Blood Ammonia Level Correlates with Severity of Cirrhotic Portal Hypertensive Gastropathy

Abstract

Background Portal hypertensive gastropathy (PHG) is a common anomaly with potential for bleeding found in portal hypertension. Blood ammonia levels correlate well with liver disease severity and existence of portosystemic shunts. Increased ammonia results in vasodilation and hepatic stellate cell activation causing and exacerbating portal hypertension. Objective To assess the relation of blood ammonia to the presence and severity of portal hypertensive gastropathy in cirrhosis. Methods This cross-sectional study included 381 cirrhotics undergoing screening for esophageal varices (EV) divided into a portal hypertensive gastropathy group (203 patients with EV and PHG), esophageal varix group (41 patients with EV but no PHG), and control group (137 patients with no EV or PHG). A full clinical examination, routine laboratory tests, abdominal ultrasonography, child score calculation, and blood ammonia measurement were performed for all patients. Results Blood ammonia, portal vein, splenic vein, and splenic longitudinal diameters were significantly higher and platelet counts lower in patients with EV and EV with PHG than controls. Patients having EV with PHG had significantly higher bilirubin and ammonia than those with EV but no PHG. Severe PHG was associated with significantly higher ammonia, EV grades, and superior location and a lower splenic longitudinal diameter than mild PHG. The PHG score showed a positive correlation with blood ammonia and a negative correlation with splenic longitudinal diameter. Conclusions Blood ammonia levels correlate with the presence, severity, and score of portal hypertensive gastropathy in cirrhosis suggesting a causal relationship and encouraging trials of ammonia-lowering treatments for the management of severe PHG with a tendency to bleed.

Risk factors for portal hypertensive gastropathy

“…Some studies have indicated [20] that the occurrence of PHG is related to staged liver function, and the incidence of PHG is high in patients with Child-Pugh B and C cirrhosis, while the occurrence of PHG has nothing to do with Child-Pugh A. In contrast, El-Kalla et al [11] pointed out that the occurrence and severity of PHG were independent of liver function. Mezawa et al [21] pointed out that PHG was relieved after TIPS, but liver function did not change significantly before or two weeks after surgery, so it was speculated that PHG had no significant relationship with liver function.…”

“…Mandhwani et al [9], Sathar et al [10] and Tiwari et al [2] showed that there was a significant association between the occurrence of PHG and Child-Pugh stage. In contrast, El-Kalla et al [11] found no difference between them with respect to Child-Pugh stage. The major purpose of this study was to retrospectively evaluate the incidence of PHG and explore the relationship between PHG and gender, laboratory parameters, liver function and varicose veins.…”

The value of ammonia as a biomarker in patients with cirrhosis

“…Additionally, a single-center cross-sectional study involving 381 patients with HCV or hepatitis B virus (HBV)-related cirrhosis revealed that plasma ammonia correlates with the presence and severity of portal hypertensive gastropathy (PHG). Cases with severe PHG had significantly higher levels of blood ammonia (192.69 ± 59.87 vs.151.39 ± 54.37 μg/dL, p=0.026) (24). Despite all the evidence correlating ammonia levels with severity of liver disease (Table 1), there are significant overlaps between different stages that challenges its role as a biomarker for disease staging.…”

Avaliação sanguínea e salivar de compostos nitrogenados em pacientes cirróticos com e sem encefalopatia hepática

“…As consequências da hiperamonemia para a hipertensão portal têm sido estudadas in vitro e in vivo. Foi demonstrado que a diminuição de amônia sérica em um modelo de ratos cirróticos, é capaz de regular negativamente a ativação de células estrelárias do fígado e, consequentemente reduzir fatores fisiopatológicos determinantes no estabelecimento da hipertensão portal, sugerindo a amônia como uma possível terapia alvo para a redução da hipertensão portal (El-Kalla et al, 2018).…”