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World J Gastroenterol. Feb 7, 2008; 14(5): 795-799
Published online Feb 7, 2008. doi: 10.3748/wjg.14.795
Portalsystemic hemodynamic changes in chronic severe hepatitis B: An ultrasonographic study
Zhong-Zhen Su, Hong Shan, Wei-Min Ke, Bing-Jun He, Rong-Qin Zheng
Zhong-Zhen Su, Wei-Min Ke, Department of Infectious Diseases, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou 510630, Guangdong Province, China
Hong Shan, Bing-Jun He, Department of Radiology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou 510630, Guangdong Province, China
Rong-Qin Zheng, Department of Ultrasound, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou 510630, Guangdong Province, China
Correspondence to: Zhong-Zhen Su, Department of Infectious Diseases, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou 510630, Guangdong Province, China. sp9313@126.com
Telephone: +86-20-85252010
Fax: +86-20-87583501
Received: September 3, 2007
Revised: December 12, 2007
Published online: February 7, 2008
Abstract

AIM: To evaluate portalsystemic hemodynamic changes in chronic severe hepatitis B.

METHODS: Hemodynamic parameters included portal vein diameter (PVD), portal vein peak velocity (PVPV), portal vein volume (PVV), spleen length (SPL), spleen vein diameter (SPVD), spleen vein volume (SPVV) and umbilical vein recanalization. They were measured by Color Doppler ultrasonography in 36 patients with chronic severe hepatitis B, compared with 51 normal controls, 61 patients with chronic hepatitis B, 46 patients with compensable cirrhosis, and 36 patients with decompensable cirrhosis.

RESULTS: In the group of chronic severe hepatitis B, PVD (12.38 ± 1.23 mm) was significantly different from the normal control, compensable cirrhosis and decompensable cirrhosis groups (P = 0.000-0.026), but not significantly different from the chronic hepatitis group. PVPV (16.15 ± 3.82 cm/s) dropped more significantly in the chronic severe hepatitis B group than the normal control, chronic hepatitis B and compensable cirrhosis groups (P = 0.000-0.011). PVV (667.53 ± 192.83 mL/min) dropped significantly as compared with the four comparison groups (P = 0.000-0.004). SPL (120.42 ± 18.36 mm) and SPVD (7.52 ± 1.52 mm) were longer in the normal control and chronic hepatitis B groups (P = 0.000-0.009), yet they were significantly shorter than those in the decompensable cirrhosis group (P = 0.000). SPVV (242.51 ± 137.70 mL/min) was also lower than the decompensable cirrhosis group (P = 0.000). The umbilical vein recanalization rate (75%) was higher than the chronic hepatitis B and compensable cirrhosis groups. In the course of progression from chronic hepatitis to decompensable cirrhosis, PVD, SPL and SPVD gradually increased and showed significant differences between every two groups (P = 0.000-0.002).

CONCLUSION: Patients with chronic severe hepatitis B have a tendency to develop acute portal hypertension, resulting in significantly reduced portal vein perfusion. Observation of the portalsystemic hemodynamic changes may be contributed to the disease progression of chronic liver disease.

Keywords: Color doppler ultrasonography; Portalsystemic hemodynamics; Chronic severe hepatitis B