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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute hepatic failure is a rare and potentially lethal complication of propylthiouracil (PTU) use for hyperthyroidism. We present a 20-year-old woman with Basedow-Graves' disease who developed PTU-induced fulminant hepatitis, which progressed to acute hepatic failure with grade III hepatic encephalopathy. Laboratory evaluation ruled out the most common causes of fulminant hepatitis. We treated her hyperthyroidism with amiodarone (average daily dose, 200 mg) for 3 weeks, achieving rapid and persistent euthyroidism, (triiodothyronine [T(3)] levels ranged between 64 and 109 ng/dL) without side effects. Amiodarone treatment did not abolish the thyroid radioactive iodine uptake (RAIU), allowing for subsequent treatment with radioactive iodine. The clinical course was favorable and the patient achieved full hepatic recovery 3 months after the hepatic failure was detected. After an extensive review of the literature, we believe that this is the first communication of the successful use of amiodarone to control hyperthyroidism in a patient with PTU-induced fulminant hepatitis.
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PMID:Successful treatment of hyperthyroidism with amiodarone in a patient with propylthiouracil-induced acute hepatic failure. 1558 85

The present study was designed to examine the effects of the donor of nitric oxide (NO), NaNO(2) and the inhibitor of NO synthase, N(omega)-nitro-L-arginine (L-NNA), on the development of dimethylnitrosamine (DMNA)-induced chronic hepatitis in rats. L-NNA decreased rat survival and enhanced the severity of hepatic encephalopathy in the DMNA-treated animals. The aggravation of the morphological signs of hepatitis, the activation of serum alanine aminotransferase and cytosolic superoxide dismutase activities and the increase in the liver malondialdehyde content were observed in this group. The treatment with NaNO(2) improved liver morphology, decreased serum marker enzyme activities, lowered the activities of alpha-D-mannosidase and N-acetyl-beta-D-glucosaminidase compared to the DMNA-treated group. The results of the morphological and biochemical studies suggest that L-NNA increased DMNA-induced liver damage, whereas NaNO(2) partially prevented the development of chronic hepatitis. It is proposed that the opposite effects of L-NNA and NaNO(2) are partially explained by a modulation of the free radical-dependent processes in the liver.
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PMID:Effect of the nitric oxide donor and the nitric oxide synthase inhibitor on the liver of rats with chronic hepatitis induced by dimethylnitrosamine. 1559 49

Acute liver failure (ALF) is a rare but often fatal disorder in childhood. Its aetiology includes infections, toxins, metabolic disorders, infiltrative diseases, autoimmune hepatitis, ischaemia, irradiation damage, but in a high proportion of cases it remains unknown. In contrast to adults, in children with ALF hepatic encephalopathy can be a late event, and may not develop at all, despite a lethal outcome, particularly in infants. Children with ALF should be managed in experienced centres with facilities for liver transplantation. Transplantation should be offered only if the underlying disease is treatable by liver replacement and if the prognosis of transplant is better than that of the underlying disease, as in many cases of ALF the liver has the potential to recover with supportive treatment, if the child is kept alive and stable long enough. Universally accepted criteria for listing for transplantation have not been defined as yet. In our centre, maximum INR, bilirubin level, and white cell count, together with age have proven to be reliable predictors of outcome. Future efforts in the management of ALF should concentrate on designing efficient supportive therapy and specific treatments to provide effective non-transplant therapeutic options.
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PMID:Approaches to acute liver failure in children. 1559 30

Hepatic encephalopathy is a complex neuropsychiatric syndrome, which derives from liver failure associated with severe liver damage such as fulminant hepatitis and liver cirrhosis, and vascular abnormalities associated with liver cirrhosis. Although the cause is explained by a multifactorial theory, the accumulation of ammonia has traditionally been considered to have an important role in the pathogenesis of hepatic encephalopathy. In addition, a number of other possible mechanisms have recently proposed, including production of false neurotransmitter, activation of central gamma-aminobutyric acid-benzodiazepine receptors by ligands of endogenous origin, altered cerebral metabolism. These pathogenetic mechanisms are not necessarily exclusive. The principle of treatment is to remove or correct aggravating factors and inhibit the transfer of toxic substances such as ammonia into the bloodstream by minimizing the interaction of intestinal bacteria and nitrogen substances. Most treatments of proved value are based on the ammonia hypothesis. Ammonia metabolism is regulated by numerous factors, among which zinc has long been indicated to be involved, and its clinical application has drawn attention recently.
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PMID:Ammonia metabolism and hepatic encephalopathy. 1560 43

The forensic pathologist is responsible for determining the cause, manner and approximate time of death and injury. After recording the detailed description of the external and internal appearances, a short summary should be offered of the major positive findings and their relationship to the cause of death. In many cases this will be obvious, however when the findings are less clear-cut, or are multiple, then the alternatives should be discussed detailing the possible sequence of events and interpreting the findings in concluding the cause of death. It is essential to causally connect the autopsy findings to the cause of death. We present a case report wherein a person who sustained avulsion injury to his left hand in an industrial accident, died due to, fulminant hepatitis, hepatic encephalopathy and acute renal failure, having undergone six operations under general anesthesia with halothane during his stay in the hospital.
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PMID:Fulminant hepatic failure following halothane anaesthesia. 1608 47

Tropical pyomyositis is a primary pyogenic infection of skeletal muscle, often caused by Staphylococcus aureus. The most common presentation of tropical pyomyositis is that of multiple acute abscesses with fever. Hepatitis is a rare manifestation of this disease. We report a case of tropical pyomyositis who presented with hepatic encephalopathy leading to initial diagnostic dilemma.
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PMID:An unusual presentation of tropical pyomyositis. 1611 67

Cirrhosis is the result of chronic inflammation and of the progressive increase of fibrosis. In France, hepatitis C infection is the second cause of cirrhosis after alcohol abuse. The other causes of cirrhosis are: hepatitis B infection, genetic haemochromatosis, autoimmune hepatitis, primary biliary cirrhosis, drug-induced cirrhosis, secondary biliary cirrhosis, Wilson's disease and al-antitrypsin deficiency. Etiological treatment is based upon: abstinence in case of alcoholic cirrhosis, the combination of pegylated interferon alpha (PEG IFN) with ribavirin in case of C viral cirrhosis, the PEG IFN and the nucleoside analogs in case of B viral cause; corticosteroids and immunosuppressive drugs in case of autoimmune cirrhosis; venesections in case of genetic haemochromatosis and stopping the drug in case of drug-induced cirrhosis. The complications of cirrhosis such as ascites, oesophageal varices, bleeding, hepatic encephalopathy and hepatocellular carcinoma mainly explain the high rate of morbidity and mortality. Liver transplantation is the established therapy for decompensated liver disease of any etiology significantly changed the outcome of patients with advanced cirrhosis.
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PMID:[Liver cirrhosis in adults: etiology and specific treatments]. 1625 95

To identify factors predicting the development of hepatic encephalopathy, 164 patients with severe acute hepatitis (SAH), defined as acute hepatitis having a prolonged prothrombin time (PT) of < 40% activity but without hepatic encephalopathy, were prospectively observed at 57 major liver centers in Japan. From the data of 65 patients enrolled from 1997 to 1998, a prediction equation was developed by multiple logistic regression analysis and prospectively evaluated using the data of 99 patients since 1999. Of the 164 patients with SAH, 51 (31%) developed hepatic encephalopathy. From the etiologic viewpoint, the percentages of patients developing encephalopathy were highest in non-A-E hepatitis (41.9%). A predictive model, logit(p) = 0.084 x age (year)+ 0.129 x serum total bilirubin (TB, in mg/dL)-0.158 x prothrombin time (%)-2.434, was developed. In conclusion, old age, prolonged PT, elevation of TB, and non-A-E hepatitis are potential risk factors for developing encephalopathy in SAH.
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PMID:Prediction of hepatic encephalopathy development in patients with severe acute hepatitis. 1653 81

A young, male miniature poodle was presented with severe neurological problems. Laboratory tests and ultrasonograph examination were consistent with extrahepatic portosystemic shunts, resulting in hepatic encephalopathy. When surgical correction proved not to be a viable option, the dog was euthanized. Postmortem examination revealed multiple shunts likely acquired after severe hepatitis.
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PMID:Acquired extrahepatic portosystemic shunts in a young dog. 1689 15

Jaundice is a common clinical presentation in severe malaria, seen in approximately 2.5% patients with falciparum infection but hepatitis is unusual. Although hepatic dysfunction is unusual and hepatic encephalopathy is almost never seen in malaria, yet, cases of hepatic dysfunction are being increasingly reported in patients with P.falciparum infection, from different parts of world. The extent of hepatocellular dysfunction varies from mild abnormalities in liver function tests to hepatic failure. Patients with hepatocellular dysfunction in malaria are more prone to develop complications, but have a favorable outcome if hepatic involvement is recognized early and managed properly. It is important to meticulously look for hepatic dysfunction in patients with severe malaria, distinguish it from fulminant hepatic failure and manage it aggressively.
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PMID:Malarial hepatopathy. 1710 60


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