Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A new viral disease (Maridi haemorrhagic fever) occurred in the South Sudan in 1976. It was obviously identical with an epidemic which occurred at the same time in Zaire. The virus is morpologically closely similar to the Marburg virus. During the Maridi epemic 124 of 238 patients died (52%). Characteristic symptoms were fever and headache (100%), diarrhoea (83%), retrosternal pain (82%), vomiting (68%), haemorrhages (62%), morbilliform or vesicular rash (52%). At post-mortem there were changes in liver, kidney, myocardium and lungs, similar to those in the Marburg virus disease, as were those observed in bone marrow and peripheral blood. Despite these analagous findings, the clinical course and results of immunofluorescence indicate that it is a new disease. The epidemic ended after suitable isolation measures had been taken. There was no specific treatment but in some cases convalescent plasma and interferon were tried. The disease is transmitted among humans by direct contact or by contact with blood or excreta of patients. No animal reservoir has been found. It is possible for this disease to be imported also into countries with a modorate climate.
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PMID:[Maridi haemorrhgic fever: a new viral disease (author's transl)]. 2 83

The symptoms of 100 hospitalised cases of rotavirus infantile gastroenteritis are described. Most patients presented with high fever between the 2nd and 5th day, having started with diarrhoea or vomiting or both. 42% of the infants had upper respiratory tract symptoms. Severe electrolyte disturbance did not occur, although there was a suggestion of a correlation between the higher blood ureas and the number of rotavirus particles in the stools. The mean duration of illness of uncomplicated cases was 13.4 days. Infants were more severely affected when enteropathic coliforms were also present, the total duration of illness being extended to 23 days. It is suggested that rotavirus or similar virus infection may be an essential precursor in the majority of coliform gastroenteritis.
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PMID:The clinical features of infantile gastroenteritis due to rotavirus. 18 18

A large outbreak of haemorrhagic fever (subsequently named Ebola haemorrhagic fever) occurred in southern Sudan between June and November 1976. There was a total of 284 cases; 67 in the source town of Nzara, 213 in Maridi, 3 in Tembura, and 1 in Juba. The outbreak in Nzara appears to have originated in the workers of a cotton factory. The disease in Maridi was amplified by transmission in a large, active hospital. Transmission of the disease required close contact with an acute case and was usually associated with the act of nursing a patient. The incubation period was between 7 and 14 days. Although the link was not well established, it appears that Nzara could have been the source of infection for a similar outbreak in the Bumba Zone of Zaire.In this outbreak Ebola haemorrhagic fever was a unique clinical disease with a high mortality rate (53% overall) and a prolonged recovery period in those who survived. Beginning with an influenza-like syndrome, including fever, headache, and joint and muscle pains, the disease soon caused diarrhoea (81%), vomiting (59%), chest pain (83%), pain and dryness of the throat (63%), and rash (52%). Haemorrhagic manifestations were common (71%), being present in half of the recovered cases and in almost all the fatal cases.Two post mortems were carried out on patients in November 1976. The histopathological findings resembled those of an acute viral infection and although the features were characteristic they were not exclusively diagnostic. They closely resembled the features described in Marburg virus infection, with focal eosinophilic necrosis in the liver and destruction of lymphocytes and their replacement by plasma cells. One case had evidence of renal tubular necrosis.Two strains of Ebola virus were isolated from acute phase sera collected from acutely ill patients in Maridi hospital during the investigation in November 1976. Antibodies to Ebola virus were detected by immunofluorescence in 42 of 48 patients in Maridi who had been diagnosed clinically, but in only 6 of 31 patients in Nzara. The possibility of the indirect immunofluorescent test not being sufficiently sensitive is discussed.Of Maridi case contacts, in hospital and in the local community, 19% had antibodies. Very few of them gave any history of illness, indicating that Ebola virus can cause mild or even subclinical infections. Of the cloth room workers in the Nzara cotton factory, 37% appeared to have been infected, suggesting that the factory may have been the prime source of infection.
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PMID:Ebola haemorrhagic fever in Sudan, 1976. Report of a WHO/International Study Team. 30 55

Reye's syndrome is difined as fatty degeneration of the viscera with encephalopathy. The signs are change in consciousness after recovery of a viral illness, vomiting, high fever, and progresseve deterioration of the level of consciousness. Signs of brain stem involvement quickly follow. The clinical findings are: mild elevations of serum transaminases (SGOT and SGPT), normal to slightly elevated bilirubin, abnormal blood-clotting functions, normal to low blood glucose, high blood ammonia, and normal cerebrospinal fluid which may be under increased pressure. Death is due to increased intracranial pressure. Therapy is used to stabilize these signs. It includes: infusion of hypertonic glucose followed by insulin, peritoneal dialysis, and exchange transfusion. Intracranial pressure was monitored continually to determine when therapy should be administered.
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PMID:Intracranial pressure monitoring in Reye's syndrome. 127 55

A case of sudden death associated with fatty liver and encephalopathy is described in a 4-year old white boy with medium-chain acyl-coenzyme A dehydrogenase (MCAD) deficiency. The death was caused by hypoglycemia triggered by fasting and vomiting associated with a minor viral infection. The differential diagnosis of the hepatoencephalopathy is discussed in relation to other conditions, especially Reye's syndrome. The forensic pathologist should be familiar with MCAD and other deficiencies of beta-oxidation of fatty acids as a cause of sudden unexpected death in children in order to advise parents in genetic counseling to prevent disability or death of other affected, but still asymptomatic siblings.
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PMID:Fatty liver, encephalopathy, and sudden unexpected death in early childhood due to medium-chain acyl-coenzyme A dehydrogenase deficiency. 128 65

The study deals with the influence of persistent hepatitis B virus infection on immediate and end results of chemotherapy for breast cancer with bony metastases. The infection was shown to be associated with lower complete and partial remission rates, lower 3-year survival rate and higher rate of combination chemotherapy toxic effects such as nausea, vomiting and increased activity of aminotransferases.
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PMID:[The effect of an infection due to the hepatitis B virus on the treatment results in breast cancer patients with bone metastases]. 130 Jul 39

Reye's syndrome, a condition characterized pathologically by cerebral edema and fatty change of the liver, has been described extensively in the medical literature as a disease manifested clinically by encephalopathy and coma. This is a report of five cases of Reye's syndrome occurring as sudden, unexpected deaths outside of the hospital. In each of these cases, there is a vague history of a previous viral illness. A history of aspirin intake is inconstant. Each child either had no significant past illnesses or there was a history of repeated upper respiratory infections. The classic progression of signs and symptoms usually described for Reye's syndrome, where vomiting usually precedes encephalopathy and coma, was not present in any of the cases. Results of autopsies showed the characteristic findings for Reye's syndrome, and additional tests showed no other explanation for the deaths. This manifestation of the disease is seldom described in medical literature, but it may be encountered occasionally by the medical examiner.
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PMID:Reye's syndrome. A diagnosis occasionally first made at medicolegal autopsy. 849 79

By analysing two patients initially diagnosed as Reye syndrome evidence is given that in some patients considered as having Reye syndrome, the syndrome is an escalation of symptoms due to viral disease and to unrecognized drug-induced encephalopathy, mainly by anti-emetics. A detailed drug history, considering all medication--not exclusively aspirin--taken during the full course of the illness is essential to differentiate between Reye syndrome and drug-induced symptoms. In addition, a critical analysis is presented of the four main case-control surveys that have lead to the proposal that salicylates are primary causative agents of Reye syndrome. In these surveys, medications given during the prodromal illness were adequately recorded, but other drugs given after the onset of vomiting have been overlooked or deliberately excluded. New epidemiological studies are needed, recording all drugs given to the patients throughout the full course of their illness until the moment of admission, in order to elucidate the mystery of Reye syndrome.
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PMID:Reye syndrome or side-effects of anti-emetics? 153 63

An outbreak of severe haemorrhagic illness began in the municipality of Guanarito, Portuguesa State, Venezuela, in September, 1989. Subsequent detailed study of 15 cases confirmed the presence of a new viral disease, designated Venezuelan haemorrhagic fever. Characteristic features are fever, toxicity, headache, arthralgia, diarrhoea, conjunctivitis, pharyngitis, leucopenia, thrombocytopenia, and haemorrhagic manifestations. Other features include facial oedema, cervical lymphadenopathy, nausea/vomiting, cough, chest or abdominal pain, and convulsions. The patients ranged in age from 6 to 54 years; all were residents of rural areas in central Venezuela, and 9 died. Infection with Guanarito virus, a newly recognised arenavirus, was shown by direct culture or by serological confirmation in all cases. Epidemiological studies suggest that the disease is endemic in some rural areas of central Venezuela and that it is rodent-borne. Venezuelan haemorrhagic fever has many similarities to Lassa fever and to the arenavirus haemorrhagic fevers that occur in Argentina and Bolivia.
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PMID:Venezuelan haemorrhagic fever. 168 54

Rhesus monkeys inoculated intravenously with Rift Valley fever (RVF) virus presented clinical disease syndromes similar to human cases of RVF. All 17 infected monkeys had high-titered viremias but disease ranged from clinically inapparent to death. Three (18%) RVF virus-infected monkeys developed signs of hemorrhagic fever characterized by epistaxis, petechial to purpuric cutaneous lesions, anorexia, and vomiting prior to death. The 14 remaining monkeys survived RVF viral infection but, 7 showed clinical signs of illness characterized by diminished food intake, cutaneous petechiae, and occasional vomiting. The other 7 monkeys showed no evidence of clinical disease. All monkeys had detectable serum interferon 24-30 h after infection, but 4 of 7 monkeys that did not develop clinical illness had serum interferon titers within 12 h after infection. In lethally infected macaques, indices of hepatic function and blood coagulation were abnormal within 2 days, implicating early pathogenetic events as critical determinants of survival. Serum transferase values were elevated in proportion to severity of clinical disease and outcome of infection. Both myocardial damage and laboratory evidence consistent with disseminated intravascular coagulation were present in fatal infections. All surviving monkeys developed neutralizing antibodies to RVF virus 4-7 days after infection, and this coincided with termination of viremia. Two fatally infected monkeys were viremic until death on days 6 and 8, and the third cleared viremia on day 5 and developed antibody on day 6 but died on day 15. There was a significant correlation between a delayed interferon response and mortality, suggesting that the early appearance of interferon was influential in limiting the severity of disease.
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PMID:Pathogenesis of Rift Valley fever in rhesus monkeys: role of interferon response. 169 May 34


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