Melatonin Levels in Serum and Ascitic Fluid of Patients with Hepatic Encephalopathy

Cezary Chojnacki,Janusz Błasiak,Jan Chojnacki,Marek Romanowski,Katarzyna Winczyk

doi:10.1155/2012/510764

Cezary Chojnacki, Janusz Błasiak + Show 3 more

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https://doi.org/10.1155/2012/510764

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Abstract

Cirrhotic patients exhibit disturbed melatonin homeostasis, which may lead to sleep disturbances, but an influence on the hepatic encephalopathy has not been elucidated. Aim. In the present study, the association of melatonin levels in serum and ascitic fluid and ammonia concentration related to the intensity of hepatic encephalopathy (HE) was investigated. Material and Methods. The study included 90 alcoholic patients with hepatic encephalopathy and 30 healthy volunteers (C). Patients were divided in three groups according to 0–4 West-Haven Score: HE1 (n = 28), HE2 (n = 30), and HE3 (n = 32). Melatonin was measured by radioimmune assay. Results. In fasting patients with hepatic encephalopathy we noted higher melatonin serum levels [pg/mL] than in healthy subjects groups: C—11.3 ± 3.9, HE1 – 34.3 ± 12.2 (P < 0.01), HE2—54.8 ± 23.9, and HE3—119.8 ± 96.4 (P < 0.001). No correlation between melatonin and ammonia levels was found. Melatonin was detected in ascetic fluid in 24 patients of group HE2 and 27 patients of group HE2 of hepatic encephalopathy. Conclusions. Our results suggest that high blood levels of melatonin in cirrhotic liver patients may account for some of the clinical manifestations of hepatic encephalopathy, for example, daytime sleepiness, fatigue.

Highlights

Hepatic encephalopathy (HE) is a complex neuropsychiatric syndrome which is characterized by disturbances in behavioral and consciousness as well as neurological symptoms
High levels of ammonia were not observed in all hepatic encephalopathy patients, indicating that other chemical substances should be considered as pathogenetic factors
Serum melatonin level in healthy subjects was 11.3 ± 3.9 pg/mL, and it was significantly higher in cirrhotic patients and strongly depended on the degree of hepatic insufficiency (Figure 1)

Summary

Introduction

Hepatic encephalopathy (HE) is a complex neuropsychiatric syndrome which is characterized by disturbances in behavioral and consciousness as well as neurological symptoms Detailed pathophysiology of this disease remains unknown, but some of the pathogenetic factors have been identified. Ammonia has been identified as a factor of hepatic encephalopathy pathogenesis It disturbs enzymatic processes in brain tissue, inhibits the activity of acetylcholine and dopamine, and increases accumulation of false neurotransmitters [1]. Possible candidates are the excess of methionine and its mercaptan derivatives as well as aromatic amino acids (phenylalanine, tyrosine, tryptophan, and methionine) These agents block the synthesis of physiological neurotransmitters and induce the production of false ones, including octopamine, which may replace normal neurotransmitters, especially noradrenaline and dopamine in synapses. The influence of melatonin on CNS in individuals with liver insufficiency has not been sufficiently recognized

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