trimethoprim-sulphamethoxazole and amikacin sulphate. The fact that even the most severe case of brucellosis can present without fever is stressed.
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PMID:Apyrexic Brucella melitensis aortic valve endocarditis. 263 55

The great majority of viral infections are not associated with significant alterations in hemostasis. Occasionally, common viral pathogens lead to illnesses in which hemostatic impairment is an important feature. In these instances, two clinical syndromes usually are present: thrombocytopenic purpura and disseminated intravascular coagulation. Immune mechanisms are implicated in the first, while the second is associated with severe disease. Hepatitis viruses produce hemorrhage by a third mechanism. In cases of fulminant hepatitis, hepatocellular injury leads to decreased production of multiple coagulation factors and impairment of other hepatic functions that modulate hemostasis. A small number of viruses stand apart by virtue of the frequency with which they cause hemorrhage. These are the hemorrhagic fever viruses. Much more needs to be learned about how these viruses cause disease and induce hemorrhage. The first line of therapy in viral infections complicated by hemorrhage is early treatment with an antiviral agent. Unfortunately, effective antiviral therapy is usually not available. There is little useful information and no controlled studies on the efficacy of therapy aimed directly at correcting hemostatic impairment.
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PMID:Viruses and hemostasis. 266 6

The presentation and subsequent course of respiratory syncytial virus (RSV) bronchiolitis may be atypical and unusually severe when simultaneous infection due to other pathogenic agents is present. During the past two years, nine of the 189 pediatric patients hospitalized with documented RSV infection were found to have the following simultaneous isolates from initial respiratory tract specimens: four adenovirus, four pneumococcus, one cytomegalovirus, and one Pneumocystis carinii. Noted complications attributable to the second pathogen included thrombocytopenia and anemia (cytomegalovirus), hepatitis and disseminated intravascular coagulation (adenovirus), and sepsis and osteomyelitis (pneumococcus). Three of the four patients with RSV and adenovirus died of severe respiratory failure despite mechanical ventilation; two of these patients received ribavirin therapy. Rapid identification of RSV is important but should not be a substitute for more comprehensive viral and bacterial evaluation.
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PMID:Simultaneous infection with respiratory syncytial virus and other respiratory pathogens. 283 76

The clinical and pathologic features of Epstein-Barr virus (EBV) hepatitis in 3 children are described. Manifestations included fever, hepatomegaly, disseminated intravascular coagulation, and failure of uptake of technetium by the reticuloendothelial system of the liver. Histologic features may mimic chronic active hepatitis and lymphoid malignancy. Two patients underwent exploratory laparotomy because of suspected tumor. Recognition of the wide spectrum of hepatic involvement in infectious mononucleosis is important in the differential diagnosis of hepatomegaly. Diagnosis should be made by measurement of IgM-specific EBV antibodies.
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PMID:The spectrum of Epstein-Barr virus hepatitis in children. 302 40

Sequential histological and fine structural changes were studied in liver from 4.5 min to 21 days after a single intravenous injection of Corynebacterium parvum in the rat. A previously unreported effect of the micro-organism, the formation of eosinophilic inclusion bodies within hepatocytes, was observed between 15 min and 24 h of injection. These structures were most common in periportal hepatocytes at 2 h. The structural, enzyme- and immunohistochemical features of these bodies suggest that they represent a consequence of sub-lethal cell injury, affecting the endoplasmic reticulum or Golgi apparatus; resolution occurred within 24 h. The ingestion of C. parvum by phagocytes and the deposition of fibrin within sinusoids preceded the development of acute and chronic parenchymal and portal tract inflammation, leading to self-limiting granulomatous hepatitis. Lethal cell injury was represented by the presence of single-cell and confluent hepatocyte necrosis. Intravenous C. parvum causes sublethal and lethal hepatocyte damage, seen as the formation of cytoplasmic bodies and hepatocyte necrosis, respectively. Disseminated intravascular coagulation may mediate these changes via local hypoxia. This model could prove useful in the study of granulomatous hepatitis and in the evaluation of anti-inflammatory agents.
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PMID:A sequential study of hepatic structural damage following the intravenous injection of Corynebacterium parvum. 352 81


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