Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 56-year-old white male painter, with a history of major electrocution and deep thermal injury, developed mental status changes initially ascribed to an acute neurological event. Unexpectedly, magnetic resonance imaging (MRI) of the head showed areas of high signal intensity in the basal ganglia, which can be observed in advanced liver disease. An electroencephalogram (EEG) suggested metabolic encephalopathy and coexistent elevation of ammonia, indicative of significant liver disease. The patient had had a long history of right upper quadrant pain and fluctuation in liver tests following the electrocution trauma. For these symptoms, he underwent surgery 7 years prior to his current presentation of portosystemic encephalopathy, and was found to have a gangrenous acalculous cholecystitis. Intraoperative cholangiogram suggested possible strictures within the right hepatic ducts. Multiple liver biopsies, however, showed only steatosis. Current evaluation including liver biopsy, MRI, magnetic resonance angiography (MRA), and magnetic resonance cholangiopancreatography (MRCP), revealed progression to biliary cirrhosis with large bile duct obstruction, and hepatic artery thrombosis/occlusion with evidence of left lobe atrophy and right lobe compensatory hypertrophy. The pathobiology of ischemic bile duct injury is discussed herein. The case is an example of serious late sequelae of an occupational injury.
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PMID:A 56-year-old man with sudden onset of portosystemic encephalopathy years after severe electrocution trauma. 1881 85

Cancer chemotherapy in chronic hepatitis B virus (HBV) carriers occasionally leads to acute hepatic failure (AHF) from viral reactivation resulting in an high mortality rate. In this situation, living donor liver transplantation (LDLT) can be life saving. Herein we have reported 2 cases of successful LDLT performed for AHF caused by reactivation of HBV infection during chemotherapy for hematologic malignancies. In case 1, a 38-year-old male HBV carrier with a neck mass was hisopathologically diagnosed as Hodgkin's lymphoma. During 4 cycles of chemotherapy he developed right upper quadrant pain and jaundice. Laboratory data (alanine amino transferase, 701 U/L, total bilirubin: 7.92 mg/dL, positive hepatitis B e antigen showed that he had experienced an acute exacerbation of chronic hepatitis. Soon, he developed grade IV hepatic encephalopathy with a total bilirubin level of 50.56 mg/dL and a model for End-Stage Liver Disease score of 40. After LDLT, he has been free of relapse for 52 months so far. In case 2, a 49-year-old male HBV carrier was diagnosed in the chronic phase of chronic myeloid leukemia. The patient had been under Imatinib treatment for 1 year until he was admitted for AHF. He developed grade II encephalopathy with a total bilirubin of 50.8 mg/dL. We performed LDLT; the patient has been free of relapse for 17 months. LDLT was a life-saving procedure for AHF caused by reactivation of HBV during chemotherapy for hematologic malignancy. It can provide long-term survival if the coexistent hematologic malignancy has been controlled.
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PMID:Living donor liver transplantation for acute hepatic failure caused by reactivation of hepatitis B virus infection after chemotherapy for hematologic malignancy: case reports. 2043 Jan 87