Blood ammonia levels in liver cirrhosis: a clue for the presence of portosystemic collateral veins
1 Department of Clinical and Experimental Medicine, Hepatology in Internal Medicine Section, Federico II University Medical School of Naples, Naples, Italy
2 Hepatology Unit of General Medicine, Mauro Scarlato Hospital, Scafati, ASL SA/1, Naples, Italy
3 Department of Gastroenterology and Digestive Endoscopy, Second University of Naples (SUN), Naples, Italy
4 Geriatric Centre Frullone ASL NA/1, Naples, Italy
5 Department of Oncology and Endocrinology, Gastrointestinal Surgery Unit, Federico II University Medical School of Naples, Naples, Italy
BMC Gastroenterology 2009, 9:21 doi:10.1186/1471-230X-9-21Published: 17 March 2009
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.
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.
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).
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.