Hepatic bile duct lesions in patients with chronic hepatitis C; prevalence and significance
September 18, 2011
Hepatic bile duct lesions in patients with chronic hepatitis C; prevalence and significance
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Title: | Hepatic bile duct lesions in patients with chronic hepatitis C; prevalence and significance |
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Article_Title: | Hepatic bile duct lesions in patients with chronic hepatitis C; prevalence and significance |
Authors: | M. Cornianu1, A. Dema1, S. Tăban1, D. Lazăr2, R. Şirli2, E. Lazăr1, A. Faur1, C. Lăzureanu1, I. Muntean3, R. Popescu3, R. Cornea1 |
Affiliation: | 1 Department of Pathology; 2 Gastroenterology Clinic; 3 Department of Cellular Biology, U.M.F. “V. Babeş” Timişoara |
Abstract: | Introduction: Hepatic bile duct lesions (BDL), lymphoid aggregates or lymphoid follicles (LA/LF) and hepatic steatosis (HS) are common histological features, often observed in patients with chronic hepatitis C (VHC). The pathogenesis and clinical significance of hepatic BDL remain unclear. Material and method: We evaluated the prevalence and clinical significance of BDL on a group of 189 liver biopsies from patients with chronic viral hepatitis (125 patients with VHC and 64 with VHB), trying therewith to compare clinical, biochemical and morphologic data in patients with and without BDL. Results: The mean age of patients with BDL was 50.5 years, slightly higher than the one of patients without BDL (48.61 years). Analyzing the frequency and pathological significance of BDL and portal lymphocyte infiltrate in patients with VHC we noted: a higher frequency of BDL in patients with VHC than in those with VHB (55/125; 44% vs.14/64; 21.8%); a high level of serum alanin-aminotransferase (ALT) (93.83 U/l), alkaline phosphatase (AP) (175.83 U/l) and gamma-glutamil-transpeptidase (gGTP) (99.76 U/l) in patients with BDL vs. 71.73 U/l, 146.76U/l and 71.24 U/l, respectively, in those without these kind of lesions; serum triglyceride (TG), cholinesterase (CHE) and total bilirubin (TB) levels were found to be significantly higher in patients without BDL. We did not observe a relationship between the sex of the patients and the presence of blood transfusions in their history, between the two groups of patients. For the group of patients with VHC and BDL we observed a higher score of necroinflammation (9.87 vs. 7.38), portal inflammation (3.01 vs. 2.44) and fibrosis (1.65 vs. 0.97) and a higher frequency of LA/LF (49 vs. 36), as compared to patients without BDL. HS was found in 96 from the 125 (76.8%) patients with VHC, in 44 from 55 (80%) patients with BDL and in 52 from 70 (74.3%) of those without BDL. Conclusion: The incidence of hepatic BDL is highly related to the severity of the histopathological lesions, being higher in patients with advanced liver disease and cholestasis. The implication and molecular role of hepatitis C virus in the pathogenesis of BDL requires further studies. |
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References: | Scheuer PJ, Ashrafzadeh P, Sherlock S, Brown D, Dusheiko GM. The pathology of hepatitis C. Hepatology 1992; 15:567-571. Bach N, Thung SN, Schaffner F. The histological features of chronic hepatitis C and autoimmune chronic hepatitis: a comparative analysis. Hepatology 1992; 15:572-577. Wong VS, Wight DGD, Palmer C.R, Alexander GJM. Fibrosis and other histological features in chronic hepatitis C virus infection: a statistical model. Journal of Clinical Pathology 1996; Vol. 49, No. 6: 465-469. Ludwig J, Czaja AJ, Dickson ER. Manifestations of nonsuppurative cholangitis in chronic hepatobiliary diseases: morphologic spectrum, clinical correlations and terminology. Liver 1984; 4: 105-10. Goldin RD, Patel NK, Thomas HC. Hepatitis C and bile duct loss. J Clin Pathol, 1996; 49:836-838. Hwang SJ, Luo JC, Chu CW et al. Clinical, virological, and pathological significance of hepatic bile duct injuries in Chinese patients with chronic hepatitis C. Journal of Gastroenterology, 2001; 36:392-398. Gerber MA, Krawczynski K, Alter MJ, Sampliner RE. Margolis HS, and the sentinel counties chronic non-A, non-B hepatitis study team. Histopathology of community acquired chronic hepatitis C. Mod Pathol, 1992; 5:483-486. Kaji K, Nakamuma Y, Sasaki M et al. Hepatitic bile duct injuries in chronic hepatitis C: histopathological and immunohistochemical studies. Mod Pathol, 1994; 7:937-945. Luo JC, Hwang SJ, Lai CR et al. Clinical significance of portal lymphoid aggretates/follicles in Chinese patients with chronic hepatitis C. Am J Gastroenterology, 1999; 94:1006-1011. Danque POV, Bach N, Schaffner F, Gerber MA, Thung SN. HLA-DR expression in bile duct damage in chronic hepatitis C. Mod Pathol 1993; 6: 327-32. Hino K, Okuda M, Konishi T et al. Analysis of lymphoid follicles in liver of patients with chronic hepatitis C. Liver, 1992; 12:387-91. Pawlotsky JM, et al. immunological disorders in C virus chronic active hepatitis: a prospective case-control study. Hepatology, 1994; 19:841-848. Haruna Y, Miyamoto T, Yasunami R, Kanda T, Fushimi H. Human leucocyte antigen DRN1 1302 protects against bile Duch damage and portal lymphocyte infiltration in patients with chronic hepatitis C. Journal of Hepatology 2000; 32: 837-42 |
Read_full_article: | pdf/21-2011/21-2-2011/SU21-2-2011Cornianu.pdf |
Correspondence: | M. Cornianu, Department of Pathology; U.M.F. “V. Babeş” Timişoara, Romania |
Read full article | |
Article Title: | Hepatic bile duct lesions in patients with chronic hepatitis C; prevalence and significance |
Authors: | M. Cornianu1, A. Dema1, S. Tăban1, D. Lazăr2, R. Şirli2, E. Lazăr1, A. Faur1, C. Lăzureanu1, I. Muntean3, R. Popescu3, R. Cornea1 |
Affiliation: | 1 Department of Pathology; 2 Gastroenterology Clinic; 3 Department of Cellular Biology, U.M.F. “V. Babeş” Timişoara |
Abstract: | Introduction: Hepatic bile duct lesions (BDL), lymphoid aggregates or lymphoid follicles (LA/LF) and hepatic steatosis (HS) are common histological features, often observed in patients with chronic hepatitis C (VHC). The pathogenesis and clinical significance of hepatic BDL remain unclear. Material and method: We evaluated the prevalence and clinical significance of BDL on a group of 189 liver biopsies from patients with chronic viral hepatitis (125 patients with VHC and 64 with VHB), trying therewith to compare clinical, biochemical and morphologic data in patients with and without BDL. Results: The mean age of patients with BDL was 50.5 years, slightly higher than the one of patients without BDL (48.61 years). Analyzing the frequency and pathological significance of BDL and portal lymphocyte infiltrate in patients with VHC we noted: a higher frequency of BDL in patients with VHC than in those with VHB (55/125; 44% vs.14/64; 21.8%); a high level of serum alanin-aminotransferase (ALT) (93.83 U/l), alkaline phosphatase (AP) (175.83 U/l) and gamma-glutamil-transpeptidase (gGTP) (99.76 U/l) in patients with BDL vs. 71.73 U/l, 146.76U/l and 71.24 U/l, respectively, in those without these kind of lesions; serum triglyceride (TG), cholinesterase (CHE) and total bilirubin (TB) levels were found to be significantly higher in patients without BDL. We did not observe a relationship between the sex of the patients and the presence of blood transfusions in their history, between the two groups of patients. For the group of patients with VHC and BDL we observed a higher score of necroinflammation (9.87 vs. 7.38), portal inflammation (3.01 vs. 2.44) and fibrosis (1.65 vs. 0.97) and a higher frequency of LA/LF (49 vs. 36), as compared to patients without BDL. HS was found in 96 from the 125 (76.8%) patients with VHC, in 44 from 55 (80%) patients with BDL and in 52 from 70 (74.3%) of those without BDL. Conclusion: The incidence of hepatic BDL is highly related to the severity of the histopathological lesions, being higher in patients with advanced liver disease and cholestasis. The implication and molecular role of hepatitis C virus in the pathogenesis of BDL requires further studies. |
Keywords: | |
References: | Scheuer PJ, Ashrafzadeh P, Sherlock S, Brown D, Dusheiko GM. The pathology of hepatitis C. Hepatology 1992; 15:567-571. Bach N, Thung SN, Schaffner F. The histological features of chronic hepatitis C and autoimmune chronic hepatitis: a comparative analysis. Hepatology 1992; 15:572-577. Wong VS, Wight DGD, Palmer C.R, Alexander GJM. Fibrosis and other histological features in chronic hepatitis C virus infection: a statistical model. Journal of Clinical Pathology 1996; Vol. 49, No. 6: 465-469. Ludwig J, Czaja AJ, Dickson ER. Manifestations of nonsuppurative cholangitis in chronic hepatobiliary diseases: morphologic spectrum, clinical correlations and terminology. Liver 1984; 4: 105-10. Goldin RD, Patel NK, Thomas HC. Hepatitis C and bile duct loss. J Clin Pathol, 1996; 49:836-838. Hwang SJ, Luo JC, Chu CW et al. Clinical, virological, and pathological significance of hepatic bile duct injuries in Chinese patients with chronic hepatitis C. Journal of Gastroenterology, 2001; 36:392-398. Gerber MA, Krawczynski K, Alter MJ, Sampliner RE. Margolis HS, and the sentinel counties chronic non-A, non-B hepatitis study team. Histopathology of community acquired chronic hepatitis C. Mod Pathol, 1992; 5:483-486. Kaji K, Nakamuma Y, Sasaki M et al. Hepatitic bile duct injuries in chronic hepatitis C: histopathological and immunohistochemical studies. Mod Pathol, 1994; 7:937-945. Luo JC, Hwang SJ, Lai CR et al. Clinical significance of portal lymphoid aggretates/follicles in Chinese patients with chronic hepatitis C. Am J Gastroenterology, 1999; 94:1006-1011. Danque POV, Bach N, Schaffner F, Gerber MA, Thung SN. HLA-DR expression in bile duct damage in chronic hepatitis C. Mod Pathol 1993; 6: 327-32. Hino K, Okuda M, Konishi T et al. Analysis of lymphoid follicles in liver of patients with chronic hepatitis C. Liver, 1992; 12:387-91. Pawlotsky JM, et al. immunological disorders in C virus chronic active hepatitis: a prospective case-control study. Hepatology, 1994; 19:841-848. Haruna Y, Miyamoto T, Yasunami R, Kanda T, Fushimi H. Human leucocyte antigen DRN1 1302 protects against bile Duch damage and portal lymphocyte infiltration in patients with chronic hepatitis C. Journal of Hepatology 2000; 32: 837-42 |
*Correspondence: | M. Cornianu, Department of Pathology; U.M.F. “V. Babeş” Timişoara, Romania |