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)

Due to its advantageous properties the volatile anesthetic enflurane is used as the main agent for all routine open heart cases in our department. The technique consists of the induction of the heavely premedicated patient with fentanyl (10 micrograms/kg i.v.) followed by pancuroniumbromide (100 micrograms/kg i.v.). For the maintenance of anesthesia, i.e. before, during, and after cardio-pulmonary bypass, enflurane together with nitrous-oxide (up to 66%) is used, in a concentration between 1.0-2.0 vol%. Compared to other volatile anesthetics we foster a technique with enflurane because it has following advantages: 1. Less negative inotropic effect on the myocardium. 2. Less tendency for ventricular arrhythmia. 3. Fast onset of action. 4. Fast recovery from the anesthetic state. 5. Spontaneous post-operative respiration. 6. Lesser incidence of toxic hepatitis (Acta anaesth. belg., 1982, 33, 141-155).
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PMID:Enflurane in cardiac surgery. 714 71

Two cases are reported of combined renal and hepatic failure following exposure to halothane anesthesia. Both patients presented with postoperative fever and rapidly deteriorating liver and kidney function. Both required peritoneal dialysis. Both patients died, and in both cases this was the second exposure to halothane. The pathologic features of the 2 cases were similar in that the liver changes were typical of those seen with halothane hepatitis and the renal lesion was similar to that of methoxyflurane nephritis. This is, to our knowledge, the third report of renal failure occurring after halothane anesthesia. Possible mechanisms regarding its toxicity are discussed.
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PMID:Halothane-induced nephrotoxicity. 722 20

After major surgery some patients, especially those with an infectiouss process or sepsis, develop jaundice which has been called reactive hepatitis, toxic hepatitis, septic hepatitis or benign postoperative cholestasis; these terms do not have a very precise connotation. Eighty patients with postoperative sepsis and jaundice where studied, excluding those with liver or biliary tract disease, hepato-toxic drugs or repeated halogenated anesthetics. All of them had complete laboratory tests, cultures and percutaneous liver biopsy when it was feasible. Thirty five patients were submitted to percutaneous liver biopsy and they are the material for this paper. There was no correlation with the type and duration of the operation, postoperative complications, shock or kind of anesthesia. The main laboratory changes were leukocytosis, neutrophilia, elevation of the bilirubins mainly the direct type and increase of the alkaline phosphatase; transaminases were within normal limits. Cultures were positive in 76% of the cases predominating E. coli, Pseudomonas a. and Proteus, anaerobics were present in 22.8% of the cases. The liver biopsy showed lymphoctic infiltration, hyperplasia of the Kupffer cells, hepatic regeneration and turbid tumefaction; pericholangitis, focal necrosis, retention of pigment and steatosis were less frequent. We consider that the best denomination of these complications is benign postoperative cholestasis.
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PMID:[Postoperative reactive hepatitis in the septic patient]. 728 Apr 56

HLA A and B locus antigens were determined in 17 patients who had recovered from unexplained hepatitis following halothane anaesthesia. The greatest deviations from expected frequencies were observed with A1, A11 and BW22, but these differences were not statistically significant when the P values were corrected for the number of antigens tested. Although a larger series might show such deviations to be significantly different, HLA typing is of no predictive value in determining those at risk to hepatitis following repeated halothane exposure.
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PMID:HLA A and B locus antigens in patients with unexplained hepatitis following halothane anaesthesia. 733 Aug 46

A patient developed fever and acute hepatitis shortly after enflurane anaesthesia. Other causes of postoperative hepatitis were excluded. Cross-sensitization with halothane may have occurred, and the enflurane hepatitis may have been aggravated by halothane hepatitis.
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PMID:Acute hepatitis following enflurane anaesthesia. 742 22

Lymphocytes from three of four patients with severe unexplained hepatitis following halothane anaesthesia were cytotoxic in vitro for liver cells isolated from rabbits following halothane anaesthesia, and less so for control hepatocytes. While the latter reaction could be blocked by addition of a purified liver membrane lipoprotein (LSP), this had no effect on the cytotoxicity to "halothane" hepatocytes. These results provide evidence that patients with severe halothane-associated hepatitis are sensitised to a liver cell antigen distinct from LSP, which arises as a result of halothane anaesthesia.
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PMID:Lymphocyte cytotoxicity to halothane altered hepatocytes in patients with severe hepatic necrosis following halothane anaesthesia. 746 74

A 36-year-old woman was scheduled for Cesarean section under spinal anesthesia. She was a carrier of hepatitis-B-virus and diabetic. She was complaining of low back pain. Spinal anesthesia was performed in the left lateral decubitus position. Because lumbar puncture in the midline was difficult, left paramedian approach was tried. Then she began to complain of right leg pain. Another attempt was made at other site, but her pain was not relieved. After confirming drop of blood-tinged cerebrospinal fluid, 0.3% dibucaine 2.0 ml was injected. Sensory anesthesia was assessed by pin-prick, but anesthesia was not effective. Then epidural catheter was inserted at Th12-L1 using median approach. She received 1.0% lidocaine 15 ml. However, sensory anesthesia was insufficient (Th4-Th12). Therefore O2-N2O was administered in addition to regional anesthesia. After the delivery, she still complained of low back pain. Later examination revealed metastatic bone tumor of L2 from hepatoma. This case suggests that in a patient with such incomplete spinal or epidural anesthesia and neurological finding, vertebral metastatic tumor should be ruled out.
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PMID:[A case of vertebral metastasis revealed by incomplete spinal analgesia for cesarean section]. 793 77

This review focuses on cellular events that modulate hepatotoxicity subsequent to initial liver insult. Cellular events that determine the nature and extent of hepatotoxic injury and the ultimate outcome of that injury are also discussed. The roles of cell types other than hepatocytes, hepatocyte organelle-specific processes, and regeneration in progression or recovery from liver injury are emphasized. Leukocyte activities are key events in two distinct hepatotoxicities. Neutrophil-mediated, periportal inflammation appears to play a primary role in progression of alpha-naphthylisothiocyanate-induced cholangiolitic hepatitis. However, a humorally mediated autoimmune response to protein adducts that occurs after anesthesia is critical in onset of halothane-induced hepatitis. New insights into specific events at the hepatocyte level are also emerging. Although reducing gap junctional communication between hepatocytes can protect against progression of liver injury, down-regulation of the subunit proteins (connexins) can isolate neoplastic cells from growth regulation. Acidic intracellular pH characteristic of hypoxia is protective against both hypoxic and toxicant-induced cell injury. In oxidative injury, a pH-mediated mitochondrial permeability transition causes mitochondrial uncoupling and ATP loss and leads to cell death. The ultimate outcome of hepatotoxic injury depends on the extent of tissue repair. Stimulation of tissue repair after a sublethal dose of CCl4 appears to be the central mechanism in protection against death from a subsequent large dose. Taken together, these examples illustrate the importance of events subsequent to initial liver injury as determinants of extent of liver damage.
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PMID:Novel mechanisms in chemically induced hepatotoxicity. 800 41

It has been shown that the circulating antibodies, which bind to rat hepatic microsomal proteins obtained after in vivo exposure to halothane, are detectable by immunoblotting in patients with "halothane hepatitis (HH)," and that rabbit immunized anti-sera against trifluoroacetylated rabbit serum albumin (TFA-RSA) recognizes rat microsomal distorted polypeptides in almost the same way as do sera from patients with HH. In this paper, we report first the development of a novel method of synthesizing TFA-RSA using p-nitrophenyl TFA, and second the results of tests for circulating anti-TFA antibodies in the serum of 86 patients who had received halothane anaesthesia and developed no (67 patients) or mild (19 patients, the maximum activity of serum alanine aminotransaminase 519 IU.L-1) liver damage. Serum was selected from stored sera of post-transfusion patients. The new method of synthesizing TFA-RSA was convenient and was able to be done at neutral pH. Rabbit sera obtained after immunization with the newly synthesized TFA-RSA recognized the same polypeptides (109 kDa, 92 kDa, 80 kDa, 76 kDa, 64 kDa and 59 kDa) as the established anti-sera against TFA-RSA, and these reactions were inhibited in the presence of TFA-lysine. Circulating antibodies were not detected in our patients who had developed no or mild liver damage. The present finding supports the hypothesis that the appearance of circulating antibodies against microsomal distorted proteins are specific to patients with HH. Furthermore, we have shown here that the halothane-induced mild increase in ALT activity is not associated with the appearance of those circulating antibodies, supporting the pathophysiological difference between HH and halothane-induced mild hepatic damage.
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PMID:Absence of anti-trifluoroacetate antibody after halothane anaesthesia in patients exhibiting no or mild liver damage. 805 7

Seventy-four responses were received from a questionnaire which had been mailed to 91 bone marrow transplantation institutes throughout Japan to assess the activity of bone marrow transplantation and complications in bone marrow donors. A total of 2329 bone marrow harvests, performed from 1688 adult donors and 641 child donors for allogeneic or syngeneic transplantation up to August 1992, were available for study. Analyses of the responses showed slight diversity regarding the marrow harvesting preparation and methods of the different bone marrow programs. The resulting perioperative complications were principally caused by anesthesia: 73 episodes of hypotension including one death 18 months later, seven of arrhythmia, one of respiratory arrest, three of mental confusion, one of asthma, one of malignant hyperthermia, one tooth injury and one broken aspiration needle. The postoperative complications were chiefly caused by marrow aspiration per se: 731 episodes of transient fever, 26 of long-lasting pain or discomfort, 10 episodes of liver dysfunction including two cases of non-A, non-B hepatitis, four cases of infection, one episode of hypotension, one of dysuria and one case of keloid formation. The study further revealed that the frequency of complications was lower in child donors than in adult donors.
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PMID:[Complications of marrow harvesting for transplantation]. 813 99


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