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)

The striking mortality in viral hepatitis associated with pregnancy, regularly observed in developing countries, has shown a significant decrease in Saudi Arabia during a period of unprecedented economic growth. However, the risk of fatal hepatitis in the pregnant Saudi woman remains approximately four times that for the nonpregnant woman. The explanation for the observed mortality trend is not apparent, but is unlikely to be the result of improved nutritional status of the population alone, or because of treatment of severe hepatitis with adrenal corticosteroids. Disseminated intravascular coagulation may be one factor that decisively influences the outcome of hepatitis in the pregnant woman.
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PMID:Viral hepatitis complicating pregnancy: mortality trends in Saudi Arabia. 3 43

Herpesvirus hominis (HVH) hepatitis, a rarely recognized manifestation of HVH infection in adults, occurred in a 36-year-old woman who had received prednisone therapy for pemphigus vulgaris continuously for seven years. After an acute terminal illness that was characterized by fulminant hepatic failure and disseminated intravascular coagulation (DIC), postmortem examination disclosed massive hepatic necrosis. Herpesvirus hominis (type 1) was isolated from the liver. The association of disseminated HVH infection with impaired immunologic defenses, as well as the occurrence of DIC in association with acute hepatic failure, are discussed. Greater awareness of the clinical manifestations of HVH hepatitis should lead to early diagnosis, although sucessful modes of therapy await development.
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PMID:Herpesvirus hominis hepatitis and disseminated intravascular coagulation. Occurrence in an adult with pemphigus vulgaris. 18 74

Between 1 September and 24 October 1976, 318 cases of acute viral haemorrhagic fever occurred in northern Zaire. The outbreak was centred in the Bumba Zone of the Equateur Region and most of the cases were recorded within a radius of 70 km of Yambuku, although a few patients sought medical attention in Bumba, Abumombazi, and the capital city of Kinshasa, where individual secondary and tertiary cases occurred. There were 280 deaths, and only 38 serologically confirmed survivors.The index case in this outbreak had onset of symptoms on 1 September 1976, five days after receiving an injection of chloroquine for presumptive malaria at the outpatient clinic at Yambuku Mission Hospital (YMH). He had a clinical remission of his malaria symptoms. Within one week several other persons who had received injections at YMH also suffered from Ebola haemorrhagic fever, and almost all subsequent cases had either received injections at the hospital or had had close contact with another case. Most of these occurred during the first four weeks of the epidemic, after which time the hospital was closed, 11 of the 17 staff members having died of the disease. All ages and both sexes were affected, but women 15-29 years of age had the highest incidence of disease, a phenomenon strongly related to attendance at prenatal and outpatient clinics at the hospital where they received injections. The overall secondary attack rate was about 5%, although it ranged to 20% among close relatives such as spouses, parent or child, and brother or sister.Active surveillance disclosed that cases occurred in 55 of some 550 villages which were examined house-by-house. The disease was hitherto unknown to the people of the affected region. Intensive search for cases in the area of north-eastern Zaire between the Bumba Zone and the Sudan frontier near Nzara and Maridi failed to detect definite evidence of a link between an epidemic of the disease in that country and the outbreak near Bumba. Nevertheless it was established that people can and do make the trip between Nzara and Bumba in not more than four days: thus it was regarded as quite possible that an infected person had travelled from Sudan to Yambuku and transferred the virus to a needle of the hospital while receiving an injection at the outpatient clinic.Both the incubation period, and the duration of the clinical disease averaged about one week. After 3-4 days of non-specific symptoms and signs, patients typically experienced progressively severe sore throat, developed a maculopapular rash, had intractable abdominal pain, and began to bleed from multiple sites, principally the gastrointestinal tract. Although laboratory determinations were limited and not conclusive, it was concluded that pathogenesis of the disease included non-icteric hepatitis and possibly acute pancreatitis as well as disseminated intravascular coagulation.This syndrome was caused by a virus morphologically similar to Marburg virus, but immunologically distinct. It was named Ebola virus. The agent was isolated from the blood of 8 of 10 suspected cases using Vero cell cultures. Titrations of serial specimens obtained from one patient disclosed persistent viraemia of 10(6.5)-10(4.5) infectious units from the third day of illness until death on the eighth day. Ebola virus particles were found in formalin-
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PMID:Ebola haemorrhagic fever in Zaire, 1976. 30 56

An outbreak of chronic liver disease was investigated in a kennel of dogs. Anorexia, depression, polyuria, polydipsia, icterus and a terminal hemorrhagic diathesis were noted in clinically affected dogs. Thrombocytopenia, hypofibrinogenemia, elevated fibrinogen degradation products and prolonged activated partial thrombosplastin times (PTT) and one-stage prothrombin times (PT) were associated with the hemorrhagic crisis. Aflatoxicosis was confirmed by the presence of significant levels of aflatoxicosis was confirmed by the presence of significant levels of aflatoxin B in the commercial dog food being fed. A subacute hepatitis was found on necropsy. Disseminated intravascular coagulation was suspected as the cause of the hemorrhage in these cases and treatment was instituted.
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PMID:Disseminated intravascular coagulation complicating aflatoxicosis in dogs. 55 87

The records of 104 patients with culture-proven enteric fever were reviewed and evaluated as to the clinical signs, laboratory findings, pathologic features and complications of the disease. One patient with fatal disseminated intravascular coagulation and enteric fever is also presented. Fever and bradycardia were the leading clinical signs followed by splenomegaly, hepatomegaly and rose spots. The principal complications of enteric fever included anemia, typhoid hepatitis, relapse and bleeding. Evidence of typhoid hepatitis was present in 30% of the patients tested. The pathology consisted of typhoid nodules of variable frequency and size depending upon the severity of the condition. The relationship of typhoid hepatitis to relapse seems to be more than coincidental as four out of seven patients who had relapse had abnormal liver tests. The occurrence of disseminated intravascular coagulation in enteric fever is rare; however, awareness of such a potential complication may be life-saving to the patient.
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PMID:Enteric fever: a clinicopathologic study of 104 cases. 64 89

The first recognised outbreak of Marburg virus disease in Africa, and the first since the original epidemic in West Germany and Yugoslavia in 1967, occurred in South Africa in February 1975. The primary case was in a young Australian man , who was admitted to the Johannesburg Hospital after having toured Rhodesia. Two secondary cases occurred, one being in the first patient's travelling companion, and the other in a nurse. Features of the illness included high fever, myalgia, vomiting and diarrhoea, hepatitis, a characteristic maculopapular rash, leucopenia, thrombocytopenia, and a bleeding tendency. The first patient died on the seventh day from haemorrhage resulting from a combination of disseminated intravascular coagulation and hepatic failure. The other two patients were given vigorous supportive treatment and prophylactic heparin and recovered after an acute phase lasting about seven days. During this period on developed pancreatitis, the serum amylase remaining raised until the 32nd day after the onset of the illness. The other developed unilateral uveitis after having been asymptomatic for two months. This persisted for several weeks and Marburg virus was cultured from the anterior chamber of the eye.
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PMID:Outbreake of Marburg virus disease in Johannesburg. 81 15

Coagulation studies were performed in 61 patients of acute infective hepatitis. 18 with clinical signs of liver failure had bleeding and all succumbed. The 47 patients without liver failure showed no haemorrhagic diathesis and all of them had uneventful recovery. Though coagulopathy was present in most of the patients, the severity and frequency of coagulation defects were more in those with signs of hepatic failure. Hypofibrinogenemia, elevated serum fibrinogen degradation products and accelerated euglobulin lysis were conspicuous in patients with hepatic failure. It appears that while diminished synthesis of coagulation factors is the main basis for coagulopathy in patients without hepatic failure, additional factors like local or disseminated intravascular coagulation and increased fibrinolysis also contribute significantly to the coagulopathy in cases of liver failure.
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PMID:Blood coagulation in patients with acute infections hepatitis in India. 81 35

The course of galactosamine hepatitis induced by 1.0 g/kg i.p. injected galactosamine (Ga1N) was investigated a sequential study in normal rats, in colectomized rats, and in rats being endotoxin resistent against both exogenous and endogenous endotoxin. Clinical symptoms of Ga1N-hepatitis such as pyrogen reaction, disseminated intravascular coagulation, arterial hypotension, and hypoglycaemia correlated significantly with the development of endotoxaemia, which was detected by means of the limulus gelation test (L.G.T.) Ga1N refractoriness was found after colectomy, a situation, in which gram negative bacterias and their endotoxins were eliminated. Ga1N refractoriness was also observed in case of endotoxin resistence. It is concluded that endotoxins contribute significantly to the pathogenesis of "Ga1N-hepatitis" and its clinical symptoms.
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PMID:Significance of endotoxaemia in experimental "galactosamine-hepatitis" in the rat. 85 60

The turnover of 125I-labelled fibrinogen and 131I-labelled albumin was studied in the course of galactosamine-induced hepatitis in rabbits. In addition to galactosamine, some animals were treated with epsilon-aminocaproic acid (EACA) to inhibit the activation of the fibrinolytic system. The infusion of galactosamine and EACA caused generation of fibrin-rich microclots in the renal glomerular capillaries in seven out of 12 rabbits. Correspondingly, the incorporation of 125I-radioactivity into liver, spleen, and kidneys was pronounced in galactosamine- and EACA-treated rabbits compared with control animals treated with EACA. An acceleration of the 125I-fibrinogen elimination from the plasma was observed between eight and 12 hours after the start of the galactosamine infusion. The administration of heparin in addition to galactosamine and EACA prevented the occurrence of intravascular coagulation, but shortened the survival times of the animals because of bleeding into visceral organs. The elimination of 131I-albumin in plasma as well as the distribution of 131I-radioactivity in organs were similar in all the rabbits independent of the treatment with galactosamine, EACA, or heparin. The experiments indicate that, in addition to diminished synthesis of coagulation factors, disseminated intravascular coagulation is involved in galactosamine-induced hepatitis and contributes to the haemostatic disorder.
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PMID:Behaviour of 125I-fibrinogen and 131I-albumin in experimental galactosamine-induced hepatitis. 87 36

Coagulation studies were made on 22 pregnant women with acute infective hepatitis and on 15 normal control pregnant women in third trimester. Fourteen hapatitis patients had clinical evidence of liver failure and all of them had a haemorrhagic diathesis; none of the patients without liver failure showed clinical evidence of haemostatic defects. Coagulopathy was present in most patients, its severity being greater in those with hepatic failure. Significant alterations were observed in bleeding time, whole blood clotting time, prothrombin time, thrombin time, plasma fibrinogen and serum levels of fibrinogen degradation products. The last three disturbances were most frequent in patients with liver failure. Increased fibrinolysis and disseminated intravascular coagulation also appeared to play a contributory role, particularly in patients with hepatic failure.
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PMID:Blood coagulations studies in pregnant patients with infective hepatitis. 88 47


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