Liver cirrhosis is the irreversible end-stage of chronic liver disease, which is associated by extensive hepatic scarring, nodular regeneration, and gradual loss of liver functions[1,2]. It is a pathological state that is a sequel to long-term hepatocellular damage caused by a variety of etiologies, namely, chronic viral hepatitis, alcoholic liver disease, non-alcoholic steatohepatitis, and metabolic disorders [1,3]. Cirrhosis as it advances, brings about serious complications including portal hypertension, esophagus varices, ascites, liver encephalopathy, and eventually hepatic failure hence a major source of morbidity and death in the whole world[2,4].

Lipid metabolism is centered and dependent on the liver, where the synthesis of cholesterol, the synthesis of lipoproteins, the oxidation of fatty acids, and the formation of the biliary acids occur[5,6]. In physiological conditions, the liver produces about 80 percent of the cholesterol demand of the body as well as important apolipoproteins such as apolipoprotein A-I, apolipoprotein B-100, and apolipoprotein E which are significant units in lipoproteins that can transport lipids across the body[7,8,9]. Lipoprotein synthesis by the liver especially very low-density lipoproteins (VLDL), low-density lipoproteins (LDL), and high-density lipoproteins (HDL) are the key to systemic lipid homeostasis[5,6].

Chronic liver disease with cirrhosis patients: The gradual loss of hepatic synthetic ability results in considerable changes in lipid metabolism and serum lipids[1,3,4] here the factors underlying these changes are numerous such as: loss of hepatocellular mass, impaired protein synthesis, loss of enzyme activity, and disarranged intrahepatic architecture[2,10]. When hepatic stellate cells become activated and differentiate into myofibroblasts, they under-secrete extracellular matrix proteins in excess which are mostly type I and III collagen and that results in fibrosis and architectural distortion[2,11]. The extent of the fibrotic process impairs metabolic capacity of liver, leading to reduced synthesis of cholesterol, triglycerides, and apolipoproteins[1,3,12].

Several studies have revealed uniform characteristics of lipid abnormalities among cirrhotic patients, where serial deteriorations in serum total cholesterol, HDL cholesterol, LDL cholesterol and triglyceride levels were associated with disease severity[1,3,12,13]. These changes are caused by multiple and interrelated processes: lower de novo cholesterol production as a result of low 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, interference with apolipoprotein production and therefore reduced lipoprotein assembly and secretion, the biliary acid metabolism, and heightened cholesterol utilization to repair the damaged hepatocyte membrane[5,12,3].

Importance of changes in the lipid profile does not lie in their biochemical curiosities only, as they are increasingly being considered important prognostic parameters in cirrhotic patients[14,15,16]. Child-Pugh score and Model for End-Stage Liver Disease (MELD) score are currently the gold standards of evaluating the severity of cirrhosis and predicting outcomes[4,17,18]. The Child-Pugh classification system uses five variables: serum bilirubin, albumin, prothrombin time/INR, ascites and hepatic encephalopathy to classify patients in classes A, B, and C with different survival rates[4,19]. The MELD score, which uses serum bilirubin, creatinine, and INR, is more objective and validated widely in the determination of liver transplant allocation[17,18,20].

Each of these systems, however, suffers certain inherent limitations, such as subjectivity inherent to the Child-Pugh system and the possibility of inaccuracy in certain patients groups when using MELD scoring[18,21]. This has provoked researchers to explore other biomarkers that have the capacity to increase the precision of prognosis. Serum cholesterol levels (HDL cholesterol in particular) were found, in more recent studies, to be independent mortality predictors in cirrhotic patients and their utility as a method of prognostication matched that of established scoring systems[15,16,22].

The clinical impact of adding assessment of the lipid profile in the management of cirrhosis is substantial. There is a strong correlation between low HDL cholesterol (<0.5 mmol/L) and high short-term mortality risk with some studies showing prognostic performance comparable to the MELD scores[16]. Likewise, low concentrations of total cholesterol have been shown to be independent predictors of mortality, even after controlling the conventional prognostic variables[15,23]. These results indicate that lipid parameters may serve as useful supplementary data in risk stratification and clinical decision-making of cirrhotic patients.

Moreover, progressive lipid abnormalities in cirrhosis provide some prospective thoughts regarding the pathophysiology of disease and targets. The correlation between hepatocellular synthetic dysfunction and changes in lipid metabolism can be used to define new therapeutic manipulation strategies and maintain or reverse the hepatic condition[14,24]. Also, the use of lipid profile could provide a non-invasive assessment of disease status and response to therapy in institutions where liver biopsy or invasive hemodynamic monitoring is unable to be performed[14,24].

The relationship between abnormalities of the lipid profile and the severity of cirrhosis can also be used to explain some of the systemic effects of liver disease. Dyslipidemia can also be a factor in determining the presence of complications in cirrhosis including cardiovascular dysfunction, systemic inflammation, and/or impaired immune response[16,25]. His findings on anti-inflammatory and antioxidant effects of HDL cholesterol imply that HDL cholesterol deficiency in cirrhotic patients can enhance the mechanisms of diseases and predispose them to complications[16].

The notion that lipid profile testing needs to be included in the protocols of the evaluation of cirrhoses deserves current evidence support[12,13,14]. Lipid measurements are easy to compute, relatively inexpensive, and provide information that can be useful in predicting outcomes, which makes them an appealing prospect to incorporate into the regular practice of clinicians. Nevertheless, uniformity of measurement methods, development of population-specific reference intervals, and validation across various patients are viable options in clinical application[24].

Design and Setting of Study:

It was a single-centered hospital-based cross sectional, observational study that was carried at the Department of general medicine at Amaltas Institute of medical sciences at Dewas. This research was conducted to evaluate the abnormalities of lipid profile among liver cirrhosis patients and identify the relation between such abnormalities and severity of liver dysfunction according to Child-Pugh and MELD system.

Ethical Clearance and study duration:

The Institutional Ethics Committee of Amaltas Institute of Medical Sciences, Dewas granted ethical clearance of the study. The research followed the declaration of Helsinki. The research assessment took place in 18 months (March 2023 to September 2024), spaced into three stages, that is, Planning Phase (3 months), participant-recruitment and data-collection phase (12 months), and datum analysis and report writing phase (3 months).

Study Participants:

A sample size of 100 adult patients with diagnosed cirrhosis of liver, which have been confirmed clinically, radiologically or by laboratory results, was used. The inclusion criteria were patients that had attained 18 years of age, and were capable of giving prevention. Excluded were known diabetes, hypertension, chronic kidney disease or use of lipid- lowering agents.

Data Collection:

Demographic information, clinical histories and laboratory tests (lipid profile, total cholesterol, HDL, LDL, triglycerides and VLDL) were obtained in data collection. Its severity was determined using the Child Pugh and MELD scores among the participants. Lipid profile in blood was done after a 1012 hour fasting state and liver functions were checked. Clinical findings were confirmed by imaging studies such as abdominal ultrasound.

Outcome Measures:

The major finding was the measuring relationship between abnormality of lipid profile and severity of the cirrhosis evaluated by the Child-Pugh score and MELD score. The dependent variable was lipid profiles, age and gender, etiology of cirrhosis, and alcohol consumption, and BMI, and comorbidities were taken as possible independent or confounding variables.

Statistical Analysis:

The data were fed to Microsoft excel and analyzed using statast version 17.0. The demographic information, clinical results and lipid analysis were descriptively analyzed. The mean and the standard deviation was used to describe continuous variables and frequencies and percentages were used to express categorical variables. The correlation analyses were carried out to estimate the connection between lipid traits and the extent of cirrhosis, and a regression analysis was conducted to review the relationship between the independent and dependent variables.

Ethical Considerations:

All participants have given the project informed consent, and the forms were available in both means, Hindi and English. It was conducted in an ethical way, as it guaranteed the confidentiality of participants and the safety of data sensitive material.

Financing and Conflict of Interest:

External funding was not received to obtain the study. The study institute incurred all costs and the Principal Investigator used his personal funds to collect data. Conflict of interests was not present.

Table 1: Age Distribution of Participants

This table shows the age distribution of participants in the study. The majority of patients were in the 41–50 years age group (33%), followed by 29% in the 51–60 years group. The 61–70 years group represented 23% of participants, and 11% were in the 71–80 years group. Only 4% of the participants were in the 31–40 years range. The data shows a predominance of middle-aged individuals in the study.

Table 2: Gender Distribution

Table 2 presents the gender distribution of the study participants, showing a significant male predominance, with 80% of participants being male and 20% female.

Table 3: BMI Category Distribution

Table 3  shows the distribution of participants based on their body mass index (BMI). The majority (40%) of participants had a normal BMI, followed closely by 39% being underweight. A smaller proportion (21%) of participants were classified as overweight.

Table 4: Association of Child-Pugh Class and Lipid Profile

Table 4 demonstrates the relationship between the severity of cirrhosis, as classified by the Child-Pugh score, and lipid profile parameters. As cirrhosis worsened from Class A to Class C, there was a noticeable decline in total cholesterol, HDL, and LDL levels, with statistically significant differences. Interestingly, triglyceride and VLDL levels showed a slight decrease but remained higher in Class A and decreased progressively in Class B and C, suggesting changes in lipid metabolism with advancing liver disease.

Table 5: Correlation between MELD Score and Lipid Profile

Table 5 shows the correlation between the MELD score and lipid profile abnormalities. A significant negative correlation was found between MELD score and total cholesterol, HDL, and LDL levels, indicating that as liver function deteriorates, these lipid parameters decrease. Conversely, triglyceride levels exhibited a weak positive correlation with MELD score, while VLDL showed no significant correlation. This highlights the complex relationship between liver function and lipid metabolism in cirrhosis.

The results of age distribution where most of the participants (majority) fell in the bracket of 41-60 years match the literature available. Among 2,017 patients with cirrhosis, a well-conducted, aggregate demographic study has revealed that the median presentation age is 51.5 10.7 years while alcoholic liver disease presents at 51 10 years[26]. On the same note, another large scale research on a sample of 150 patients found incidence of cirrhosis maximum among the age group of 51-60 years[27]. This invariance in a number of studies confirms the fact that the disease of cirrhosis is mostly prevalent in middle aged persons and that this is a demonstration of the same chronic liver damage as accumulated over a long period of time[28].

Investigation has also shown that various etiologies of cirrhosis are characterized by different presenting ages and that autoimmune disease causes cirrhosis at a younger age (43 17 years) than that of cryptogenic/ NAFLD/NASH (60 12 years)[26]. To understand why the climax of incidence is in the age group of 41-60, several risk factors will come into play, such as the chronic alcohol consumption, the development of viral hepatitis and the occurrence of metabolic disorders which are the hepatotoxicities that are expected to become manifest following a wide range of exposures[29].

The current is in line with the known pattern of epidemiology of liver cirrhosis. This gender difference has been substantiated by other large-scaled studies, one of which revealed that it occurs twice or thrice among males compared to females[30,31]. In a study done on 553,017 patients, it was discovered that women formed a mere 39 percent of cirrhotic patients whereas 61 percent was formed by men[31].

Various factors are linked to the male preponderance, which includes the increased alcohol intake, more exposure to hepatotoxic drugs, and proliferation of risk behavior[30,32]. It has been demonstrated that the prevalence of the male to female relationship varies depending on the modality of etiology, where alcohol related cirrhosis exhibits high degrees of male predominance[30]. Genetic factors are involved as well as the association of the male specific gene SRY, found to be contributive to hepatocarcinogenesis and a possible male liver disease progression that is more aggressive[30].

Notably, gender variations do not only become apparent in incidence but also in clinical outcomes. The course of the disease in women with cirrhosis is usually less severe, better responses to the therapy and superior overall survival is observed than in men, especially younger age groups[30,31].

The complexity of the nutritional problems in cirrhosis is expressed in the results of the study related to the BMI distribution when 40 percent of patients had normal BMI, 39 percent were underweight, whereas 21 percent were overweight. This allocation can be substantiated by the studies showing that the prevalence of malnutrition depends considerably on the methods of measuring it and the severity of a disease[33,34].

Research employing the BMI as a marker of malnutrition has given fluctuating rates of prevalence. Malnutrition has also been identified in 7 percent of cirrhotic patients on BMI criteria[33] and 23.5 percent of Child-Pugh C patients were underweight against 9.3 percent of Child-Pugh B patients[33]. A large percentage (39%) of underweight patients in the study corresponds to the results of a research that finds the prevalence of malnutrition as being directly proportional to the severity of the disease, with Child-Pugh C patients demonstrated to have the highest incidences of protein-energy malnutrition[33,35].

Significance of metabolic liver disease and NAFLD as major contributory factors to cirrhosis is shown by the presence of overweight patients (21%) in the study[33]. Studies indicate that the use of BMI to measure the body composition of cirrhotic patients needs to be interpreted cautiously since they have fluid retention, ascites and also the other changes in body composition that obscure the fact that the patient is malnourished[33,36].

The fact that the levels of total cholesterol, HDL, and LDL has been shown to diminish progressively till the highest severity identified as Child-Pugh is well cited by various studies. A landmark study involving 50 patients with Cirrhosis indicated that average total cholesterol in patients with Child-Pugh A was 166.517.9 mg/dL and the Child-Pugh C had 121.231.7 mg/dL of total cholesterol[37]. In the same way, the HDL cholesterol levels reduced to 37.4+15.5 mg/DL (Class C) compared to 49.0+21.6 mg/DL (Class A)[37].

Detailed correlation investigations have always revealed excessive negative relationship between Child-Pugh scores and lipid parameters. Correlation coefficients on total cholesterol, HDL cholesterol and LDL cholesterol were cited to be -0.681, -0.465 and -0.406 respectively in one study[37]. The other study showed similar trends with the total cholesterol having association coefficients that ranged between -0.491 and -0.681 among different studies[39,40,41].

Increment in mild VLDL at an increasing course of the disease has been interchangeably reported. Other research concluded that the level of VLDL did not fluctuate significantly or differ much to that of other lipid fractions[42][38]. It may indicate various metabolic variations occurring in severe liver disease, in which synthesis and VLDL assemblage of triglycerides may be altered compared to cholesterol metabolism[42].

The result of the study that MELD score has a significant negative correlation with the total cholesterol, and HDL and LDL, is widely investigated in the literature. A study of Brazilian cirrhotic patients has shown that a high MELD score association with reduced values of total cholesterol (< 100 mg/dL), VLDL (< 16 mg/dL), and LDL (< 70 mg/dL) is also significant[43]. There were statistically significant inverse relations between MELD scores as well as other major lipid fractions but not triglycerides through the correlation analysis[43].

The prognostic significance of lipid parameters combined with the scores of MELD was proved in multiple studies. A study indicated that, MELD 18 and above, together with low total cholesterol level (108 mg /dL), is an independent marker of short term survival in cirrhotic patients[44]. The correlation coefficients factors between MELD scores and lipid parameters are usually between 0.3 to 0.7 in the dependence concerning the particular lipid percentage analyzed[43,45].

The study finding that indicates weak positive correlation between MELD score and triglyceride levels is consistent with the observation of other studies indicating that triglyceride metabolism can differ in patients with advanced liver disease. It has been indicated in studies that the magnitude of the triglyceride concentrations can be maintained at a higher level or they can decrease less actively than that of cholesterol fractions or in people with multiple steatosis or metabolic impairment[42,43].

The conclusion made by the study on the prospects of lipid profiles as biomarkers on monitoring the progress of the disease is highly justified by evidence that has been emerging. It was reported that high-density lipoprotein cholesterol was an independent mortality predictor in patients with cirrhosis, where its prognostic value was as accurate as any other scoring system[46,47,48]. It has been reported that the degree of reduced HDL-C (<0.13 mmol/L) is a key factor to becoming highly transplant-free mortal at 90 days (hazard ratio is greater than 4.0)[46].

Studies have revealed that the inclusion of lipid parameters into the established prognostic models is able to increase their predictive validity. It has been demonstrated that the incorporation of the HDL-C levels in the MELD scores enhances 30-day mortality in Asians with cirrhosis[49]. In predicting the 90-day outcomes, HDL-C (AUC 0.732) has been found to be similar to MELD score (AUC 0.729)[46].

The prognostic value of the level of abnormalities of lipids is caused by the fact that they are the indication of both the state of hepatic synthetic activity and instate inflammation. It has been demonstrated that the HDL dysfunction in cirrhosis is not only quantitative as substantially reduced, but also qualitative as the cholesterol efflux capacity and anti-inflammatory potential decrease[48][50]. It has been found that low HDL concentration is associated with high levels of inflammatory factors such as IL-4, IL-6, and TNF-alpha, which indicates that lipid anomalies reflect more pathophysiological disorders[46].

Implications Therapeutic and Future Directions

The focus of the research on the necessity of additional research to investigate the targeted therapy of the abnormalities in the lipid system agrees with the principles of the emerging treatments. Lipids have become an area of interest in research and thus studies have been carried out on areas in which lipid supplementation, statin therapy and metabolic interventions have a role to play in cirrhotic patients[50]. These inabilities of lipid profile as a prognostic indicator have prompted recommendations of inclusion of such parameters in the standard clinical evaluation procedures[50,51].

The existing data justify the use of lipid profile measurement as a component of a full set of cirrhosis evaluations, especially when it comes to risk stratification and prognostic determination[50,52]. Nevertheless, implementation of uniform standards of measurement use, development of population-specific reference ranges, and verification in spectrums of distinct patients is a significant factor in clinical use[51].

In this study, it is out of point to note that the process of lipid metabolism in liver cirrhotic patients undergoes significant changes. There is a definite worsening of lipid parameters especially the reduced levels of total cholesterol, HDL as well as LDL levels as the cirrhosis escalates to indicate the lost hepatic activity. The fact that the correlation of the MELD scores and these lipid parameters is negative make the lipid parameters even more promising as prognostic markers of CTP in cirrhotic patients. Further, the mapping implies that the markers may serve as an addition to the conventional scoring models such as Child-Pugh and MELD, to provide a convenient and non-invasive tool to evaluate the evolution of the disease and risk stratification. They should be confirmed in the results of further studies and also on other groups of patients to adjust their clinical applicability to predicting the long-term outcomes and treatment response.

1. Jatav HK, Pathak A, Vaidya A, Sharma R, Jain NK. Study of lipid profile changes in cirrhosis of liver. Int J Sci Study. 2018;6(3):110-114.
2. Ghadir MR, Riahin AA, Avazpour A, Nooranipour M, Habibinejad AA. The relationship between lipid profile and severity of liver damage in cirrhotic patients. Hepat Mon. 2010;10(4):285-288.
3. Nguyen P, Leray V, Diez M, et al. Liver lipid metabolism. J Anim Physiol Anim Nutr (Berl). 2008;92(3):272-283.
4. Radu M, Moldoveanu AC, Popa SG, et al. The relationship between lipid profile and severity of liver damage in cirrhotic patients. Hepat Mon. 2011;11(4):285-288.
5. Ramcharran D, Wahed AS, Conjeevaram HS, et al. Serum cholesterol is a significant and independent mortality predictor in advanced liver disease. Ann Hepatol. 2019;18(4):556-563.
6. Siagris D, Christofidou M, Theocharis GJ, et al. Serum lipid pattern in chronic hepatitis C: histological and virological correlations. J Viral Hepat. 2006;13(1):56-61.
7. Janaki Rama Raju SD. Study on lipid profile and its correlation to the severity of cirrhosis of liver. MedPulse Int J Med. 2020;14(2):38-41.
8. Nguyen P, Leray V, Diez M, et al. Liver lipid metabolism. J Anim Physiol Anim Nutr (Berl). 2008;92(3):272-283.
9. Tessitore A, Pastore A, Sorrentino P, et al. Lipid and lipoprotein metabolism in liver disease. Endotext [Internet]. 2015 May 18.
10. Perales FR, Manzano ML, Arguelles F, et al. Lipoprotein profile in cirrhosis of liver. Eur J Gastroenterol Hepatol. 2007;19(6):521-527.
11. Siagris D, Christofidou M, Theocharis GJ, et al. The effect of the severity of liver cirrhosis on the level of lipids and lipoproteins. BMC Gastroenterol. 2013;13:142.
12. Habib A, Mihas AA, Abou-Assi SG, et al. High-density lipoprotein cholesterol as an indicator of liver function and prognosis in noncholestatic cirrhotics. Clin Gastroenterol Hepatol. 2005;3(3):286-291.
13. Salimoghlou N, Hanai T, Ashihara E, et al. Lipid profiles as markers for the severity of liver diseases in patients with chronic hepatitis B virus infection. J Med Virol. 2018;90(2):263-271.
14. Nassir F, Bonen DK, Davidson NO. Apolipoprotein(a) synthesis and secretion from hepatoma cells is coupled to triglyceride synthesis and secretion. J Biol Chem. 1998;273(28):17793-17800.
15. Ma Y, Huang Y, Yan L, et al. Synthetic and natural regulation of cholesterol homeostasis: the liver as a metabolic power station. Pharmacol Res. 2012;66(4):292-311.
16. Chen TC, Parker JC, Nassir F, et al. Liver X receptor inhibits the synthesis and secretion of apolipoprotein A1 by human liver-derived cells. Biochemistry. 2006;45(50):15068-15074.
17. Piano S, Brocca A, Mareso S, et al. Infections complicating cirrhosis. Liver Int. 2018;38 Suppl 1:126-133.
18. Kerbert AJ, Montano-Loza AJ, Carbone M, et al. Prognostic value of high-density lipoprotein cholesterol in patients with decompensated cirrhosis and overt hepatic encephalopathy. J Gastroenterol Hepatol. 2024;39(8):1547-1555.
19. Su TH, Liu CH, Yang HC, et al. Serum cholesterol is a significant and independent mortality predictor in advanced liver disease. Ann Hepatol. 2019;18(4):556-563.
20. Okamura T, Hashimoto Y, Majima S, et al. Low cholesterol is associated with mortality from stroke, heart disease, and cancer: the Jichi Medical School Cohort Study. J Epidemiol. 2021;31(1):67-74.
21. Tsoukalas N, Kiagia M, Schizas D, et al. Child-Pugh score for chronic liver disease and cirrhosis. Healthline. 2022 Mar 29.
22. Kamath PS, Wiesner RH, Malinchoc M, et al. A model to predict survival in patients with end-stage liver disease. Hepatology. 2001;33(2):464-470.
23. Wiesner R, Edwards E, Freeman R, et al. Model for end-stage liver disease (MELD) and allocation of donor livers. Gastroenterology. 2003;124(1):91-96.
24. Child CG, Turcotte JG. Surgery and portal hypertension. Major Probl Clin Surg. 1964;1:1-85.
25. Pugh RN, Murray-Lyon IM, Dawson JL, et al. Transection of the oesophagus for bleeding oesophageal varices. Br J Surg. 1973;60(8):646-649.
26. Jatav HK, Pathak A, Vaidya A, Sharma R, Jain NK. Study of lipid profile changes in cirrhosis of liver. Int J Sci Study. 2018;6(3):110-114.
27. Ghadir MR, Riahin AA, Avazpour A, Nooranipour M, Habibinejad AA. The relationship between lipid profile and severity of liver damage in cirrhotic patients. Hepat Mon. 2010;10(4):285-288.
28. Łapiński TW, Łapińska M. Evaluation of the nutritional status of patients with liver cirrhosis. PMC. 2023;27:401412.
29. Moreau R, Elkrief L, Bureau C, et al. Age and Ethnicity in Cirrhosis. PMC. 2014;172494.
30. Thabut D, Zafrani ES, Hanoun N, et al. Gender differences among patients hospitalized with cirrhosis in the United States. PMC. 2019;6706332.
31. Mishra AK, Nangliya VL, Sharma RK, et al. Assessment of Nutritional Status of Liver Cirrhotic Patients by the Anthropometrics measurements. Int J Pharm Clin Res. 2022;14(3):505.
32. Asrani SK, Devarbhavi H, Eaton J, Kamath PS. Epidemiology of liver cirrhosis and associated complications. PMC. 2022;9669831.
33. Buzzetti E, Kalafateli M, Thorburn D, et al. Sex differences in chronic liver disease and benign liver lesions. Sci Direct. 2023.
34. Sorrentino P, Tarantino G, Perrella A, et al. Validation of body mass index for the diagnosis of malnutrition in cirrhotic patients. Pub Med. 2006;28:1547.
35. FastStats - Chronic Liver Disease or Cirrhosis. 2025.
36. Shaheen AA, Kaplan GG, Hubbard JN, Myers RP. Global Epidemiology of Cirrhosis in Women. LWW. 2024.
37. Nunes G, Santos CA, Barosa R, et al. Review Nutritional assessment of patients with liver cirrhosis in the 21st century. Sci Direct. 2024.
38. Pimpin L, Cortez-Pinto H, Negro F, et al. Changing epidemiology of cirrhosis from 2010 to 2019. Taylor Francis. 2023.
39. Shalimar, Kumar A, Kedia S, et al. Sex disparities in acute-on-chronic liver failure. Sci Direct. 2024.
40. Wang X, Men K, Zhang X, et al. Screening and assessment of malnutrition in patients with liver cirrhosis. Front Nutr. 2024;11:1398690.
41. Asrani SK, Devarbhavi H, Eaton J, Kamath PS. The Global Burden of Liver Disease. Sci Direct. 2023.
42. Burra P, Senzolo M, Adam R, et al. Gender specific medicine in liver diseases: A point of view. WJG. 2014;20(9):2127.
43. Huisman EJ, Trip EJ, Siersema PD, et al. Nutritional assessment in patients with liver cirrhosis. WJG. 2022;14(9):1694.
44. Bernardi M, Moreau R, Angeli P, et al. Trends and the course of liver cirrhosis and its complications in Germany. Sci Direct. 2021.
45. Buzzetti E, Kalafateli M, Thorburn D, et al. Gender differences in liver disease and the drug-dose gender gap. UCL Discovery. 2017.
46. Ghadir MR, Riahin AA, Avazpour A, Nooranipour M, Habibinejad AA. The relationship between lipid profile and severity of liver damage in cirrhotic patients. PMC. 2012;3271321.
47. Bassani L, Fernandes SA, Raimundo FV, Harter DL, Gonzalez MC, Marroni CA. Lipid profile of cirrhotic patients and its association with prognostic scores: a cross-sectional study. Scielo. 2015.
48. Siagris D, Christofidou M, Theocharis GJ, et al. The effect of the severity of liver cirrhosis on the level of lipids and lipoproteins. PMC. 2013;4213382.
49. Verma AK, Singh SP, Mishra AK, Gupta MK, Tiwari S. Study of serum lipid profile in patients with chronic liver disease and its correlation with Child Pugh score. Int J Adv Med. 2023;10(5):388-391.
50. Verma AK, Singh SP, Mishra AK, Gupta MK, Tiwari S. Study of serum lipid profile in patients with chronic liver disease and its correlation with Child Pugh score. Int J Adv Med. 2023;10(5):388-391.
51. Jatav HK, Pathak A, Vaidya A, Sharma R, Jain NK. Study of Lipid Profile Changes in Cirrhosis of Liver. IJSS. 2018.
52. Mahapatra S, Rout C, Jena RK. A cross-sectional study for lipid profile as an indicator of severity in liver cirrhosis. Med Paper. 2020.