Exp Clin Endocrinol Diabetes 2005; 113(5): 268-274
DOI: 10.1055/s-2005-837546
Article

J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York

Fasting Hyperglucagonemia in Patients with Transjugular Intrahepatic Portosystemic Shunts (TIPS)

D. Raddatz1 , C. Roßbach1 , A. Buchwald2 , K.-H. Scholz2 , G. Ramadori1 , W. Nolte1
  • 1Department of Gastroenterology and Endocrinology, Georg-August-Universität Göttingen, Göttingen, Germany
  • 2Department of Cardiology, Georg-August-Universität Göttingen, Göttingen, Germany
Further Information

Publication History

Received: February 3, 2004 First decision: June, 28, 2004

Accepted: November 21, 2004

Publication Date:
30 May 2005 (online)

Abstract

Background: Hyperglucagonemia has been described to be associated with insulin resistance in patients with liver cirrhosis. Portosystemic shunts may be involved in the etiology of hyperglucagonemia. To test this hypothesis we investigated fasting peripheral plasma glucagon levels before and after portal decompression by transjugular intrahepatic portosystemic shunting (TIPS). Methods: Glucagon, insulin, plasma glucose, HbA1c, and C-peptide were determined in peripheral venous samples from 21 non-diabetic (ND)- and 15 diabetic patients (D; 3 treated with insulin, 3 with sulfonylurea, 9 with diet alone) with liver cirrhosis, showing comparable clinical features (gender, age, BMI, creatinine, Child-Pugh-score, complications, and etiology of liver cirrhosis) before, 3 and 9 months after elective TIPS implantation. Insulin resistance was calculated as RHOMA according to the homeostasis model assessment (HOMA). Results: Glucagon levels before TIPS were elevated in patients with diabetes compared to patients without diabetes (D: 145.4 ± 52.1 pg/ml vs. ND: 97.3 ± 49.8 pg/ml; p = 0.057). 3 and 9 months after TIPS implantation glucagon levels increased significantly in ND (188.9 ± 80.3 pg/ml and 187.2 ± 87.6 pg/ml) but not in D (169.6 ± 62.4 pg/ml and 171.9 ± 58.4 pg/ml). While plasma glucose, HbA1c, and C-peptide were significantly higher in D than in ND, they did not change significantly 3 and 9 months after TIPS implantation. Insulin was increased in D before TIPS (D: 31.6 ± 15.9 mU/l vs. ND: 14.8 ± 7.1 mU/l; p = 0.0001). 3 and 9 months after TIPS insulin significantly increased in ND (26.6 ± 14.7 mU/l and 23.2 ± 10.9 mU/l vs. 14.8 ± 7.1 mU/l before TIPS) but not in D. In ND RHOMA also increased from 3.5 ± 2 mU × mmol/l² to 5.7 ± 3.3 mU × mmol/l² after 3 and 5.4 ± 2.6 mU × mmol/l² after 9 months. BMI, liver and kidney function did not change with time. Conclusion: In non-diabetic cirrhotic patients TIPS implantation is followed by an increase of glucagon. However, this does not result in a worsening of glycemic control, probably because of a simultaneous increase of insulin.

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Dr. med. Dirk Raddatz

Department of Gastroenterology and Endocrinology, Georg-August-Universität

Robert-Koch-Straße 40

37075 Göttingen

Germany

Phone: + 49551396326

Fax: + 49 55 13 91 91 25

Email: draddat@gwdg.de

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