Extrahepatic portal biliopathy

Proposed etiology on the basis of anatomic and clinical features

Eric Walser, Brandon R. Runyan, Michael G. Heckman, Mellena D. Bridges, Darrin L. Willingham, Ricardo Paz-Fumagalli, Justin H. Nguyen

Research output: Contribution to journalArticle

43 Citations (Scopus)

Abstract

Purpose: To compare the anatomic and clinical features in patients with chronic portal vein thrombosis (PVT) to determine why some patients develop portal biliopathy (PB) while most do not and propose an etiology for PB. Materials and Methods: This project satisfied HIPAA regulations and received institutional review board approval for a retrospective review without the need for consent. From 100 patients with PVT, 60 were extracted who had chronic, nonmalignant PVT, after exclusion of those with sclerosing cholangitis, liver transplants, choledocholithiasis, or portosystemic shunts. Clinical and imaging data from 19 patients with biliary dilatation (PB group) were compared with data from 41 patients without biliary dilatation (no-PB group). Statistical analysis was performed with the Fisher exact test for categorical variables or the Wilcoxon rank-sum test for numerical and ordered categorical variables. P values of.05 or less were considered to indicate a significant difference. Results: The etiology of PVT differed between the groups (P <.001); cirrhosis was infrequently seen in the PB group (two of 19, 11%) but was common in the no-PB group (31 of 41, 76%). Only two of 33 (6 %) patients with cirrhosis and PVT had PB. Extension of PVT into the mesenteric veins was significantly more common in the PB group (18 of 19, 95%) than in the no-PB group (one of 41, 2%) (P <.001). Compared with the no-PB group, patients in the PB group had more acute angulation of the bile duct (median, 110° vs 128°; P =.008), less frequent gastroesophageal varices (three of 19 [16%] vs 20 of 41 [49%], P =.021), and a smaller mean coronary vein diameter (median, 5 vs 6 mm; P =.014). Conclusion: Noncirrhotic patients with hypercoagulable states tend to develop PB when PVT extends to the splenomesenteric veins. A possible etiology is the formation of specific peribiliary venous pathways responsible for bile duct compression and tethering.

Original languageEnglish (US)
Pages (from-to)146-153
Number of pages8
JournalRadiology
Volume258
Issue number1
DOIs
StatePublished - Jan 2011
Externally publishedYes

Fingerprint

Portal Vein
Thrombosis
Nonparametric Statistics
Bile Ducts
Dilatation
Fibrosis
Surgical Portasystemic Shunt
Health Insurance Portability and Accountability Act
Choledocholithiasis
Mesenteric Veins
Sclerosing Cholangitis
Research Ethics Committees
Varicose Veins
Veins
Coronary Vessels
Transplants
Liver

ASJC Scopus subject areas

  • Radiology Nuclear Medicine and imaging

Cite this

Walser, E., Runyan, B. R., Heckman, M. G., Bridges, M. D., Willingham, D. L., Paz-Fumagalli, R., & Nguyen, J. H. (2011). Extrahepatic portal biliopathy: Proposed etiology on the basis of anatomic and clinical features. Radiology, 258(1), 146-153. https://doi.org/10.1148/radiol.10090923

Extrahepatic portal biliopathy : Proposed etiology on the basis of anatomic and clinical features. / Walser, Eric; Runyan, Brandon R.; Heckman, Michael G.; Bridges, Mellena D.; Willingham, Darrin L.; Paz-Fumagalli, Ricardo; Nguyen, Justin H.

In: Radiology, Vol. 258, No. 1, 01.2011, p. 146-153.

Research output: Contribution to journalArticle

Walser, E, Runyan, BR, Heckman, MG, Bridges, MD, Willingham, DL, Paz-Fumagalli, R & Nguyen, JH 2011, 'Extrahepatic portal biliopathy: Proposed etiology on the basis of anatomic and clinical features', Radiology, vol. 258, no. 1, pp. 146-153. https://doi.org/10.1148/radiol.10090923
Walser E, Runyan BR, Heckman MG, Bridges MD, Willingham DL, Paz-Fumagalli R et al. Extrahepatic portal biliopathy: Proposed etiology on the basis of anatomic and clinical features. Radiology. 2011 Jan;258(1):146-153. https://doi.org/10.1148/radiol.10090923
Walser, Eric ; Runyan, Brandon R. ; Heckman, Michael G. ; Bridges, Mellena D. ; Willingham, Darrin L. ; Paz-Fumagalli, Ricardo ; Nguyen, Justin H. / Extrahepatic portal biliopathy : Proposed etiology on the basis of anatomic and clinical features. In: Radiology. 2011 ; Vol. 258, No. 1. pp. 146-153.
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abstract = "Purpose: To compare the anatomic and clinical features in patients with chronic portal vein thrombosis (PVT) to determine why some patients develop portal biliopathy (PB) while most do not and propose an etiology for PB. Materials and Methods: This project satisfied HIPAA regulations and received institutional review board approval for a retrospective review without the need for consent. From 100 patients with PVT, 60 were extracted who had chronic, nonmalignant PVT, after exclusion of those with sclerosing cholangitis, liver transplants, choledocholithiasis, or portosystemic shunts. Clinical and imaging data from 19 patients with biliary dilatation (PB group) were compared with data from 41 patients without biliary dilatation (no-PB group). Statistical analysis was performed with the Fisher exact test for categorical variables or the Wilcoxon rank-sum test for numerical and ordered categorical variables. P values of.05 or less were considered to indicate a significant difference. Results: The etiology of PVT differed between the groups (P <.001); cirrhosis was infrequently seen in the PB group (two of 19, 11{\%}) but was common in the no-PB group (31 of 41, 76{\%}). Only two of 33 (6 {\%}) patients with cirrhosis and PVT had PB. Extension of PVT into the mesenteric veins was significantly more common in the PB group (18 of 19, 95{\%}) than in the no-PB group (one of 41, 2{\%}) (P <.001). Compared with the no-PB group, patients in the PB group had more acute angulation of the bile duct (median, 110° vs 128°; P =.008), less frequent gastroesophageal varices (three of 19 [16{\%}] vs 20 of 41 [49{\%}], P =.021), and a smaller mean coronary vein diameter (median, 5 vs 6 mm; P =.014). Conclusion: Noncirrhotic patients with hypercoagulable states tend to develop PB when PVT extends to the splenomesenteric veins. A possible etiology is the formation of specific peribiliary venous pathways responsible for bile duct compression and tethering.",
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AU - Bridges, Mellena D.

AU - Willingham, Darrin L.

AU - Paz-Fumagalli, Ricardo

AU - Nguyen, Justin H.

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N2 - Purpose: To compare the anatomic and clinical features in patients with chronic portal vein thrombosis (PVT) to determine why some patients develop portal biliopathy (PB) while most do not and propose an etiology for PB. Materials and Methods: This project satisfied HIPAA regulations and received institutional review board approval for a retrospective review without the need for consent. From 100 patients with PVT, 60 were extracted who had chronic, nonmalignant PVT, after exclusion of those with sclerosing cholangitis, liver transplants, choledocholithiasis, or portosystemic shunts. Clinical and imaging data from 19 patients with biliary dilatation (PB group) were compared with data from 41 patients without biliary dilatation (no-PB group). Statistical analysis was performed with the Fisher exact test for categorical variables or the Wilcoxon rank-sum test for numerical and ordered categorical variables. P values of.05 or less were considered to indicate a significant difference. Results: The etiology of PVT differed between the groups (P <.001); cirrhosis was infrequently seen in the PB group (two of 19, 11%) but was common in the no-PB group (31 of 41, 76%). Only two of 33 (6 %) patients with cirrhosis and PVT had PB. Extension of PVT into the mesenteric veins was significantly more common in the PB group (18 of 19, 95%) than in the no-PB group (one of 41, 2%) (P <.001). Compared with the no-PB group, patients in the PB group had more acute angulation of the bile duct (median, 110° vs 128°; P =.008), less frequent gastroesophageal varices (three of 19 [16%] vs 20 of 41 [49%], P =.021), and a smaller mean coronary vein diameter (median, 5 vs 6 mm; P =.014). Conclusion: Noncirrhotic patients with hypercoagulable states tend to develop PB when PVT extends to the splenomesenteric veins. A possible etiology is the formation of specific peribiliary venous pathways responsible for bile duct compression and tethering.

AB - Purpose: To compare the anatomic and clinical features in patients with chronic portal vein thrombosis (PVT) to determine why some patients develop portal biliopathy (PB) while most do not and propose an etiology for PB. Materials and Methods: This project satisfied HIPAA regulations and received institutional review board approval for a retrospective review without the need for consent. From 100 patients with PVT, 60 were extracted who had chronic, nonmalignant PVT, after exclusion of those with sclerosing cholangitis, liver transplants, choledocholithiasis, or portosystemic shunts. Clinical and imaging data from 19 patients with biliary dilatation (PB group) were compared with data from 41 patients without biliary dilatation (no-PB group). Statistical analysis was performed with the Fisher exact test for categorical variables or the Wilcoxon rank-sum test for numerical and ordered categorical variables. P values of.05 or less were considered to indicate a significant difference. Results: The etiology of PVT differed between the groups (P <.001); cirrhosis was infrequently seen in the PB group (two of 19, 11%) but was common in the no-PB group (31 of 41, 76%). Only two of 33 (6 %) patients with cirrhosis and PVT had PB. Extension of PVT into the mesenteric veins was significantly more common in the PB group (18 of 19, 95%) than in the no-PB group (one of 41, 2%) (P <.001). Compared with the no-PB group, patients in the PB group had more acute angulation of the bile duct (median, 110° vs 128°; P =.008), less frequent gastroesophageal varices (three of 19 [16%] vs 20 of 41 [49%], P =.021), and a smaller mean coronary vein diameter (median, 5 vs 6 mm; P =.014). Conclusion: Noncirrhotic patients with hypercoagulable states tend to develop PB when PVT extends to the splenomesenteric veins. A possible etiology is the formation of specific peribiliary venous pathways responsible for bile duct compression and tethering.

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