The Experts below are selected from a list of 372 Experts worldwide ranked by ideXlab platform
Jenny Heathcote - One of the best experts on this subject based on the ideXlab platform.
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cholestatic liver disease with Ductopenia vanishing bile duct syndrome after administration of clindamycin and trimethoprim sulfamethoxazole
The American Journal of Gastroenterology, 1994Co-Authors: Ibrahim Altraif, Les Lilly, Ian R Wanless, Jenny HeathcoteAbstract:Two patients who developed cholestatic liver disease after exposure to antibiotics are described. One patient who received clindamycin had liver biopsy findings of marked cholestasis, portal inflammation, bile duct injury and bile duct paucity (Ductopenia). A second biopsy after clinical improvement showed resolution of cholestasis but persistence of duct paucity. Three years later, treatment with ampicillin caused another episode of cholestatic hepatitis with cholestasis and duct paucity on rebiopsy. The second patient, who developed cholestasis after receiving trimethoprim-sulfamethoxazole, had marked duct paucity in the liver biopsy. This is the first description, to our knowledge, of Ductopenia apparently caused by clindamycin
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cholestatic liver disease with Ductopenia vanishing bile duct syndrome after administration of clindamycin and trimethoprim sulfamethoxazole
The American Journal of Gastroenterology, 1994Co-Authors: Ibrahim Altraif, Les Lilly, Ian R Wanless, Jenny HeathcoteAbstract:Two patients who developed cholestatic liver disease after exposure to antibiotics are described. One patient who received clindamycin had liver biopsy findings of marked cholestasis, portal inflammation, bile duct injury and bile duct paucity (Ductopenia). A second biopsy after clinical improvement showed resolution of cholestasis but persistence of duct paucity. Three years later, treatment with ampicillin caused another episode of cholestatic hepatitis with cholestasis and duct paucity on rebiopsy. The second patient, who developed cholestasis after receiving trimethoprim-sulfamethoxazole, had marked duct paucity in the liver biopsy. This is the first description, to our knowledge, of Ductopenia apparently caused by clindamycin. Cross-reactivity between clindamycin and ampicillin is also demonstrated in one patient. This report documents that duct paucity may occur within 10 days of onset of jaundice and appears to be confined to ducts less than 0.03 mm in diameter.
Joan Rodes - One of the best experts on this subject based on the ideXlab platform.
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nonsyndromic paucity of intrahepatic bile ducts in infancy and idiopathic Ductopenia in adulthood the same syndrome
Hepatology, 1992Co-Authors: M Bruguera, Josep Llach, Joan RodesAbstract:Eleven patients with chronic intrahepatic cholestasis in whom a liver biopsy specimen showed unexplained bile duct paucity were investigated. Cholestasis developed during the neonatal period in three, at infancy (before 14 yr) in four and after 14 yr in the remaining four patients. In all patients other conditions characterized by chronic cholestasis associated with Ductopenia such as primary biliary cirrhosis, primary sclerosing cholangitis, drug-induced liver disease, sarcoidosis or graft-vs.-host disease were excluded. Cardiovascular abnormalities in the three patients who had neonatal cholestasis permitted diagnosis of Alagille's syndrome. Clinical, biochemical and histological features were similar in the remaining eight patients, independent of the age at which the disease appeared. Idiopathic adulthood Ductopenia may be a late-onset form of the nonsyndromic paucity of interlobular bile ducts seen in children, or it may be due to a still-unidentified cause that strikes later in life.
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nonsyndromic paucity of intrahepatic bile ducts in infancy and idiopathic Ductopenia in adulthood the same syndrome
Hepatology, 1992Co-Authors: M Bruguera, Josep Llach, Joan RodesAbstract:Eleven patients with chronic intrahepatic cholestasis in whom a liver biopsy specimen showed unexplained bile duct paucity were investigated. Cholestasis developed during the neonatal period in three, at infancy (before 14 yr) in four and after 14 yr in the remaining four patients. In all patients other conditions characterized by chronic cholestasis associated with Ductopenia such as primary biliary cirrhosis, primary sclerosing cholangitis, drug-induced liver disease, sarcoidosis or graft-vs.-host disease were excluded. Cardiovascular abnormalities in the three patients who had neonatal cholestasis permitted diagnosis of Alagille's syndrome. Clinical, biochemical and histological features were similar in the remaining eight patients, independent of the age at which the disease appeared. Idiopathic adulthood Ductopenia may be a late-onset form of the nonsyndromic paucity of interlobular bile ducts seen in children, or it may be due to a still-unidentified cause that strikes later in life. (HEPATOLOGY 1992;15:830–834).
Vicente Carreno - One of the best experts on this subject based on the ideXlab platform.
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association of hla dr genes with mild idiopathic adulthood biliary Ductopenia
The American Journal of Gastroenterology, 2001Co-Authors: Manuel Esteban Garciajimenez, Juan Antonio Quiroga, Maria Luisa Gutierrez, Margarita Pardo, Vicente CarrenoAbstract:OBJECTIVE: Mild idiopathic adulthood Ductopenia (MIAD) is an asymptomatic chronic cholestatic liver disease characterized by the loss of interlobular bile ducts in <50% of the portal tracts. Although the underlying cause of MIAD is unknown, the host factors may contribute to the patient’s susceptibility to the disease. The aim of this work was to investigate the immunogenetics in the pathogenesis of MIAD. METHODS: We prospectively studied 22 Caucasian patients with MIAD. Peripheral blood was collected, and HLA-DR typing was performed by polymerase chain reaction with sequence-specific primers followed by sequencing for subtyping. Results were compared with those from 140 age- and sex-matched controls. RESULTS: There was no significant association between HLA-DRB1 alleles and the disease, although a trend was found in MIAD patients with the DRB1∗1502 allele (five of 44 vs four of 280 in controls; p corrected = 0.055; χ2 = 13.9). Multiple HLA-DRB1 alleles (∗04, ∗11, ∗15) showed increased frequencies in MIAD patients. Further subtyping revealed a motif (positions 25–32 of the β1 chain) present in 17 (77.3%) patients, which was significantly associated with MIAD (p = 0.049; χ2 = 3.87). Seven patients (31.8%) and 21 (15%) controls coded for this motif in their two alleles (p = 0.068; χ2 = 3.76). Among MIAD patients, those seven had abnormal ALT levels (p = 0.017) and their γ-glutamyltransferase and ALT values tended to be more increased. CONCLUSIONS: These results provide evidence of an immunogenetic basis of susceptibility to MIAD in Caucasian individuals.
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idiopathic biliary Ductopenia in adults without symptoms of liver disease
The New England Journal of Medicine, 1997Co-Authors: Alberto Moreno, Vicente Carreno, Ana Cano, Cecilia GonzalezAbstract:Background Idiopathic adulthood Ductopenia is a severe cholestatic liver disease of unknown cause characterized by loss of the interlobular bile ducts in more than 50 percent of the portal tracts. In most reported cases, cirrhosis and liver failure develop. Methods We studied 24 adults with abnormal results on liver-function tests but no symptoms of liver disease. All had liver biopsies that showed a lack of bile ducts in many of the portal tracts. Results The 17 women and 7 men had a mean age of 41 years (range, 27 to 57). All were asymptomatic and had high serum γ-glutamyltransferase concentrations (mean [±SD], 179±84 U per liter); 75 percent also had abnormal serum alanine aminotransferase concentrations. The proportion of portal tracts that had bile ducts was 62±7 percent (range, 55 to 78 percent). Three patients had a second liver biopsy three to nine years after the first; there were no changes over time. In four of the five patients treated with 600 to 900 mg of ursodiol two to three times daily, r...
Ibrahim Altraif - One of the best experts on this subject based on the ideXlab platform.
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cholestatic liver disease with Ductopenia vanishing bile duct syndrome after administration of clindamycin and trimethoprim sulfamethoxazole
The American Journal of Gastroenterology, 1994Co-Authors: Ibrahim Altraif, Les Lilly, Ian R Wanless, Jenny HeathcoteAbstract:Two patients who developed cholestatic liver disease after exposure to antibiotics are described. One patient who received clindamycin had liver biopsy findings of marked cholestasis, portal inflammation, bile duct injury and bile duct paucity (Ductopenia). A second biopsy after clinical improvement showed resolution of cholestasis but persistence of duct paucity. Three years later, treatment with ampicillin caused another episode of cholestatic hepatitis with cholestasis and duct paucity on rebiopsy. The second patient, who developed cholestasis after receiving trimethoprim-sulfamethoxazole, had marked duct paucity in the liver biopsy. This is the first description, to our knowledge, of Ductopenia apparently caused by clindamycin
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cholestatic liver disease with Ductopenia vanishing bile duct syndrome after administration of clindamycin and trimethoprim sulfamethoxazole
The American Journal of Gastroenterology, 1994Co-Authors: Ibrahim Altraif, Les Lilly, Ian R Wanless, Jenny HeathcoteAbstract:Two patients who developed cholestatic liver disease after exposure to antibiotics are described. One patient who received clindamycin had liver biopsy findings of marked cholestasis, portal inflammation, bile duct injury and bile duct paucity (Ductopenia). A second biopsy after clinical improvement showed resolution of cholestasis but persistence of duct paucity. Three years later, treatment with ampicillin caused another episode of cholestatic hepatitis with cholestasis and duct paucity on rebiopsy. The second patient, who developed cholestasis after receiving trimethoprim-sulfamethoxazole, had marked duct paucity in the liver biopsy. This is the first description, to our knowledge, of Ductopenia apparently caused by clindamycin. Cross-reactivity between clindamycin and ampicillin is also demonstrated in one patient. This report documents that duct paucity may occur within 10 days of onset of jaundice and appears to be confined to ducts less than 0.03 mm in diameter.
Mary Kay Washington - One of the best experts on this subject based on the ideXlab platform.
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the concept of hepatic artery bile duct parallelism in the diagnosis of Ductopenia in liver biopsy samples
The American Journal of Surgical Pathology, 2011Co-Authors: Roger K Moreira, William Chopp, Mary Kay WashingtonAbstract:Absence of bile ducts (BDs) in >50% of portal tracts is currently the most widely accepted criterion for the diagnosis of Ductopenia. In this study, we describe an alternative method for the quantitative assessment of BDs based on the percentage of portal tracts containing unpaired hepatic arteries
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the concept of hepatic artery bile duct parallelism in the diagnosis of Ductopenia in liver biopsy samples
The American Journal of Surgical Pathology, 2011Co-Authors: Roger K Moreira, William Chopp, Mary Kay WashingtonAbstract:Absence of bile ducts (BDs) in >50% of portal tracts is currently the most widely accepted criterion for the diagnosis of Ductopenia. In this study, we describe an alternative method for the quantitative assessment of BDs based on the percentage of portal tracts containing unpaired hepatic arteries (HAs). Diagnostic criteria for Ductopenia were defined as follows: 1. presence of at least 1 unpaired HA in >10% of all portal tracts; 2. at least 2 unpaired HAs present in different portal tracts in a given sample. In liver biopsies from patients with primary biliary cirrhosis and suspected chronic allograft rejection (n = 32), loss of BD was detected in 59.4% of patients using the unpaired HA method compared with 43.7% (P = 0.31), 21.9% (P = 0.005), and 12.5% (P = 0.001) by the traditional method, depending on specific adequacy criteria used (no adequacy criteria, >10 portal tracts, or >5 complete portal tracts per biopsy, respectively). The percentage of portal tracts containing BD(s) was significantly affected by the degree of portal inflammation, fibrosis stage, percentage of complete portal tracts, and biopsy width, whereas none of these factors influenced the prevalence of unpaired arteries. The unpaired HA method showed higher sensitivity for the detection of mild degrees of loss of BD compared with the traditional method, and was not influenced by factors that affected the percentage of portal tracts containing BDs.
