Journal of Gastroenterology, volume 50, issue 6, pages 683-693

Pancreatic congestion in liver cirrhosis correlates with impaired insulin secretion

Taira Kuroda 1
Masashi Hirooka 1
Mitsuhito Koizumi 1
Hironori Ochi 1
Yoshiko Hisano 2
Kenji Bando 3
Bunzo Matsuura 1
Teru Kumagi 1
Yoichi Hiasa 1
Show full list: 9 authors
Publication typeJournal Article
Publication date2014-10-05
scimago Q1
SJR2.099
CiteScore12.2
Impact factor6.9
ISSN09441174, 14355922
Gastroenterology
Abstract
Although impaired glucose tolerance is common in cirrhosis, this condition’s pathogenesis remains undefined. This study aimed to clarify pathogenesis related to the pancreas in cirrhotic patients, and to evaluate associations between insulin secretion and pancreatic congestion due to portal hypertension. Pancreatic perfusion parameters were analyzed by dynamic contrast-enhanced ultrasound (CE-US) in 41 patients (20 cirrhotic, 21 non-cirrhotic; age, 67.9 ± 13.3; female, 19), and prospectively compared to delta C-peptide immunoreactivity (ΔCPR). In a separate study, a retrospective chart review with human autopsy specimens was conducted, and vessels and islets of the pancreas were analyzed in 43 patients (20 cirrhotic, 23 controls; age, 71.5 ± 11.6; female, 15). In the CE-US study, the clinical characteristics indicative of portal hypertension (e.g., ascites and varices) had significantly higher incidences in the cirrhotic group than in the control group. Pancreatic drainage times were greater in the cirrhotic group (p < 0.0001), and had a significant negative correlation with ΔCPR (R = 0.42, p = 0.0069). In the histopathological study, the islets were enlarged in the cirrhotic group (p < 0.0001). However, the percentage of insulin-positive area per islet was decreased in the cirrhotic group (p < 0.0001), and had a significant negative correlation with the wall thickness of the pancreatic vein (R = 0.63, p < 0.0001). Pancreatic congestion was present in cirrhotic patients. Moreover, pancreatic congestion and insulin secretion were significantly correlated. This pathogenesis could be a key factor underlying the development of hepatogenous diabetes in cirrhotic patients.
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