Folic acid, Homocysteine and CT Brain Findings in Patients of Liver Cell Failure

Eissa, Somaya Suliman; Tawfiq, Hend Mohammed; El Toukhy, Safinaz Ebrahim; Sherif, Hala Maghraby Maghraby; El-Naggar, Zeinab Abdo Mohammed

doi:10.21608/ejchem.2025.386788.11796

Folic acid, Homocysteine and CT Brain Findings in Patients of Liver Cell Failure

Articles in Press

Document Type : Original Article

Authors

¹ Professor of Internal Medicine, Faculty of Medicine (for girls), Al-Azhar University

² Professor of Medical Biochemistry, Medical Research & Clinical Studies Institute, National Research Centre

³ Professor of Radio Diagnosis, Faculty of Medicine (for girls), Al-Azhar University

⁴ Assistant Lecturer of Internal Medicine , Faculty of Medicine (for girls), Al-Azhar University. Cairo- Egypt

10.21608/ejchem.2025.386788.11796

Abstract

Liver cell failure is the final stage of chronic liver disease that results in disruption of liver architecture due to formation of widespread regeneration nodules surrounded by dense fibrotic septa. Cirrhosis is the 6th cause of death in developed countries. According to global burden of disease study in 2019, cirrhosis was associated with 4% of global deaths worldwide. The aim of our study is the assessment of serum Folic acid and Homocysteine in liver Cell Failure (LCF) patients and its correlation with CT brain Findings. This is a comparative study which was conducted on 80 subjects divided into two groups: Group I: 40 diagnosed cases of LCF, Group I then subdivided into: Sub group A (decompensated LCF presented with hepatic encephalopathy) (8 patients) and Sub Group B (decompensated LCF presented without hepatic encephalopathy) (32 patients), they were 30 males and 10 females, their age ranged from 50 to 65 years. group II: 40 healthy control subjects, they were 26 males and 14 females, their age ranged from 25 to 42 years. Results show significantly decrease in serum folic acid levels (< 0.001) in LCF patients as compared with control group. Liver plays an important role in metabolism of folic acid. In decompensated cirrhosis (LCF), there is defect in folic acid metabolism to THF resulting in folate deficiency. In the present work, we observed statistically significant increased serum Hcy levels (>0.001) in LCF patients as compared with control group. This is due to impaired Hcy metabolism in liver cirrhosis which is related to decreased availability or utilization of folates. Folates are methyl donor in the process of remethylation of Hcy into methionine which occurs in the healthy liver. Our work revealed presence of lacunar infarctions in 8 patients (20%) in CT brain and all patients with lacunar infarctions had hepatic encephalopathy. Presence of lacunar infarction may be explained by hyperhomocyteinemia (HHcy)which has cytopathic and cytotoxic effects on the endothelium and the platelets. HHcy makes the person more prone to endothelial cell injury and platelet aggregation leading to atherogenesis and ischemic injury especially in the small blood vessels of the brain. It can be concluded that the folic acid deficiency and hyperhomocyteinemia in LCF patients may play an etiological role in pathogenesis of lacunar infarction and hepatic encephalopathy.

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