Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In-vitro sensitisation (inhibiton or stimulation of leucocyte migration) in response to a liver homogenate obtained from rabbits pretreated with halothane was found in eight of twelve patients with halothane-associated hepatitis. Sensitisation was not observed when the homogenates were obtained from animals pretreated with ether. Furthermore, leucocyte migration in response to "halothane homogenate" was normal in eleven patients who had shown no abnormality in liver function after halothane anaesthesia and in thirty patients with other liver diseases. These studies provide direct evidence that sensitisation to halothane-altered liver-cell components is present in those occasional patients in whom severe liver damage develops after halothane anaesthesia.
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PMID:Sensitisation to halothane-altered liver components in severe hepatic necrosis after halothane anaesthesia. 8 59

A patient developed pyrexia and jaundice following repeated anaesthesia. The evidence suggests that thiopentone was the causative agent. This incident emphasizes the need for caution in associating jaundice and hepatitis with halothane in patients who have received thiopentone and halothane.
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PMID:Hepatitis following thiopentone. A case report. 49 78

Hepatitis from halothane is usually diagnosed by excluding other possible causes. Whether preexisting hepatic damage, which can occur in certain autoimmune disorders, contraindicates the use of halothane has yet to be proven. The case of a 14-year-old boy with early-onset juvenile rheumatoid arthritis who developed fatal hepatic necrosis 13 days after halothane anesthesia is presented.
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PMID:Fatal hepatic necrosis after halothane anesthesia in a boy with juvenile rheumatoid arthritis: a case report. 56 Jan 52

A survey of postoperative jaundice throughout the United Kingdom allowed the detailed analysis of 76 patients with unexplained hepatitis following halothane anesthesia ("halothane hepatitis"). In 16 patients liver biopsy specimens were examined by light and/or electron microscopy to determine whether the liver morphology could aid the differentiation between "halothane" and "acute viral" hepatitis. The mitochondrial changes often claimed to be characteristic of holothane hepatitis were unremarkable in our patients. Since lipid vacuolation and a predominantly centrilobular distribution of necrosis are not classically described in fatal viral hepatitis, the presence of these features in some of our fatal cases was of some diagnostic interest. In general, however, the results of light and electron microscopy in patients with unexplained postoperative hepatitis is considered to have little differential diagnositc value.
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PMID:A morphologic study of unexplained hepatitis following halothane anesthesia. 64 15

For over a decade there has been concern about hepatitis related to halothane anesthesia. No dose relationship or other direct cause has ever been established, and jaundice has been found to occur after other anesthetics for surgical operations. Enflurane is a newer halogenated compound with a remarkable record of safety, yet a few cases of hepatitis are reported to be associated with its administration. We have compared effects on the liver of the two anesthetics by testing hepatic serum enzymes and sulfobromophthalein in 12 patients who received halothane and 12 who received enflurane. No significant differences between the two groups were found. Both had similar but minimal elevations of the hepatic serum enzymes and retention of sulfobromophthalein. More than half the patients had enzyme increases over normal levels but reasons for this were not obvious. Since hepatic change may take place in many postoperative patients, it is not surprising to have an occasional one develop hepatitis. The exact cause is unknown and therefore it is impossible to predict the patient who will develop the disease, regardless of the anesthetic.
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PMID:Changes in liver enzyme values after halothane and enflurane for surgical anesthesia. 66 20

Causes of maternal deaths at the Lagos University Hospital were reviewed in order to highlight the problems associated with the practice of obstetrics in the hospital. Focus was on maternal deaths that occurred during the January 1, 1970-December 1970 period. There were a total of 11,041 births and 38 maternal deaths during this 1 year. The case notes of maternal deaths were studied; causes of death were extracted from them. The maternal mortality rate was 3.4/1000 total births, excluding abortions. Most of the hospitals booked cases are drawn from the mainland of Lagos and staff of both the Teaching Hospital and the Lagos University. Other high risk cases are referred from general practitioners. The unbooked cases are either referred from the neighboring private maternity homes or brought by relatives from native doctors and midwives because of impending fetal or maternal risk. 65.2% of the maternal deaths occurred in the unbooked cases in the 15-25 year age group. 17 deaths were due to eclampsia; 1 was a booked patient and 16 were unbooked patients. 10 booked patients died as a result of hemorrhage. Obstructed labor was the cause of death in 4 booked and 2 unbooked cases. 2 booked and 1 unbooked patient died following anesthesia, and 1 unbooked patient died because of infective hepatitis. Death occurred in 1 unbooked case suspected of having a ruptured uterus on admission. In the majority of cases the deaths were avoidable. Maternal death can be avoided if the general public is educated regarding good antenatal care and delivery in hospitals.
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PMID:Maternal mortality in the Lagos University Teaching Hospital. A 5-year survey--1970-1974. 72 69

The authors report 6 cases of fulminant hepatitis in patients treated with isoniazid and rifampin. In 4 of these patients, the treatment had been started within 3 days after a general anesthesia. The course of the disease was remarkably similar in all 6 patients: (1) the time interval from the beginning of the isoniazid-rifampin administration to the onset of jaundice was 6 to 10 days; (2) disorders of consciousness appeared less than 3 days after the onset of jaundice; (3) serum transaminases were 26 to 80 times the upper limit of normal; (4) the main liver lesion was centrilobular necrosis; (5) hypersensitivity manifestations were absent; (6) all 6 patients recovered. Fulminant hepatitis might be attributable to a hepatotoxic metabolite of isoniazid, the production of which would be attributable to a hepatotoxic metabolite of isoniazid, the production of which would be increased as a consequence of the enzyme-inducing effect of rifampin and, possibly, other drugs administered for general anesthesia.
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PMID:Isoniazid-rifampin fulminant hepatitis. A possible consequence of the enhancement of isoniazid hepatotoxicity by enzyme induction. 83 May 77

The value of ERCP in children is demonstrated on 3 cases. By using a usual duodenofiberscope (JF-B2), in 2 cases under general anesthesia and in one case after premedication with 1 ml Buscopan i.m., a similar technique is used as in adults. In congenital choledochal cyst only ERCP allowed the exact judgement of the distal part of the common bile duct and its relation to the pancreatic duct. Therefore, an exact preoperative diagnosis can be established. When duodenofiberscope will be more improved ERCP will also be possible in the newborn infant. Than the differential diagnosis of congenital biliary atresia, other congenital failures in infants causing jaundice and hepatitis in infant will be established endoscopically.
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PMID:Endoscopic retrograde cholangiopancreatography (ERCP) performed in children. 89 84

A case report is given on two patients receiving halothane anesthesia while beeing treated with isoniacid, ethambutol and rifampicin. Following halothane anesthesia, both patients developed a severe liver disease with encephalopathy grade III. We observed a moderate increase of bilirubin and SGOT and a more severe increase of serum ammonia. Histologically, both patients had alterations compatible with drug hepatitis. Within 14 days remission occurred spontaneously. The two case reports do not fit with typical isoniacid hepatitis or typical halothane hepatitis. The possibility of combined drug toxicity on liver during halothane and isocianid treatment is discussed.
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PMID:[Halothane and antituberculous drugs--a hepatotoxic combination? (author's transl)]. 90

142 patients with postoperative jaundice following anaesthesia with halothane were divided into two groups:-group A (76 cases) in which halothane appeared to be the sole responsible agent for jaundice, and- group B (66 cases) in which other causes were detected. The incidence of clinical signs considered to be specific for halothane-induced hepatitis (skin rash, arthralgia, bronchospasm, fever of unexplained origin, leukocytosis) was the same in both groups. Only a high eosinophil count was more common in group A. The author found a clear-cut relationship between the frequency of exposure and the onset of hepatitis as well as a shortening of the latent period with increasing numbers of exposures.
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PMID:[Relevance of clinical signs of hypersensitivity in cases of halothane hepatitis]. 98 17


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