Mohamed Yousri Taher1, Abeer El-Hadidi2, Assem El-Shendidi1, Ahmed Sedky1. 1. Department of Internal Medicine (Hepatology Division), Faculty of Medicine, Alexandria University, Alexandria, Egypt. 2. Department of Clinical and Chemical Pathology, Faculty of Medicine, Alexandria University, Alexandria, Egypt.
Abstract
Introduction: Activation of hepatic macrophages in liver disease is pathogenically related to portal hypertension (PH). Soluble CD163 (sCD163) is shed in blood by activated macrophages and may predict PH progression noninvasively. This study was designed to investigate the relation of serum sCD163 to the grade and bleeding risk of esophageal varices (EV) and its role for prediction of variceal hemorrhage (VH). Methods: The study included cirrhotic patients divided into 3 groups: patients who presented with acute upper gastrointestinal bleeding (UGIB) proved to originate from EV on endoscopy, patients without any history of UGIB but who revealed EV on surveillance endoscopy, and patients without endoscopic evidence of varices. Variceal grade and risk signs and bleeding stigmata were noted simultaneously with measurement of serum sCD163 concentration. Results: Serum sCD163 concentration showed a significant increase in cirrhotic patients compared to healthy subjects (p < 0.001) with a stepwise increase among the group without varices, nonbleeder group, and bleeder group sequentially. Serum sCD163 levels correlated positively with the variceal grade and risk signs in both the bleeder and nonbleeder groups (p = 0.002, p < 0.001 and p = 0.004, p < 0.001, respectively). Serum sCD163 at a cutoff value of 3.6 mg/L performed significantly for prediction of EV presence (AUC = 0.888). Serum sCD163 at a cutoff value >4 mg/L significantly predicted large-size and high-risk EV (AUC = 0.910 and AUC = 0.939, respectively) and the index bleed risk (AUC = 0.977). Serum sCD163 at a cutoff value >4.05 mg/L modestly discriminated bleeding EV from those that had never bled (AUC = 0.811). Conclusions: Serum sCD163 levels accurately predicted high-grade and high-risk EV and could help plan for primary prophylaxis. However, it modestly identified VH occurrence, and endoscopy would be required to make a definitive diagnosis.
Introduction: Activation of hepatic macrophages in liver disease is pathogenically related to portal hypertension (PH). Soluble CD163 (sCD163) is shed in blood by activated macrophages and may predict PH progression noninvasively. This study was designed to investigate the relation of serum sCD163 to the grade and bleeding risk of esophageal varices (EV) and its role for prediction of variceal hemorrhage (VH). Methods: The study included cirrhotic patients divided into 3 groups: patients who presented with acute upper gastrointestinal bleeding (UGIB) proved to originate from EV on endoscopy, patients without any history of UGIB but who revealed EV on surveillance endoscopy, and patients without endoscopic evidence of varices. Variceal grade and risk signs and bleeding stigmata were noted simultaneously with measurement of serum sCD163 concentration. Results: Serum sCD163 concentration showed a significant increase in cirrhotic patients compared to healthy subjects (p < 0.001) with a stepwise increase among the group without varices, nonbleeder group, and bleeder group sequentially. Serum sCD163 levels correlated positively with the variceal grade and risk signs in both the bleeder and nonbleeder groups (p = 0.002, p < 0.001 and p = 0.004, p < 0.001, respectively). Serum sCD163 at a cutoff value of 3.6 mg/L performed significantly for prediction of EV presence (AUC = 0.888). Serum sCD163 at a cutoff value >4 mg/L significantly predicted large-size and high-risk EV (AUC = 0.910 and AUC = 0.939, respectively) and the index bleed risk (AUC = 0.977). Serum sCD163 at a cutoff value >4.05 mg/L modestly discriminated bleeding EV from those that had never bled (AUC = 0.811). Conclusions: Serum sCD163 levels accurately predicted high-grade and high-risk EV and could help plan for primary prophylaxis. However, it modestly identified VH occurrence, and endoscopy would be required to make a definitive diagnosis.
Authors: Lehn K Weaver; Katharine A Hintz-Goldstein; Patricia A Pioli; Kathleen Wardwell; Nilofer Qureshi; Stefanie N Vogel; Paul M Guyre Journal: J Leukoc Biol Date: 2006-07 Impact factor: 4.962
Authors: Anthony Rode; Amanda Nicoll; Holger Jon Møller; Lucy Lim; Peter W Angus; Ian Kronborg; Niranjan Arachchi; Alexandra Gorelik; Danny Liew; Konstantin Kazankov; Hendrik Vilstrup; Henning Grønbæk Journal: Gut Date: 2013-02-26 Impact factor: 23.059