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C‐reactive protein and model for end‐stage liver disease score: Have we found the fifth element?
Author(s) -
Ruf Andres E.,
Villamil Federico G.
Publication year - 2015
Publication title -
liver transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.814
H-Index - 150
eISSN - 1527-6473
pISSN - 1527-6465
DOI - 10.1002/lt.24140
Subject(s) - medicine , decompensation , cirrhosis , ascites , liver transplantation , model for end stage liver disease , liver disease , portal hypertension , gastroenterology , transplantation , natural history , hepatorenal syndrome , chronic liver disease , liver function , creatinine
The natural history of cirrhosis varies from patient to patient, depends on a number of factors, and is largely unpredictable. The transition from the compensated phase to the decompensated phase is dictated on one hand by the loss of liver cell mass and on the other hand by the development of complications of portal hypertension. Many studies have confirmed that the Model for End-Stage Liver Disease (MELD) is highly accurate for assessing the degree of hepatic insufficiency and short-term prognosis (90 days) in patients with cirrhosis in both transplant and nontransplant settings. However, approximately 15% to 20% of candidates for liver transplantation are not well served by MELD. A few years ago, our group showed that the addition of serum sodium to the MELD formula significantly increased its efficacy. The replacement of MELD by MELD-Na will allow earlier access to liver transplantation, especially for patients with severe portal hypertension and ascites but with relatively well-preserved liver function and normal serum creatinine. Serum sodium thus became the fourth element of MELD. The transition to the decompensated stage of cirrhosis is usually a slow and gradual process evolving over months or even years. However, the natural course of cirrhosis is often complicated by acute episodes of decompensation triggered by a precipitating event. The outcome and reversibility of decompensation vary according to the nature and severity of the acute hepatic insult and according to the degree of dysfunction of extrahepatic organ systems. Recent studies have shown that in acutely ill patients with cirrhosis, systemic inflammatory response syndrome (SIRS), with or without a documented bacterial infection, is an independent predictor of survival and is also associated with the development of portal hypertension–related complications. Liver function appears not to be the main determinant of outcome in patients with cirrhosis who experience multiorgan failure. Therefore, the negative impact of systemic inflammation in this scenario may be poorly predicted by MELD. Conventional parameters for diagnosing SIRS lack sensitivity and specificity in patients with advanced cirrhosis because of hypersplenism, hyperventilation associated with encephalopathy, hyperkinetic circulation, or the use of beta-blockers. C-reactive protein (CRP) is considered a surrogate marker for acute or chronic systemic inflammation and bacterial infection, although elevated levels have been described in many other conditions, such as acute alcoholic hepatitis, malignant tumors (including hepatocellular carcinoma), tissue necrosis, and bacterial translocation. In a series of 148 consecutive patients with predominantly alcoholic cirrhosis and a Child-Pugh status B8, Cervoni et al. found that CRP was a statistically significant predictor of death [area under the receiver operating characteristic curve (AUROC), 0.63] and SIRS (AUROC, 0.73). The prognostic value of CRP was independent of SIRS, bacterial infection, and alcoholic hepatitis. Interestingly, the majority of patients with