One of the leading causes of chronic liver disease worldwide is fatty liver disease (FLD) [1]. FLD may result from non-alcoholic causes, such as non-alcoholic fatty liver disease (NAFLD), or from excessive alcohol usage, such as alcoholic fatty liver disease (AFLD). While nonalcoholic fatty liver disease (NAFLD) encompasses a range of liver disorders from simple steatosis to non-alcoholic steatohepatitis (NASH), advanced fibrosis, and cirrhosis, alcoholic fatty liver disease (AFLD) is the initial stage of alcoholic liver disease (ALD), which follows acute alcohol ingestion and is typically reversible with alcohol abstinence [2]. One of the most prevalent public health issues in emerging nations these days is alcohol usage. The most prevalent chronic liver illness, nonalcoholic fatty liver disease (NAFLD), is typified by an abnormal

buildup of hepatic triglycerides. NAFLD is thought to affect 25% of people worldwide [3]. In 2020, Eslam and George were part of a worldwide team of experts that suggested changing the name of NAFLD to metabolic associated fatty liver disease (MAFLD) in order to better reflect metabolic events [4]. Type 2 diabetes mellitus (T2DM), metabolic syndrome (Mets), cardiovascular disease (CVD), and other metabolic illnesses that are linked by systemic inflammation are all based on non-alcoholic fatty liver disease (NAFLD) [5].  The major immune cells that make up the complete blood count (CBC) compartments platelets, lymphocytes, monocytes, and neutrophils all mediate inflammatory and metabolic processes at the same time [6]. While platelets and neutrophils contribute to the generation of cytokines and chemokines,

monocytes, which are a component of the phagocytic immune system, play crucial roles in inflammation [7]. ].  Recently, there has been a lot of interest in clinical settings in systemic inflammatory indices (SIIs), such as monocyte-to-lymphocyte ratio (MLR), neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and monocyte-to-high-density lipoprotein cholesterol (HDL-C) ratio (MHR) [8]. SIIs are straightforward, non-invasive, and helpful indicators of the prognosis, diagnosis, and risk assessment for metabolic disorders, notwithstanding the viability of these blood standard tests [9].

This was a comparative observational study were recruited 100 patients with fatty liver disease (50 alcoholic fatty liver diseases and 50 non-alcoholic fatty liver diseases).

Inclusion criteria:

• Patients age ranged from 21-50 years with both gender
• Patients who had a significant history of alcohol consumption exceeding 210 gm/ week in males and 140gm/week in females for the last 2 year and ultrasound showing fatty liver taken for AFLD
• Patients with no history of alcohol consumption and ultrasound showing fatty liver were taken for NAFLD
• Patients who given written informed consent for the study

Exclusive criteria

• Patients with history of hepatitis, diabetes mellitus, thyroid disorders, heart disease
• Patients who were using drugs which can affect Heart Rate Variability (HRV)
• Patients who not given consent for the study

Complete history, socio-demographic features (age, gender, residential status, socio-economic class, education, occupation, etc) and examination was done in all the patients

Venous blood samples for all the patients were taken in the morning after an overnight fast of more than 10 hours. Total leukocyte count (TLC), neutrophil and lymphocyte count were done in an automated hematology analyzers. Neutrophil lymphocyte ratio (N/L ratio) was calculated by dividing the absolute neutrophil count by the absolute lymphocyte count. The erythrocyte sedimentation rate (ESR) is determined by Westergren’s method. Total bilirubin, direct bilirubin, indirect bilirubin, AST, ALT, GGT, Alkaline phosphatase (ALP), total protein, albumin, and globulin levels were estimated.

Statistical Analysis: Statistical Package for Social Sciences (SPSS) version 22.0 was used for statistical analysis. Comparison of mean values between two groups was done by using Student t-test (un-paired). Pearson correlation test was used to see the relationship between the variables. ‘P’ value of <0.05 was considered statistically significant.

Our study was enrolled 50 confirmed cases of AFLD and 50 cases of NAFLD. Majority of the patients were males (82% in AFLD and 66% in NAFLD) in both the groups. The mean age of AFLD was 43.62±2.82 years and that of NAFLD was 48.94±1.63 years. So, there was a significant difference between the ages and gender of AFLD and NAFLD (p<0.05). Most of them resided in rural area (68% and 62% in AFLD and NAFLD groups respectively), education up to primary school (40% and 42% respectively). 24% AFLD were obese with BMI > 29.9 kg/m and 46% cases were overweight with BMI of 25-29.9 kg/m², whereas among NAFLD 28% had obese and 42% were overweight.

Table 1: Demographic profile among alcoholic and non alcoholic liver disease

Table 2 shows the distribution of liver function test of all the subjects. The mean values of total bilirubin, direct bilirubin, indirect bilirubin and alkaline phosphatase were higher in AFLD as compared to NAFLD, but not significant (p>0.05). Liver enzymes AST and GGT were significantly higher in AFLD, whereas ALT was significantly lower in AFLD as compared to NAFLD (p<0.05). Total protein, albumin and globulin were significantly higher in NAFLD as compared to AFLD, while A/G ratio slightly lower in AFLD as compared to NAFLD.

Table 2: Distribution of liver function test in Alcoholic and non alcoholic fatty liver disease

The mean values of TLC, ESR, CRP, IL-6 and TNF-α were statistically significantly higher in alcoholic fatty liver disease patients as compared to non alcoholic fatty liver diseases patients (p<0.05), while lymphocyte count was significantly lower in AFLD patients as compared with the NAFLD (p<0.05). The mean value of Neutrophil count, and N/L ratio was higher in AFLD

patients when compared with the NAFLD patients, but not significantly significant (p>0.05).

Table 3: Comparison of inflammatory markers in AFLD versus NAFLD patients

Non-alcoholic Fatty livers have inflammation and liver cell damage, as well as fat in the liver. Liver steatosis, or fibrosis, can be brought on by inflammation and damage to the liver's cells. Later on, it could result in liver cancer or cirrhosis. TNF-α, IL, interferon, and high-sensitivity C-reactive protein are examples of pro-inflammatory cytokines that are involved in the pathogenesis of liver disease. Additionally, an excess of reactive oxygen species (ROS) generated by hepatic cell lipid accumulation leads to oxidative stress, which in turn produces hepatic inflammation, cytokine release, and hepatic cell lipid peroxidation [10].

In our study AFLD and NAFLD both are predominantly occurs in males as compared to females and male percentage were significantly higher in AFLD as compared to NAFLD, our results were correlates with the Ashwiani, et al [11].

We have observed that BMI were significantly higher among alcoholic and non alcoholic fatty liver disease patients as compared to normal population, in agreement with the a study done by Khura J et al [12].

The mean age of AFLD patients was 43.62±2.82 years in the current research in accordance with the Arefhosseini, et al [13].

The present study found that the values of TLC and ESR were significantly higher, whereas the value of lymphocytes was significantly lower in AFLD as compared to NAFLD, our finding are consistent with the Das et al [14] and Wang et al [15].

This could be due to various inflammatory mediators is increased in ALD and NAFLD which promote liver damage and inflammatory reactions in early ALD and NAFLD. The higher values of neutrophils, TLC and ESR are suggestive of presence of chronic low-grade inflammation in patients with fatty liver disease.

Inflammatory markers such as CRP, IL-6 and TNF-α were statistically significantly higher in alcoholic fatty liver disease patients as compared to non alcoholic fatty liver diseases in this research, similar findings were reported by Nigma et al [16] and Wu Suna, et al [17].

The mechanism linking the inflammatory markers with fatty liver disease remains unclear although several explanations could be offered. An important step in the development of fatty liver disease is hepatic lipid accumulation which provides a source of oxidative stress triggering the inflammatory process.

In the present study liver enzymes AST and GGT were significantly higher in AFLD, whereas ALT was significantly lower in AFLD as compared to NAFLD, our results comparable with the Devi, et al [18] and Dyson JK, et al [19].

In our study total serum protein, albumin and globulin were significantly higher in NAFLD as compared to AFLD, accordance with the Duan Y, et al [20] and Niemela O, et al [21].

Inflammatory markers and liver enzymes are significantly elevated in both AFLD and NAFLD patients, indicating the presence of low grade inflammation. Inflammatory markers like TLC, neutrophils, ESR, CRP, IL-6 and TNF-α are raised more in AFLD as compared to NAFLD.  Because increased inflammatory markers in fatty liver disease indicate liver injury, assessing inflammatory markers should be prioritized in the therapy of fatty liver disease patients.

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