Liver cirrhosis is a major burden on public health, and causes a significant number of deaths globally [1] and also in Bangladesh [2]. It is estimated that around one million deaths are attributed to liver cirrhosis each year [3]. The significant causes of mortality and morbidity in patients of cirrhosis are hepatic encephalopathy (HE), ascites, hepatorenal syndrome (HRS), and esophageal variceal bleeding [4]. Hepatic encephalopathy is a complex neuropsychiatric syndrome manifested by a wide spectrum of changes in consciousness, ranging from subtle behavioral abnormalities to deep coma and death [5]. The mechanism of hepatic encephalopathy is complex and has not been conclusively established [6]. The common precipitating factors are gastrointestinal bleeding, infection, azotemia, constipation, high protein diet, and electrolyte imbalance. Sedatives, analgesics, diuretics, and large-volume paracentesis have also been considered as precipitants of hepatic encephalopathy in a stable patient of cirrhosis [7]. Still, definite precipitating factors could not be identified in a significant number of patients ranging from 10 % to 30 % [8], [9], [10]. The risk for the first bout of overt hepatic encephalopathy is 5 %-25 % within 5 years after cirrhosis diagnosis, depending on the presence of risk factors [11] and the survival probability was 42 % at 1 year of follow-up and 23 % at 3 years after developing the first episode of acute hepatic encephalopathy [12]. In addition to increased morbidity and mortality, overt hepatic encephalopathy negatively affects both physical and mental aspects of quality of life, whereas subclinical encephalopathy affects mainly the mental aspects, independently of liver disease severity [13].

Vitamin D is a fat-soluble vitamin, mostly synthesized in the skin from exposure to sunlight [14], further metabolized in the liver to 25-hydroxyvitamin D [25 (OH) D] and in the kidneys to its active form, 1,25-dihydroxy vitamin D [15]. Vitamin D plays an important role in bone metabolism and maintaining normal skeletal architecture. The role of vitamin D has also been demonstrated in the immune system, anti-fibrotic effect, neurodevelopment, and brain function [15], [16], [17]. Besides, studies have also demonstrated an association between low vitamin D with increased risk of mortality [18], and decompensation [19] in patients with cirrhosis. Patients with hepatic encephalopathy have been shown to have significantly lower serum 25 (OH) D levels than non-encephalopathy patients [20], [21], [22], [23]. This correlation suggests that vitamin D deficiency may have an unrecognized role in the development of hepatic encephalopathy. However, there are very few studies that have examined the association of serum 25 (OH) D deficiency in hepatic encephalopathy. Thus, this study aimed to see the association of serum 25 (OH) D with hepatic encephalopathy in patients with liver cirrhosis.