Abstract
Background: The inflammatory process has an important role in the pathophysiology of hepatic encephalopathy (HE) in liver cirrhosis. IL-18 is a key mediator who plays a role in neuroinflamation processes that can lead to symptoms of HE. This study aimed to determine serum IL-18 levels in liver cirrhosis patients and to assess the association of serum IL-18 levels with HE.Method: A total of 52 subjects (32 patients with liver cirrhosis and 20 healthy controls) were enrolled in this study. Thirty two (32) patients with liver cirrhosis will be assessed for HE based on West-Haven criteria. All subjects were examined for serum IL-18 levels which is measured by ELISA method. We performed a comparative analysis between serum IL-18 levels of liver cirrhosis patients and healthy controls, a correlation analysis between serum IL-18 levels and HE, and a comparative analysis of serum IL-18 levels among degrees of HE.Results: Mean serum IL-18 levels in the liver cirrhosis group were 688.5 ± 674.3 pg/mL, and in the healthy controls group were 163.9 ± 100 pg/mL with p value = 0.01 (p 0.05). There was a significant correlation between IL-18 and HE (r = 0.85; p = 0.00). Serum IL-18 levels in covert and overt HE groups were significantly higher than those without HE (p 0.05).Conclusion: Serum IL-18 levels were significantly higher in liver cirrhosis patients than in healthy controls. There was a positive correlation between IL-18 and HE. Serum IL-18 levels in liver cirrhosis patients with HE were significantly higher than those without HE.
Highlights
Hepatic encephalopathy (HE) is a neuropsychiatric syndrome associated with chronic and acute liver dysfunction, with clinical spectrum of neuropsychological disorders range from mild to coma.[1]
Serum IL-18 levels were significantly higher in liver cirrhosis patients than in healthy controls
There were 52 subjects were enrolled during this study that consist of 32 patients with liver cirrhosis and 20 people as healthy control
Summary
Hepatic encephalopathy (HE) is a neuropsychiatric syndrome associated with chronic and acute liver dysfunction, with clinical spectrum of neuropsychological disorders range from mild (subclinical) to coma.[1]. The inflammatory process appears to be a key factor for HE, in addition to disturbed gastrointestinal tract disorders which lead to microbiota dysbiosis, overgrowth of bacteria, bacterial translocation, systemic endotoxaemia and immune dysfunction.[1] Shawcross shows that patients with liver cirrhosis with hyperamonia due to amino acid oral administration to sepsis conditions, there are increases in proinflammatory mediators such as TNF-α, IL-1β and IL-6, and poor neuropsychiatric examination results. This is different than patients with hyperamonia without an inflammatory condition.[7] This suggests that hyperamonia alone is not enough to make patients with liver cirrhosis fall into HE. This study aimed to determine serum IL-18 levels in liver cirrhosis patients and to assess the association of serum IL-18 levels with HE
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