ROLE OF PLASMA AMMONIA AS A PREDICTOR OF LIVER-RELATED MORBIDITY, HOSPITALIZATION, AND MORTALITY IN CLINICALLY STABLE CIRRRHOTIC PATIENTS | ||
ALEXMED ePosters | ||
Volume 7, Issue 3, July 2025, Pages 64-65 | ||
Document Type: Preliminary preprint short reports of original research | ||
DOI: 10.21608/alexpo.2025.427464.2277 | ||
Authors | ||
Amr Ali Abd El Moety1; Sameh Aldesoky Anwar Lashen2; Hend Naguib Abd El Motelub1; Eman Zakareya AbdElrahman3; Elsayed Khamis Abdraboh Elrashidy* 1 | ||
1Department of Internal Medicine, Faculty of Medicine, Alexandria University | ||
2Department of Internal Medicine, HPB Unit, Faculty of Medicine, Alexandria University. | ||
3Department of Clinical and Chemical Pathology, Faculty of Medicine Alexandria University | ||
Abstract | ||
Cirrhosis is the end-stage of chronic liver injury, characterized by fibrosis and regenerative nodules, most commonly caused by viral hepatitis, alcohol abuse, metabolic dysfunction, autoimmune, biliary, and genetic disorders. Staging distinguishes compensated (preserved function) from decompensated (ascites, bleeding, encephalopathy) phases. Prognosis and disease severity are guided by scoring systems, most notably Child-Pugh and MELD, each with unique strengths and limitations.(1) Ammonia is a gut-derived neurotoxin central to hepatic encephalopathy (HE), with a clear link to cerebral edema in acute liver failure, but its role in cirrhosis-related HE is less defined and remains controversial in routine practice. It also contributes to complications like liver cell injury, immune dysfunction, sarcopenia, and portal hypertension.(2) AIM The aim of the current study was to test the hypothesis that level of hyperammonemia is a predictive factor for liver-related complications and mortality in clinically stable cirrhotic patients. PATIENTS AND METHODS: This prospective, observational cohort study enrolled 100 adult patients aged over 18 years with established cirrhosis, confirmed by clinical features and characteristic ultrasonographic findings, from the Hepatobiliary Unit, Alexandria University Hospitals. Both compensated and decompensated but clinically stable patients were included, provided they had no acute decompensation, major bleeding, or any event requires hospital admission in the past 30 days, and no chronic kidney disease, malignancy, hematological disorders, prior organ transplant, or inherited hyperammonemia. All patients underwent clinical and laboratory assessments, including CBC, liver and renal function tests, serum electrolytes, AFP, and coagulation profile. | ||
Keywords | ||
Hyperammonemia; Liver disease biomarkers; Cirrhosis complications; Hepatic encephalopathy | ||
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