The reason for the close association between primary biliary cirrhosis and the appearance of antibodies that recognize the E2 component of pyruvate dehydrogenase complex is not understood. The distribution of the three pyruvate dehydrogenase complex subunits was examined in the liver and lymph nodes of patients with primary biliary cirrhosis, patients with other liver diseases and normal subjects by immunohistochemistry using affinity-purified antibodies. Intensity of staining was assessed semiquantitatively and validated by scanning laser confocal microscopy. In primary biliary cirrhosis tissue, the E2 staining pattern did not parallel the reported distribution of mitochondria. E2 staining in biliary epithelial cells was consistently stronger than in hepatocytes. In primary biliary cirrhotic liver, staining of biliary epithelium was significantly stronger than in normal or other liver disease controls; many bile ducts in primary biliary cirrhotic liver demonstrated very high intensity, diffuse distribution of stain. No differences in staining intensity were seen between perivenular hepatocytes in primary biliary cirrhotic liver and those in controls; periportal hepatocytes in primary biliary cirrhotic liver were, however, more intensely stained than perivenular cells. In primary biliary cirrhotic portal lymph nodes, a subset of macrophages showed high-intensity, diffuse distribution of stain. By contrast, staining with antibodies to E1 and E3 (other components of pyruvate dehydrogenase complex) produced uniform-intensity, mitochondrial distribution both in primary biliary cirrhosis and control tissue. The increased intensity of E2 in primary biliary cirrhotic tissue could be explained in terms of abnormal metabolism of E2 by biliary epithelial cells.(ABSTRACT TRUNCATED AT 250 WORDS)
In the article entitled Characterization and Isolation of Ductular Cells Coexpressing Neural Cell Adhesion Molecule and Bcl-2 from Primary Cholangiopathies and Ductal Plate Malformations (Volume 156, pages 1599–1612) the author affiliations should have read as follows: In the article entitled Characterization and Isolation of Ductular Cells Coexpressing Neural Cell Adhesion Molecule and Bcl-2 from Primary Cholangiopathies and Ductal Plate Malformations (Volume 156, pages 1599–1612) the author affiliations should have read as follows:
Background. In the United Kingdom, 1 in 3 patients on the National Kidney Transplant Waiting List (NKTWL) is suspended from the list at least once during their wait. The mortality of this large cohort of patients remains underreported and poorly described. Methods. We linked patient records from the UK transplant registry to mortality data from the Office of National Statistics and evaluated the impact of a clinically induced suspension event by estimating hazard ratios (HRs) that compared mortality and graft survival between those who had experienced a suspension event and those who had not. Results. Between January 1, 2000, and December 31, 2010, 16.7% (2221/13 322) of all patients registered on the NKTWL were suspended. Forty-eight percent (588/1225) of those who were suspended and who were never transplanted died, most often from cardiothoracic causes. A suspension event was associated with increased mortality from the time of listing (adjusted HR [aHR], 1.79; 1.64-1.95) and from the time of transplantation (aHR, 1.20; 1.06-1.37; P = 0.005). Graft survival was also poorer in those who had been suspended (aHR, 1.13; 1.01-1.28; P = 0.04). Conclusions. Patients suspended on the NKTWL have a significantly higher rate of mortality both on the waiting list and following transplantation. Earlier prioritization of patients at risk of experiencing a suspension event may improve their outcomes.
Background —Uncertainty exists about the extent and consequences of a return to alcohol consumption after liver transplantation for alcoholic liver disease (ALD). Aims —To determine the prevalence and consequences of alcohol consumption in patients transplanted for ALD. Methods —A retrospective case controlled study of all patients transplanted for ALD at the Queen Elizabeth Hospital, Birmingham, between 1987 and 1996. Results —Seventy patients with ALD were transplanted, of which 59 survived more than three months; 56 were interviewed. Twenty eight had consumed some alcohol after transplantation; for the nine “heavy drinkers” (HD), the median time to resumption of alcohol intake was six months and for the 19 “moderate drinkers” (MD) it was eight months. There was no significant difference in episodes of acute rejection or compliance with medication between those who were abstinent, MD, or HD. Histological evidence of liver injury was common in ALD patients who had returned to drink. Mild fatty change was found in 1/11 biopsy specimens from abstinent patients but moderate to severe fatty change and ballooned hepatocytes were seen in 3/5 MD and 2/5 HD specimens. Two HD patients had early fibrosis. One HD patient has died of alcohol related complications. Conclusions —Moderate to heavy alcohol consumption occurs in patients transplanted for ALD. Patient recall of abstinence advice is unreliable, and patients return to alcohol mainly within the first year after liver transplantation. Return to alcohol consumption after liver transplantation is associated with rapid development of histological liver injury including fibrosis.
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