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)

There has been significant decrease in maternal morbidity and mortality of sickle cell disease patients during pregnancy due to better understanding of the pathophysiology of the disease and physiologic changes during pregnancy. Prophylactic blood transfusion does not appear to reduce complications in patients with sickle cell anemia. Patients with sickle hemoglobin C disease and with S beta thalassemia+ have fewer complications but still need close monitoring. Blood transfusion therapy should be made available for medical and obstetrical complications to include increasing hypoxemia, progressive anemia, acute chest syndrome, twin pregnancy, splenic sequestration syndrome, preeclampsia, septicemia, or prior to general anesthesia and surgery. Blood transfusion therapy is associated with hepatitis, allergic reaction, alloimmunization, AIDS, and iron overload states. These aspects should be considered prior to using blood transfusion therapy. Excellent prenatal monitoring and aggressive intervention should be instituted when problems arise for the successful management of the pregnant patient with sickle cell disease. Prenatal diagnosis and cord blood screening should be made available for the infant. Appropriate pediatric referral and prophylactic penicillin is recommended for the infant with sickle cell disease.
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PMID:Management of sickle cell anemia and pregnancy. 181 45

Inhalation anesthesia first with halothane followed by enflurane relieved a patient with status asthmaticus who was refractory to conventional therapy including mechanical ventilation. After 13 days of anesthesia while on mechanical ventilation and employing nondepolarizing muscle relaxants, significant neuromuscular impairment, manifested by tetraplegia and sensory disturbance, developed. Anesthesia was discontinued on day 14, and the patient was weaned from mechanical ventilation on day 16. Over the next two months, the neuromuscular impairment markedly improved. Halothane was associated with cardiac arrhythmias and hepatitis necessitating replacement by enflurane. Enflurane appeared to be as effective a treatment for refractory asthma as halothane. The most probable cause of the neuromuscular impairment in our patient was the long-term use of inhalation anesthetics or nondepolarizing muscle relaxants.
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PMID:Transient neuromuscular impairment resulting from prolonged inhalation of halothane and enflurane. 214 34

Despite early controversy, it is now recognised that halothane anaesthesia may be followed by abnormalities of liver function. The resulting hepatitis may take 1 of 2 forms: in type I, there is a minor degree of disturbance of liver function shown by increased serum transaminases or glutathione-S-transferase in up to 25 to 30% of patients; subsequent re-exposure to halothane is not necessarily associated with evidence of liver damage. In contrast, type II hepatitis is often associated with massive liver cell necrosis, frequently leading to fulminant hepatic failure. This type of liver damage has clinical, serological and immunological features compatible with an immune-mediated idiosyncratic reaction. The incidence is low (between 1 in 3500 and 1 in 35,000 anaesthetic procedures), but the mechanism of halothane hepatitis remains uncertain: there have been extensive animal models showing that halothane has a direct hepatotoxic potential, although the relevance of this to the human patient is not yet clear. Prevention of halothane hepatitis may be difficult, and the only clear way of reducing the incidence is to avoid re-exposure to halothane in those patients who have had a previous adverse reaction to the drug, demonstrated either by unexplained pyrexia or by jaundice. Halothane should also be avoided in those patients where there is a family history of sensitisation to the drug. In such cases, halothane-free equipment should be used, and exposure to other volatile non-halogenated anaesthetics should be avoided.
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PMID:Halothane and hepatitis. Incidence, predisposing factors and exposure guidelines. 217 33

Halothane hepatitis is now a well-recognized distinct entity in adults, but there prevails an often-taught "axiom" that halothane hepatitis "does not occur" in children. We describe 2 children who developed cholestatic hepatitis following halothane anesthesia. The first patient had no antecedent liver disease, and presented with anorexia, abdominal pain and delayed onset of jaundice after multiple halothane exposures. Halothane-specific antibodies were positive, and liver tests resolved completely. The second patient had antecedent liver disease and presented with delayed onset of unexplained high fevers for 10 days following a single halothane exposure. Gradually increasing cholestasis ensued in the absence of other causes of liver disease. Halothane antibodies were negative. These cases illustrate different clinical presentations of halothane hepatitis, such as delayed onset of jaundice or fever following halothane exposure. The difficulties in making a definitive diagnosis and the need to exclude other causes of liver disease are detailed. Risk factors and other presentations are discussed. While halothane hepatitis appears to be an uncommon entity in children, it does occur, and may present with manifestations less than fulminant hepatic failure. A high index of suspicion and a detailed history of the time sequence of events are necessary as the diagnosis is primarily clinical. Halothane-specific antibodies are helpful if positive. In any child developing unexplained jaundice or high fevers following halothane anesthesia, further exposures should be avoided and halothane-specific antibodies obtained.
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PMID:Halothane hepatitis in children. 178 63

In this article, we reported the analysis of two severe diseases complicating pregnancy: 1,918 cases of heart disease in last 36 years and 22 cases of severe hepatitis in last 16 years. The conclusion was that on active therapy and close cooperation with cardiologist, pregnancy complicated with heart disease of grade III-IV cardiac function can be taken as an indication of Cesarean section. This operation performed at a proper time is good for the mother and also the baby. The traditional idea that Cesarean section could only be done for an obstetrical reason is not quite adequate. For primiparas with severe hepatitis, a supportive therapy with fresh blood transfusion, albumin and Cesarean section under local anesthesia might be the method of choice, its mortality rate being much lower than a vaginal delivery.
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PMID:[Cesarean section in pregnancy complicated by severe hepatitis and heart disease]. 232 68

Halothane (1% v/v inspired) was administered for 60 min to six children of mean age 74 months (range 14-119 months). Uptake of halothane was measured from the difference in the concentration in inspired and expired gas and varied from 176 to 310 mg kg-1, depending on minute ventilation. After administration of halothane ceased, its elimination in expired gas was measured in four patients until the conclusion of anaesthesia; 32-37% of the absorbed halothane was expired 90 min after halothane administration ceased. Urinary excretion of trifluoroacetic acid, fluoride and bromide was measured for up to 1 week. Of the absorbed halothane, 11.4% (range 6.3-18.2%) was excreted in urine as trifluoroacetic acid and 0.37% (range 0.10-0.64%) as inorganic fluoride. The urinary half-life of trifluoracetic acid was 41.8 h (range 10.4-59.1 h). The quantitative and qualitative metabolism of halothane via the reductive and oxidative pathways in children are comparable to values found in adults. No differences in the metabolism of halothane by children were found which would explain the different incidence of halothane-associated hepatitis compared with adults.
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PMID:Halothane metabolism in children. 233 22

Patients with liver damage following halothane anaesthesia (halothane hepatitis) have circulating antibodies reacting with plasma membrane determinants present on hepatocytes isolated from rabbits previously exposed to halothane. In an attempt to develop an animal model of halothane hepatitis, rabbits were immunised with hepatocytes isolated from litter mates previously exposed to halothane; this resulted in the generation of antibodies to both normal and halothane related liver cell determinants detected by both immunofluorescence and indirect cytotoxicity. Exposure of these immunised rabbits to halothane resulted in the disappearance of the halothane-related antibody, presumably due to its reaction with the liver-cell membrane halothane-related antigen; this, however, could not be proved since immunisation with halothane hepatocytes induced the presence of antibodies on the recipient hepatocytes. Although both human and rabbit lymphocytes were directly cytotoxic in vitro to these antibody coated hepatocytes, no evidence of liver damage could be detected. Thus, if immune mechanisms are involved in the pathogenesis of halothane hepatitis, other factors, probably related to idiosyncratic host immune responses, must be implicated.
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PMID:Halothane hepatitis: attempt to develop an animal model. 243 40

Pharmacokinetic analysis of lidocaine (Lid) and its metabolites, monoethylglycinexylidide (MEGX) and glycinexylidide (GX), was performed in a dog bearing carbon tetrachloride (CCl4, 0.75 ml/kg ip)-induced acute hepatitis. Following pentobarbital sodium (25 mg/kg iv) anesthesia, lidocaine hydrochloride (2.5 mg/kg iv) was given and arterial blood was drawn 2, 5, 10, 15, 30, 45, 60, 90, and 120 min after administration. Lid and its metabolites in plasma were extracted with chloroform-hexane-isopropanol (60 : 30 : 10), and organic layer was dried down at 50 degrees C under N2. The residue was dissolved in 50mM phosphoric acid and subjected to HPLC analysis. 4-compartment model was introduced to analyze pharmacokinetic parameters, and which gave the most reasonable fit with actual results. Control experiment was carried out using identical dog with acute hepatitis. The following results were given: 1) Elimination of Lid was slightly depressed, but T1/2 was not altered. Plasma level of Lid was kept higher. 2) As for MEGX, the formation was depressed, and upto 23 min after Lid administration, MEGX concentration in the dog with acute hepatitis was lower than that of control, but after 23 min it was vice versa. 3) As for GX, the formation was depressed, but the elimination was not affected. In the dog with CCl4-induced hepatitis, metabolism of Lid was suppressed, and which resulted in maintaining a relatively higher levels of Lid and MEGX concentration in plasma. These results suggested that care should be taken to avoid acute poisoning with Lid especially in patients with acute hepatitis.
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PMID:[Pharmacokinetics of lidocaine and its metabolites in dog. Comparison between normal and CCl4-induced hepatic lesion]. 248 93

Twenty patients undergoing various surgical procedures were anaesthetised using hypotensive anaesthesia using labetalol and halothane. The technique is safe, predictable and cheap. This technique also offers the advantage of usage of less blood, thus minimising the complications of transfusion induced diseases like hepatitis and AIDS.
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PMID:Experience with hypotensive anaesthesia in a peripheral general hospital. 252 36

Helothane hepatitis is a rare but sometimes fatal complication of halothane anaesthesia. Examination of case reports has pointed to a number of risk factors. Studies in animals and humans in the laboratory have provided evidence of a complex multifactorial basis for halothane hepatotoxicity, with the following factors playing a part: genetic predisposition; metabolism of halothane; repeated halothane anaesthetics; female sex; age of patient; intrahepatic hypoxia; and enzyme induction. Immunologic changes can be detected in a high percentage of cases of halothane hepatitis; however, studies establishing a cause-effect relationship are not available to determine if these changes cause, or result from, hepatic damage.
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PMID:Risk factors for halothane hepatitis. 264 40


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