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Blood ammonia levels in liver cirrhosis: a clue for the presence of portosystemic collateral veins.

Tarantino G, Citro V, Esposito P, Giaquinto S, de Leone A, Milan G, Tripodi FS, Cirillo M, Lobello R - BMC Gastroenterol (2009)

Bottom Line: The resulting shunting is responsible for the development of portosystemic encephalopathy.Although ammonia plays a certain role in determining portosystemic encephalopathy, the venous ammonia level has not been found to correlate with the presence or severity of this entity.Realizing the need for non-invasive markers mirroring the presence of esophageal varices in order to reduce the number of endoscopy screening, we came back to determine whether there was a correlation between blood ammonia concentrations and the detection of portosystemic collateral veins, also evaluating splenomegaly, hypersplenism (thrombocytopenia) and the severity of liver cirrhosis.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Clinical and Experimental Medicine, Hepatology in Internal Medicine Section, Federico II University Medical School of Naples, Naples, Italy. tarantin@unina.it

ABSTRACT

Background: Portal hypertension leads to the formation of portosystemic collateral veins in liver cirrhosis. The resulting shunting is responsible for the development of portosystemic encephalopathy. Although ammonia plays a certain role in determining portosystemic encephalopathy, the venous ammonia level has not been found to correlate with the presence or severity of this entity. So, it has become partially obsolete. Realizing the need for non-invasive markers mirroring the presence of esophageal varices in order to reduce the number of endoscopy screening, we came back to determine whether there was a correlation between blood ammonia concentrations and the detection of portosystemic collateral veins, also evaluating splenomegaly, hypersplenism (thrombocytopenia) and the severity of liver cirrhosis.

Methods: One hundred and fifty three consecutive patients with hepatic cirrhosis of various etiologies were recruited to participate in endoscopic and ultrasonography screening for the presence of portosystemic collaterals mostly esophageal varices, but also portal hypertensive gastropathy and large spontaneous shunts.

Results: Based on Child-Pugh classification, the median level of blood ammonia was 45 mcM/L in 64 patients belonging to class A, 66 mcM/L in 66 patients of class B and 108 mcM/L in 23 patients of class C respectively (p < 0.001).The grade of esophageal varices was concordant with venous ammonia levels (rho 0.43, p < 0.001). The best area under the curve was given by ammonia concentrations, i, e., 0.78, when comparing areas of ammonia levels, platelet count and spleen longitudinal diameter at ultrasonography. Ammonia levels predicted hepatic decompensation and ascites presence (Odds Ratio 1.018, p < 0.001).

Conclusion: Identifying cirrhotic patients with high blood ammonia concentrations could be clinically useful, as high levels would lead to suspicion of being in presence of collaterals, in clinical practice of esophageal varices, and pinpoint those patients requiring closer follow-up and endoscopic screening.

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Hidden relationships unravelled by the Factor Analysis. Percent of Total Variance Explained by factors: 1 (24.4); 2 (16.3); NH4, Ammonia; PLTs, Platelets count; SLD, Spleen Longitudinal Diameter; EV, Esophageal Varices; PHG, Portal Hypertensive Gastropathy; LSS, Large Spontaneous Shunts; ALT, ALanin Transferase; the critical value was calculated by the formula: Pearson's correlation coefficient for 1% level of significance/square root of patients minus 2, i.e., 419.
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Figure 1: Hidden relationships unravelled by the Factor Analysis. Percent of Total Variance Explained by factors: 1 (24.4); 2 (16.3); NH4, Ammonia; PLTs, Platelets count; SLD, Spleen Longitudinal Diameter; EV, Esophageal Varices; PHG, Portal Hypertensive Gastropathy; LSS, Large Spontaneous Shunts; ALT, ALanin Transferase; the critical value was calculated by the formula: Pearson's correlation coefficient for 1% level of significance/square root of patients minus 2, i.e., 419.

Mentions: An inverse correlation, i.e., rho -0.53 (p = < 0.0001) was detected between SLD and PLTS count. By detecting the structure in the relationships among variables (Factor Analysis), the EV presence showed the highest value, i.e., 0.716 followed by the classic sign of portal hypertension, i.e., splenomegaly at US and by the severity of liver cirrhosis, weighted as Child-Pug's classification, but not the PHG evidence, Figure 1. In the same setting, interestingly, LSS were correlated to the liver cirrhosis aetiology, being more frequent, but not statistically different, in cryptogenic form (chi square for trend 3.1, p = 0.07).


Blood ammonia levels in liver cirrhosis: a clue for the presence of portosystemic collateral veins.

Tarantino G, Citro V, Esposito P, Giaquinto S, de Leone A, Milan G, Tripodi FS, Cirillo M, Lobello R - BMC Gastroenterol (2009)

Hidden relationships unravelled by the Factor Analysis. Percent of Total Variance Explained by factors: 1 (24.4); 2 (16.3); NH4, Ammonia; PLTs, Platelets count; SLD, Spleen Longitudinal Diameter; EV, Esophageal Varices; PHG, Portal Hypertensive Gastropathy; LSS, Large Spontaneous Shunts; ALT, ALanin Transferase; the critical value was calculated by the formula: Pearson's correlation coefficient for 1% level of significance/square root of patients minus 2, i.e., 419.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2662872&req=5

Figure 1: Hidden relationships unravelled by the Factor Analysis. Percent of Total Variance Explained by factors: 1 (24.4); 2 (16.3); NH4, Ammonia; PLTs, Platelets count; SLD, Spleen Longitudinal Diameter; EV, Esophageal Varices; PHG, Portal Hypertensive Gastropathy; LSS, Large Spontaneous Shunts; ALT, ALanin Transferase; the critical value was calculated by the formula: Pearson's correlation coefficient for 1% level of significance/square root of patients minus 2, i.e., 419.
Mentions: An inverse correlation, i.e., rho -0.53 (p = < 0.0001) was detected between SLD and PLTS count. By detecting the structure in the relationships among variables (Factor Analysis), the EV presence showed the highest value, i.e., 0.716 followed by the classic sign of portal hypertension, i.e., splenomegaly at US and by the severity of liver cirrhosis, weighted as Child-Pug's classification, but not the PHG evidence, Figure 1. In the same setting, interestingly, LSS were correlated to the liver cirrhosis aetiology, being more frequent, but not statistically different, in cryptogenic form (chi square for trend 3.1, p = 0.07).

Bottom Line: The resulting shunting is responsible for the development of portosystemic encephalopathy.Although ammonia plays a certain role in determining portosystemic encephalopathy, the venous ammonia level has not been found to correlate with the presence or severity of this entity.Realizing the need for non-invasive markers mirroring the presence of esophageal varices in order to reduce the number of endoscopy screening, we came back to determine whether there was a correlation between blood ammonia concentrations and the detection of portosystemic collateral veins, also evaluating splenomegaly, hypersplenism (thrombocytopenia) and the severity of liver cirrhosis.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Clinical and Experimental Medicine, Hepatology in Internal Medicine Section, Federico II University Medical School of Naples, Naples, Italy. tarantin@unina.it

ABSTRACT

Background: Portal hypertension leads to the formation of portosystemic collateral veins in liver cirrhosis. The resulting shunting is responsible for the development of portosystemic encephalopathy. Although ammonia plays a certain role in determining portosystemic encephalopathy, the venous ammonia level has not been found to correlate with the presence or severity of this entity. So, it has become partially obsolete. Realizing the need for non-invasive markers mirroring the presence of esophageal varices in order to reduce the number of endoscopy screening, we came back to determine whether there was a correlation between blood ammonia concentrations and the detection of portosystemic collateral veins, also evaluating splenomegaly, hypersplenism (thrombocytopenia) and the severity of liver cirrhosis.

Methods: One hundred and fifty three consecutive patients with hepatic cirrhosis of various etiologies were recruited to participate in endoscopic and ultrasonography screening for the presence of portosystemic collaterals mostly esophageal varices, but also portal hypertensive gastropathy and large spontaneous shunts.

Results: Based on Child-Pugh classification, the median level of blood ammonia was 45 mcM/L in 64 patients belonging to class A, 66 mcM/L in 66 patients of class B and 108 mcM/L in 23 patients of class C respectively (p < 0.001).The grade of esophageal varices was concordant with venous ammonia levels (rho 0.43, p < 0.001). The best area under the curve was given by ammonia concentrations, i, e., 0.78, when comparing areas of ammonia levels, platelet count and spleen longitudinal diameter at ultrasonography. Ammonia levels predicted hepatic decompensation and ascites presence (Odds Ratio 1.018, p < 0.001).

Conclusion: Identifying cirrhotic patients with high blood ammonia concentrations could be clinically useful, as high levels would lead to suspicion of being in presence of collaterals, in clinical practice of esophageal varices, and pinpoint those patients requiring closer follow-up and endoscopic screening.

Show MeSH
Related in: MedlinePlus