High prevalence of normal serum albumin in NASH patients with ascites: A retrospective analysis

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• 作者：Achuthan Sourianarayanane^a ; ^{souria@upmc.edu} ; Robert S. O'Shea^a ; ^b ; David S. Barnes^a ; Arthur J. McCullough^a ; ^b
• 关键词：HVPG ; Hepatic venous pressure gradient ; SAAG ; Serum ascites albumin gradient ; CTP ; Child Turcotte Pugh ; MELD ; Model for End-Stage Liver Disease ; NASH ; Non-alcoholic steatohepatitis ; HCV ; Hepatitis C virus ; TIPS ; Transjugular Intrahepatic Porto-systemic Sh
• 刊名：Clinics and Research in Hepatology and Gastroenterology
• 出版年：2013
• 出版时间：June, 2013
• 年：2013
• 卷：37
• 期：3
• 页码：246-253
• 全文大小：572 K

文摘

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Summary

Background

Ascites usually occurs in the setting of end-stage liver disease and low serum albumin and is associated with increased mortality. However, some patients develop ascites despite normal serum albumin (NSA), when a higher portal pressure and/or enhanced renal sodium retention would be expected. This study investigated the relationship between the hepatic venous pressure gradient (HVPG) and serum albumin in ascitic patients with different etiologies of cirrhosis and mortality.

Methods

Records of all patients with non-malignant ascites who underwent HVPG measurement from 2005 to 2009 were reviewed.

Results

One hundred and thirty-eight 138 patients met inclusion criteria; 18.8 % had NSA. No difference in sodium excretion or diuretic use was noted in patients with and without NSA. NASH patients were more likely to have a NSA (34.2 % vs 12.4 % ; P = 0.001) as well as lower HVPG (15 vs 17.9 mmHg; P = 0.009) compared to other etiologies. MELD and HVPG predicted overall survival. However, mortality did not differ by disease etiology, though NASH patients had lower CTP (7.6 vs 8.5; P < 0.001) and MELD (15.6 vs 18.1; P = 0.09) scores, particularly among patients who died.

Conclusions

In patients with ascites and NSA, there were no increase in HVPG or urinary sodium retention. NASH patients with ascites had lower HVPG and a higher prevalence of NSA. They also had a higher mortality relative to MELD and CTP scores in other patients. In these patients, mechanisms other than portal and oncotic pressures and sodium retention play a role in ascites development, and increase mortality rate when complicated by low albumin.