Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0008370 (cholestasis)
 9,378 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The etiology of 72 episodes of liver disease that developed in 62 of 162 renal-transplant recipients was evaluated. Infection with hepatitis B virus was a minor problem, and none of our patients had evidence of infection with hepatitis A. Cytomegalovirus infection was ubiquitous in the population and probably accounted for many episodes of acute liver disease. This agent's role in causing chronic hepatitis is less secure. Infections with other viruses including Epstein-Barr virus, adenovirus, and the herpes viruses were only rarely associated with hepatic disease. Azathioprine was responsible for some episodes of acute cholestasis but could not be incriminated as a direct cause of chronic disease. A cause could be identified for the majority of episodes of acute hepatic dysfunction, but the cause of most of the chronic hepatitis remains undetermined. It is likely that infection with non-A, non-B hepatitis virus accounts for much of this serious, often fatal, complication of renal transplantation.
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PMID:Etiology of liver disease in renal-transplant patients. 22 42

In hepatic transplantation, the recipient and the graft must manage a difficult symbiosis. The causes that can unbalance the mutual adaptation are various, but the clinical-biochemical hepatic graft syndromes they produce are not specific. Morphological study of the graft shows a distinct pattern for each type of dysfunction etiopathogeny. Such study may find: (1) immune attack: acute rejection or chronic rejection; (2) technical complications in the biliary tract or in the blood perfusion of the graft; (3) nonspecific cholestasis secondary to graft cold ischemia or preceding development of chronic rejection; (4) recurrence of the previous illness: graft infected by hepatitis virus; (5) opportunistic viral infections (cytomegalovirus, Epstein-Barr virus, herpesvirus, adenovirus); (6) reactions to drugs and toxics; and (7) combinations of several etiologies. Morphological knowledge enables the pathologist to collaborate in hepatic transplantation programs: elaborating protocols, selecting patients, diagnosing hepatic graft dysfunction, and assessing program quality.
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PMID:The role of histopathology in hepatic transplantation. 152 58

Diphenylhydantoin-induced hepatitis and mononucleosis are uncommon in children. The occurrence of these two diseases in the same individual, with progression to hepatic failure is rare and has not been reported in infants. This report represents a 6-month-old male infant who developed an infectious mononucleosis-like syndrome and hepatic failure 16 days after diphenylhydantoin administration. He took this anticonvulsant for controlling seizures after a head injury. Fever, skin rash, hepatosplenomegaly, lymphadenopathy, and atypical lymphocytosis led to the initial diagnosis of infectious mononucleosis. However, negative heterophil antibody did not support the diagnosis. Jaundice ensued in the following course and became more and more profound. Meanwhile, physical examination showed shrinking in liver size. Negative virology studies, including Epstein-Barr virus, cytomegalovirus, and hepatitis B virus, excluded them as causative agents. The patient lapsed into a stage I hepatic coma, but gradually recovered clinically and biochemically after eight successive exchange transfusions and supportive care. Two liver biopsies were performed 20 and 50 days after the onset of disease, respectively. Remarkable hepatic parenchymal loss, cholestasis, and fatty change were found on histologic examination of the first biopsy specimen, and portal fibrosis was noted on the second.
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PMID:Mononucleosis and hepatic failure associated with diphenylhydantoin treatment in an infant. 167 17

The 9-month-old daughter of human immunodeficiency virus (HIV)-seropositive parents presented with cholestasis and was found on liver biopsy to have giant cell hepatitis. No viral inclusions or particles were seen by light or electron microscopy. Ultrastructural studies of the liver biopsy demonstrated tubuloreticular structures in the endothelium and cylindrical confronting cisternae in inflammatory cells in the portal tracts. Serologic studies for hepatitis B, hepatitis A, and Epstein-Barr viruses were negative. Cytomegalovirus (CMV) was cultured from the urine, but buffy coat, nasopharyngeal, and liver cultures were negative and CMV antibody titer was low. The hepatitis responded dramatically to prednisone therapy. A repeat biopsy several months later revealed similar morphologic findings. AIDS was suspected on clinical and immunologic grounds, and was confirmed by the demonstration of HIV-specific IgG and IgM in serum. Five months after initial presentation, the infant developed Pneumocystis pneumonia, disseminated CMV infection, and died. This appears to be the first reported association of infantile giant cell hepatitis with HIV infection.
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PMID:HIV as a cause of giant cell hepatitis. 283 97

Acute liver failure with cholestasis, histologic and serologic evidence of Epstein-Barr viral infection, and associated autoimmune hemolytic anemia occurred in a patient with lifelong protoporphyria. Changes in previously established baseline protoporphyrin distribution dynamics in erythrocyte, plasma, and fecal excretion compartments were observed during the period of severe hepatic dysfunction and recovery. These changes were consistent with predictions of a previously described conceptual model for human protoporphyria.
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PMID:Changes in protoporphyrin distribution dynamics during liver failure and recovery in a patient with protoporphyria and Epstein-Barr viral hepatitis. 301 Jul 17

While mild to moderate hepatic dysfunction is commonly encountered in infectious mononucleosis induced by Epstein-Barr virus (EBV), clinical jaundice with high bilirubin levels (greater than or equal to 6.0 mg/dL [greater than or equal to 103 mumol/L] is only occasionally encountered. In this study, seven patients with primary EBV infections had peak bilirubin levels of 10.2 to 23.0 mg/dL (174 to 393 mumol/L) and, for the most part, presented initial diagnostic problems. Complications included the virus-associated hemophagocytic syndrome and acute respiratory distress syndrome in one patient and transient renal failure in another. The laboratory data suggested that a combination of hemolysis and viral-induced cholestasis was responsible for the intense hyperbilirubinemia in at least five patients. Physicians should be aware that marked hyperbilirubinemia can occur with EBV-induced infectious mononucleosis and, thereby, obviate the need for costly diagnostic laboratory tests and, occasionally, invasive procedures.
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PMID:Marked hyperbilirubinemia in infectious mononucleosis. Analysis of laboratory data in seven patients. 303 77

An infant with uncorrectable extrahepatic bile duct atresia was found to have evidence of Epstein-Barr virus infection during the neonatal period. It is probable that the infection was acquired in utero. In view of the association of hepatitis with the Epstein-Barr virus in later life, it is possible that this infection was responsible for the development of bile duct obstruction.
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PMID:The association of extrahepatic bile duct atresia and neonatal Epstein-Barr virus infection. 632 9

During the last 31 months, 50 children between 3 months and 15 years of age have undergone living related liver transplantation (LRLT) for end-stage liver diseases (39 biliary atresia, 2 Budd-Chiari syndrome, 2 progressive intrahepatic cholestasis, 3 liver cirrhosis, 1 Wilson disease, 1 protoporphyria, 1 tyrosinemia, and 1 fulminant hepatitis). Combined FK-506 and low-dose steroids were routinely used for immunosuppression. There were seven deaths, two of which were related to infection (Candida pneumonia and Epstein-Barr virus [EBV]-associated lymphoproliferative syndrome [LPS]). Five patients had a bacterial infection, all of which were associated with surgical complications. Three patients had Candida infection, all of which were malnourished, had biliary atresia, and had been managed with prolonged antibiotics against obstinate ascending cholangitis. There were 14 symptomatic viral infections (1 herpes simplex virus, 1 herpes zoster virus, 5 cytomegalovirus [CMV], 6 EBV, and 1 EBV-associated LPS). Three of the five CMV infections appeared in patients whose graft was ABO-incompatible, who were managed with prophylactic OKT-3. Most of the viral infections (except 1 EBV-associated LPS) were minor and were treated successfully. The low incidence and successful treatment of CMV infection are related to the high compatibility and low incidence of allograft rejection in LRLT. Bacterial and fungal infections can be decreased by greater refinement of surgical technique and more aggressive preoperative management. Treatment of EBV infection is still an unsolved problem.
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PMID:Infectious complications in living related liver transplantation. 801 5

A 27-yr-old Jamaican male presented with a 2-month history of jaundice, pruritus, intermittent diarrhea, and right upper quadrant abdominal pain. Over the next month, his abdominal pain and diarrhea improved, but his jaundice and pruritus worsened. He was afebrile and profoundly jaundice, with a benign abdominal examination. Medical workup included a normal abdominal ultrasound, iron studies, ceruloplasm, and serum electrophoresis. Negative viral (Epstein-Barr virus, cytomegalovirus, mononucleosis, hepatitis A, B, C) studies, ANA, AMA, ASMA, RPR were noted. He denied any alcohol, drug, or toxin exposure. Liver tests revealed total bilirubin of 25.6 mg/dl, direct bilirubin of 13.9 mg/dl, alkaline phosphatase 278 IU/L, AST 45 IU/L, and ALT 71 IU/L. Liver biopsy demonstrated centrilobular zonal necrosis and cholestasis most consistent with a toxic reaction. The patient was again interviewed regarding potential toxins, and he admitted to the ingestion of ackee fruit, a native Jamaican fruit that is illegal in the United States. Shortly after he had ceased intake of the fruit, his symptoms resolved and his liver function tests returned to normal. We present a case of chronic ackee fruit ingestion that led to cholestatic jaundice, vomiting, and abdominal pain.
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PMID:Cholestatic jaundice due to ackee fruit poisoning. 807 44

Jaundice is a common problem in marrow transplant recipients. The incidence of bile duct obstruction in this setting is unknown. The purpose of this study was to determine the incidence of biliary obstruction, the causes, and outcomes following marrow transplant. Consecutive cases were reviewed at two major transplant centers in the United States from 1969 to 1996 at the Fred Hutchinson Cancer Research Center and 1989 to 1996 at the City of Hope National Medical Center. Nine cases of biliary obstruction were identified as a cause of jaundice in 7412 marrow transplant recipients, an incidence of 0.12%. The presentation was bimodal, with seven cases occurring prior to day 100 and two occurring 2 to 4 years after transplantation. The age distribution was 15 to 50 years and all patients had received allogeneic transplants. The causes of obstruction included gallbladder sludge (n=1), a duodenal hematoma (n=1), choledocholithiasis with biliary pancreatitis (n=1), bile duct infection (n=2), recurrent malignancy (n=1), choledocholithiasis associated with a benign stricture (n=1), Epstein-Barr virus-related lymphoproliferative disorder (n=1), and a benign stricture of unknown etiology (n=1). Biliary obstruction is a rare cause of jaundice in the post-transplant period. The presentation was similar to that of other post-transplant hepatobiliary problems, but with disparate causes.
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PMID:Biliary obstruction in hematopoietic cell transplant recipients: an uncommon diagnosis with specific causes. 1033 48


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