Abstract
Introduction
Patients with chronic liver disease are expected to report derangements in serum lipid profiles. Lipid profile monitoring is not a part of the routine management of these patients in our hospital. Few recent studies show how lipid profile varies with the severity of disease and should be considered in the management planning of such patients. The objective of this study was to determine the pattern of dyslipidemia in chronic liver disease patients.
Materials and methods
A cross-sectional study was conducted involving 171 patients of all genders aged between 18 years and 60 years presenting with chronic liver disease with disease severity graded on Child-Pugh class as A, B, and C. Lipid profile was acquired in all these patients and was compared across various subgroups. Individual serum lipid parameters were graded as normal, high, or very high. Each patient was required to provide written informed consent. Statistical Package for Social Sciences (SPSS) version 21.0 (IBM Corp. Armonk, NY) was used to analyze data statistically, taking a p-value of ≤0.05 as significant.
Results
The mean age of patients was 51.2±7.3 years. The male to female ratio came out to be 1.5:1, with 103 (60.2%) male and 68 (39.8%) female patients included in the study. The disease was classified as Child-Pugh A in 20 (11.7%) patients, Child-Pugh B in 67 (39.2%) patients, and Child-Pugh C in 84 (49.1%) patients. Forty-four (25.7%) patients were hypertensive while 62 (36.3%) were diabetic. The mean body mass index (BMI) of these patients was 25.9±2.4 kg/m2. Mean serum values among Child-Pugh A, Child-Pugh B, and Child-Pugh C of low-density lipoproteins (LDL) (113.15±14.08 vs. 95.58±14.25 vs. 53.46±5.90 mg/dl; p-value 0.001), high-density lipoproteins (HDL) (50.60±3.19 vs. 40.70±2.95 vs. 35.40±3.88 mg/dl; p-value 0.001), total cholesterol (174.20±17.33 vs. 164.00±17.82 vs. 128.64±24.73 mg/dl; p-value 0.001), and triglycerides (127.15±8.98 vs. 100.84±27.12 vs. 93.36±25.56 mg/dl; p-value 0.001) decreased significantly with increasing severity of disease. Nineteen (11.1%) patients had hyperlipidemia (serum values of two or more parameters above normal) while 152 (88.9%) patients had normal lipid profile. When stratified, no statistically significant difference was found in the frequency of hyperlipidemia across various subgroups based on the patient's gender, age, duration, and severity of the disease, BMI, or diabetic and hypertensive status.
Conclusions
A substantial proportion of patients with chronic liver disease had hyperlipidemia which varied with the severity of disease on Child-Pugh classification. Routine monitoring of the lipid profile of such patients is necessary for timely identification and management of dyslipidemia to improve the outcome of such patients. It also suggests an important role of lipid profile in the risk stratification and treatment of chronic liver disease patients and warrants further studies in this regard.
Keywords: child-pugh classification, chronic liver disease, lipid profile, dyslipidemia, severity of disease, management, monitoring, risk stratification, cld, liver cirrhosis
Introduction
Several hepatic disorders in which normal liver tissue is replaced by fibrotic tissue are collectively termed chronic liver disease (CLD) [1]. Several metabolic abnormalities are common in CLD like dyslipidemias, clotting factor deficiencies, and in some cases venous thromboembolism due to deficiency of anticoagulation factors [2]. Dyslipidemia is a metabolic anomaly that causes an imbalance in lipids or lipoproteins [3]. Fat-soluble vitamins, dietary cholesterol, and long-chain fatty acids are absorbed and transported by lipoproteins. Lipids are present in the cell membrane and are important regulators of cellular function and the internal body environment. Exogenous and endogenous lipid metabolism cycles are controlled by the liver. The liver is also responsible for the formation of apolipoproteins, which activate enzymes responsible for lipoprotein metabolism and attachment to their specific receptors [4].
Imbalance in serum lipoprotein can be due to cirrhosis of the liver, where cholesterol of low-density lipoprotein (LDL) variant and high-density lipoprotein (HDL) variant are reduced [5]. Dyslipidemia reported in patients of CLD is remarkable in contrast with other causes of secondary dyslipidemia as the composition, appearance, serum levels, and mobility of lipoproteins is disturbed [3,6]. Ress and Kaser have reported that CLD interferes with the metabolism of lipid by disrupting the functionality of the liver, resulting in the accumulation of lipid drops in hepatocytes. Abnormal secretion of very-low-density lipoprotein (VLDL) leads to hepatic steatosis [7].
A previous study reported that the total cholesterol was markedly decreased in 15% of patients. Overall, 82.5% of patients presented with hypocholesterolemia, and 2.5% of patients presented with hypercholesterolemia. Whereas, 63.13% of patients reported low triglyceride levels, 88.13% of patients reported decreased LDL, and increased levels were reported in 4.38% of patients [4]. In another study, 69.09% of patients had decreased total cholesterol, hypercholesterolemia was not reported, and 12.72% of patients had low serum triglyceride [8].
As variation in results is mentioned in the studies above, the present study is conducted to see the pattern of dyslipidemia and lipid metabolism derangement in CLD patients and to have an idea of local prevalence. This study will help the patients and healthcare providers by early identification of the pattern of dyslipidemia and taking steps to improve the survival and outcomes of the patients.
Materials and methods
This cross-sectional study was done for six months from August 2019 to January 2020 at the Department of General Medicine, Peoples Medical College, and Hospital, Nawabshah, Pakistan.
Sample size, inclusion, and exclusion criteria
A sample size of 171 was calculated using the World Health Organization (WHO) software, taking the prevalence of low serum triglyceride levels in patients 12.72%, the margin of error 5%, and confidence level 95%. Patients suffering from the CLD aged between 18 years and 60 years, confirmed by history and medical record of either gender were enrolled in the study. Whereas, the patients undergoing concomitant illnesses like heart failure, renal failure, or a thyroid problem, patients taking lipid-lowering drugs, patients consuming alcohol, or patients with a body mass index (BMI) of >30 kg/m2 were excluded from the study sample.
Sampling technique and data collection
Non-probability consecutive sampling technique was employed to sample patients. The study was conducted after approval from the ethical committee of the institute. Informed consent was also taken from all the patients enrolled before including them in the study. After taking a complete history and physical examination, a lipid profile was done to investigate the pattern of dyslipidemia. The data was entered in a predesigned proforma. Confounding variables and bias were controlled by strictly following inclusion criteria.
Statistical analysis
Statistical Package for Social Sciences (SPSS) version 21.0 (IBM, Armonk, NY) was used to analyze the collected data. Continuous variables, such as age, BMI, duration of liver disease, LDL, total cholesterol, HDL, and triglycerides, were presented as mean±SD. Serum levels of triglycerides, LDL, total cholesterol, and HDL have been compared across various subgroups using independent sample t-test/ANOVA. A p-value of ≤0.05 was considered significant. Categorical variables like gender, the severity of liver disease (Child-Pugh class), diabetes mellitus, hypertension, and pattern of dyslipidemia were presented using percentages and frequencies. Age, gender, BMI, duration, the severity of the disease, diabetes mellitus, and hypertension were stratified to address the effect of modifiers. Chi-square test was applied to assess categorical variables, taking a p-value of ≤0.05 as significant.
Results
The mean age of the patients enrolled was 51.2±7.3 years. There were 103 (60.2%) male and 68 (39.8%) female patients who comprised the study population; male to female ratio was reported to be 1.5:1. The duration of disease ranged from six to 18 months with a mean of 12.1±3.7 months. The disease was classified as Child-Pugh A in 20 (11.7%) patients, Child-Pugh B in 67 (39.2%) patients, and Child-Pugh C in 84 (49.1%) patients. Forty-four (25.7%) patients were hypertensive while 62 (36.3%) were diabetic. BMI of these patients ranged from 21.3 kg/m2 to 29.9 kg/m2 with a mean of 25.9±2.4 kg/m2 as shown in Table 1.
Table 1. Baseline characteristics of the study sample.
BMI- body mass index
| Characteristics | Participants n=171 |
| Age (years) | 51.2±7.3 |
| <45 years | 20 (11.7%) |
| ≥45 years | 151 (88.3%) |
| Gender | |
| Male | 103 (60.2%) |
| Female | 68 (39.8%) |
| Duration of disease (months) | 12.1±3.7 |
| <1 year | 76 (44.4%) |
| ≥1 year | 95 (55.6%) |
| Severity of disease | |
| Child-Pugh A | 20 (11.7%) |
| Child-Pugh B | 67 (39.2%) |
| Child-Pugh C | 84 (49.1%) |
| Hypertension | |
| Yes | 44 (25.7%) |
| No | 127 (74.3%) |
| Diabetes | |
| Yes | 62 (36.3%) |
| No | 109 (63.7%) |
| BMI (kg/m2) | 25.9±2.4 |
| 20-25 kg/m2 | 69 (40.4%) |
| 25-30 kg/m2 | 102 (59.6%) |
Serum LDL level varied from 44 mg/dl to 165 mg/dl with a mean of 76.95±26.10 mg/dl, while HDL varied from 28 mg/dl to 56 mg/dl with a mean of 39.26±5.93 mg/dl. Triglycerides levels were reported to vary from 79 mg/dl to 207 mg/dl with a mean of 100.24±26.88 mg/dl, and serum total cholesterol levels were recorded to vary from 104 mg/dl to 209 mg/dl with a mean of 147.82±28.67 mg/dl as shown in Table 2.
Table 2. Serum lipid profile of patients with chronic liver disease (n=171).
LDL- low-density lipoprotein; HDL- high-density lipoprotein
| Lipid profile | Serum level (mg/dl) |
| LDL | 76.95±26.10 |
| HDL | 39.26±5.93 |
| Total cholesterol | 147.82±28.67 |
| Triglycerides | 100.24±26.88 |
There was no statistically significant difference in the mean serum values of LDL, HDL, triglycerides, and total cholesterol across various subgroups based on patient's age, gender, duration of disease, BMI, and diabetic and hypertensive status was reported. However, mean serum values of LDL (113.15±14.08 vs. 95.58±14.25 vs. 53.46±5.90 mg/dl; p-value 0.001), HDL (50.60±3.19 vs. 40.70±2.95 vs. 35.40±3.88 mg/dl; p-value 0.001), total cholesterol (174.20±17.33 vs. 164.00±17.82 vs. 128.64±24.73 mg/dl; p-value 0.001), and triglycerides (127.15±8.98 vs. 100.84±27.12 vs. 93.36±25.56 mg/dl; p-value 0.001) decreased significantly with increasing severity of disease as shown in Tables 3-6.
Table 3. Stratification of serum LDL level (mg/dl) across various subgroups of patients with chronic liver disease (n=171).
LDL- low-density lipoprotein; BMI- body mass index
| Subgroups | n | Serum LDL level (mean±SD) | P-value |
| Age (years) | |||
| <45 years | 20 | 75.45±24.68 | 0.786 |
| ≥45 years | 151 | 77.15±26.36 | |
| Gender | |||
| Male | 103 | 76.19±25.80 | 0.644 |
| Female | 68 | 78.09±26.72 | |
| Duration of disease (months) | |||
| <1 year | 76 | 76.74±25.41 | 0.925 |
| ≥1 year | 95 | 77.12±26.78 | |
| Severity of disease | |||
| Child-Pugh A | 20 | 113.15±14.08 | 0.001 |
| Child-Pugh B | 67 | 95.58±14.25 | |
| Child-Pugh C | 84 | 53.46±5.90 | |
| Hypertension | |||
| Yes | 44 | 77.36±27.63 | 0.903 |
| No | 127 | 76.80±25.67 | |
| Diabetes | |||
| Yes | 62 | 74.90±30.56 | 0.442 |
| No | 109 | 78.11±23.27 | |
| BMI (kg/m2) | |||
| 20-25 kg/m2 | 69 | 74.07±25.34 | 0.237 |
| 25-30 kg/m2 | 102 | 78.89±26.56 |
Table 6. Stratification of serum triglycerides level (mg/dl) across various subgroups of patients with chronic liver disease (n=171).
BMI- body mass index
| Subgroups | n | Serum triglycerides level (mean±SD) | P-value |
| Age (years) | |||
| <45 years | 20 | 94.25±11.09 | 0.290 |
| ≥45 years | 151 | 101.03±28.24 | |
| Gender | |||
| Male | 103 | 100.81±27.34 | 0.736 |
| Female | 68 | 99.38±26.34 | |
| Duration of disease (months) | |||
| <1 year | 76 | 101.45±27.84 | 0.601 |
| ≥1 year | 95 | 99.27±26.18 | |
| Severity of disease | |||
| Child-Pugh A | 20 | 127.15±8.98 | 0.001 |
| Child-Pugh B | 67 | 100.84±27.12 | |
| Child-Pugh C | 84 | 93.36±25.56 | |
| Hypertension | |||
| Yes | 44 | 102.14±25.86 | 0.588 |
| No | 127 | 99.58±27.29 | |
| Diabetes | |||
| Yes | 62 | 97.95±22.64 | 0.403 |
| No | 109 | 101.54±29.03 | |
| BMI (kg/m2) | |||
| 20-25 kg/m2 | 69 | 100.10±29.05 | 0.956 |
| 25-30 kg/m2 | 102 | 100.33±25.45 |
Table 4. Stratification of serum HDL level (mg/dl) across various subgroups of patients with chronic liver disease (n=171).
HBL- high-density lipoprotein; BMI- body mass index
| Subgroups | n | Serum HDL level (mean±SD) | P-value |
| Age (years) | |||
| <45 years | 20 | 39.10±3.70 | 0.900 |
| ≥45 years | 151 | 39.28±6.17 | |
| Gender | |||
| Male | 103 | 38.94±5.84 | 0.393 |
| Female | 68 | 39.74±6.08 | |
| Duration of disease (months) | |||
| <1 year | 76 | 39.58±6.03 | 0.527 |
| ≥1 year | 95 | 39.00±5.86 | |
| Severity of disease | |||
| Child-Pugh A | 20 | 50.60±3.19 | 0.001 |
| Child-Pugh B | 67 | 40.70±2.95 | |
| Child-Pugh C | 84 | 35.40±3.88 | |
| Hypertension | |||
| Yes | 44 | 39.50±6.22 | 0.754 |
| No | 127 | 39.17±5.85 | |
| Diabetes | |||
| Yes | 62 | 39.08±5.84 | 0.770 |
| No | 109 | 39.36±6.01 | |
| BMI (kg/m2) | |||
| 20-25 kg/m2 | 69 | 39.91±5.39 | 0.235 |
| 25-30 kg/m2 | 102 | 38.81±6.26 |
Table 5. Stratification of serum total cholesterol level (mg/dl) across various subgroups of patients with chronic liver disease (n=171).
BMI- body mass index
| Subgroups | n | Serum total cholesterol level (mean±SD) | P-value |
| Age (years) | |||
| <45 years | 20 | 146.35±30.62 | 0.807 |
| ≥45 years | 151 | 148.02±28.51 | |
| Gender | |||
| Male | 103 | 147.91±29.38 | 0.961 |
| Female | 68 | 147.69±27.78 | |
| Duration of disease (months) | |||
| <1 year | 76 | 147.76±29.24 | 0.980 |
| ≥1 year | 95 | 147.87±28.36 | |
| Severity of disease | |||
| Child-Pugh A | 20 | 174.20±17.33 | 0.001 |
| Child-Pugh B | 67 | 164.00±17.82 | |
| Child-Pugh C | 84 | 128.64±24.73 | |
| Hypertension | |||
| Yes | 44 | 148.52±26.59 | 0.852 |
| No | 127 | 147.58±29.46 | |
| Diabetes | |||
| Yes | 62 | 144.47±27.95 | 0.249 |
| No | 109 | 149.73±29.03 | |
| BMI (kg/m2) | |||
| 20-25 kg/m2 | 69 | 145.91±28.46 | 0.475 |
| 25-30 kg/m2 | 102 | 149.12±28.88 |
Nineteen (11.1%) patients had hyperlipidemia (serum values of two or more parameters above normal), while 152 (88.9%) patients had normal lipid profiles. Three (1.8%) patients had higher LDL, 77 (45.0%) patients had higher HDL, 19 (11.1%) patients had higher total cholesterol, and eight (4.7%) patients had higher triglyceride levels as shown in Table 7. Very high or low levels were not observed in any patient.
Table 7. Pattern of dyslipidemia in patients with chronic liver disease (n=171).
HDL- high-density lipoprotein; LDL- low-density lipoprotein
| Lipid profile | Participants n=171 |
| LDL | |
| Normal | 168 (98.2%) |
| High | 3 (1.8%) |
| HDL | |
| Normal | 94 (55.0%) |
| High | 77 (45.0%) |
| Total cholesterol | |
| Normal | 152 (88.9%) |
| High | 19 (11.1%) |
| Triglycerides | |
| Normal | 163 (95.3%) |
| High | 8 (4.7%) |
| Hyperlipidemia | |
| Yes | 19 (11.1%) |
| No | 152 (88.9%) |
A significant difference was not found in the frequency of hyperlipidemia across various subgroups based on the patient's gender, age, BMI, duration of disease, or diabetic and hypertensive status. The frequency of hyperlipidemia decreased with the increasing severity of the disease, however, a statistically significant p-value of less than 0.05 was not reached (p-value=0.192), as shown in Table 8.
Table 8. Stratification of hyperlipidemia across various subgroups of patients with chronic liver disease (n=171).
BMI- body mass index
| Subgroups | n | Hyperlipidemia n (%) | P-value |
| Age (years) | |||
| <45 years | 20 | 2 (10.0%) | 0.866 |
| ≥45 years | 151 | 17 (11.3%) | |
| Gender | |||
| Male | 103 | 12 (11.7%) | 0.782 |
| Female | 68 | 7 (10.3%) | |
| Duration of disease (months) | |||
| <1 year | 76 | 9 (11.8%) | 0.786 |
| ≥1 year | 95 | 10 (10.5%) | |
| Severity of disease | |||
| Child-Pugh A | 20 | 4 (20.0%) | 0.192 |
| Child-Pugh B | 67 | 9 (13.4%) | |
| Child-Pugh C | 84 | 6 (7.1%) | |
| Hypertension | |||
| Yes | 44 | 5 (11.4%) | 0.951 |
| No | 127 | 14 (11.0%) | |
| Diabetes | |||
| Yes | 62 | 7 (11.3%) | 0.955 |
| No | 109 | 12 (11.0%) | |
| BMI (kg/m2) | |||
| 20-25 kg/m2 | 69 | 8 (11.6%) | 0.869 |
| 25-30 kg/m2 | 102 | 11 (10.8%) |
Discussion
Liver injury persisting six months or more is a manifestation of CLD, which can be caused by infection, inflammation, toxic, or congenital predisposition. Dyslipidemia is one of the systemic effects produced by CLD. Healing response due to liver injury causes hepatic fibrosis [9,10]. Liver impairment causes disturbed protein anabolism, excretion of bilirubin, and lipid metabolism. Such patients should be managed to improve liver metabolism [9]. Lipid profile monitoring is not a part of the routine management of such patients in our hospital; however, recent studies showed that lipid profile varies with the severity of disease and should be considered in the management of such patients [4,7].
Patients with CLD in our study had a mean age of 51.2±7.3 years. A similar mean age of 52±9 years was reported by Ali et al. (2008) in patients presenting with CLD at Muhammad Medical College Hospital, Mirpurkhas, while Hussain et al. (2014) reported it to be 51.12±6.03 years at Services Hospital, Lahore [11,12]. Achakzai et al. in 2016 and Almani et al. in 2008 also reported similar mean age of 54±11 years and 53.09±8.86 years respectively among such patients in their local population [13,14]. A similar mean age of 55.03±12.05 years has been reported by Mansour-Ghanaei et al. (2012) among Iranian such patients while Penteado et al. reported it to be 51.4±7.6 years in Brazil [15,16]. However, Bhattacharyya et al. (2016) and Deepika et al. (2015) had a much younger mean age of 45.8±10.45 years and 44±13.7 years respectively in Indian patients with CLD [17,18].
We observed a male to female ratio of 1.5:1 in our study. A similar male predominance among such patients has been reported previously by Ali et al. who observed it to be 1.5:1 in the local population [11]. El-Feki et al. in 2016 reported a similar male to female ratio of 1.5:1 among Egyptian patients with CLD [19]. Mansour-Ghanaei et al. in 2012 reported a male to female ratio of 1.9:1 among CLD patients in Iran [15]. Achakzai et al. in 2016 however observed a female predominance in CLD patients presenting at Dow University Hospital, Karachi with a male to female ratio of 1:1.5 [13].
In the present study, the disease was classified as Child-Pugh A in 20 (11.7%) patients, Child-Pugh B in 67 (39.2%) patients, and Child-Pugh C in 84 (49.1%) patients. Our observation is similar to that of Shaikh et al. (2011) who had a similar frequency of Child-Pugh Class-A (12.2%), Class-B (39.2%), and Class-C (48.6%) among cirrhotic patients at Liaquat University Hospital, Jamshoro [20]. While Naqvi et al. (2016) observed the frequency of Class-A, Class-B, and Class-C to be 11.4%, 31.4%, and 57.2%, respectively, among such patients at Dow University of Health Sciences, Karachi [21].
We observed that 25.7% of patients with CLD were hypertensive while 36.3% of patients were diabetic. Our results are similar to those of Arshad et al. (2016) who reported a similar frequency of 33.5% for diabetes among CLD patients presenting at Medical Unit III, Services Hospital, Lahore [22]. Similar diabetic rates have also been reported by Sigal et al. in 2006 (30.8%) in the American population, while Garcia-Compean et al. in 2009 reported the frequency of diabetic patients (30.0%) in Mexican patients with CLD [23, 24]. Unger et al. in 2009 reported a comparable frequency of 23.6% for hypertension in Australian patients [25].
We observed that the mean BMI of patients in our study was 25.9±2.4 kg/m2. Our observation is in line with that of Zou et al. (2016) who reported a similar mean BMI of 26.2±3.8 kg/m2 among Chinese patients with CLD [26].
The mean serum values of LDL, HDL, total cholesterol, and triglycerides decreased significantly with increasing severity of disease on Child-Pugh Classification as mentioned in Tables 3-6. Our observation is in line with a local study where Subhan et al. (2012) observed CLD patients at Khyber Teaching Hospital, Peshawar, and reported a similar significant decrease in serum LDL (110.6±29.5 vs. 96.3±49.2 vs. 56.5±26.6 mg/dl; p-value≤0.05), HDL (47.0±19.2 vs. 42.0±12.2 vs. 35.3±13.3 mg/dl; p-value≤0.05), total cholesterol (165.6±36.6 vs. 156.6±63.9 vs. 119.9±32.9 mg/dl; p-value≤0.05), and triglycerides (127.8±58.6 vs. 98.7±55.6 vs. 96.0±42.3 mg/dl; p-value≤0.05) levels with increasing severity of disease from Child-Pugh Class A vs Child-Pugh Class B vs Child-Pugh Class C [27].
Our observation is also in line with that of Ghadir et al. (2010) who observed CLD patients in Iran and reported similar remarkable decrease in serum LDL (107.6±29.5 vs. 96.4±58.5 vs. 59.5±28.9 mg/dl; p-value≤0.05), HDL (49.0±21.6 vs. 40.0±14.3 vs. 37.4±15.5 mg/dl; p-value≤0.05), total cholesterol (166.5±37.9 vs. 161.2±71.5 vs. 121.2±31.7 mg/dl; p-value≤0.05), and triglycerides (121.9±57.7 vs. 90.6±50.5 vs. 92.0±48.7 mg/dl; p-value≤0.05) levels with increasing severity of disease [28].
We observed that 11.1% of CLD patients had hyperlipidemia (serum values of two or more parameters above normal), while 88.9% of patients had normal lipid profile. Our observation is in line with that of Deeb et al. (2018) who had a similar frequency of 11.7% for hyperlipidemia in patients with CLD in the United Arab Emirates (UAE) [29]. Unger et al. in 2019 reported a comparable frequency of 13.0% for hyperlipidemia among Australian CLD patients [25]. Mehboob et al. in 2007 conducted a similar study at Sheikh Zayed Medical College, Rahim Yar Khan observed a relatively lower frequency of hyperlipidemia among CLD patients and reported it to be 7.5%, while a much higher frequency of 23.9% has been reported by Sohail et al. in 2020 at Bahawal Victoria Hospital, Bahawalpur [4,30].
A large sample size of 171 cases, strict exclusion criteria, and stratification of the results to minimize bias were the strengths of our study. However, a possible limitation could be our inability to account for serum lipid profile’s role in terms of response to treatment and mortality which could have highlighted its role in CLD patients and could have helped in the risk stratification and management of these patients.
Conclusions
A remarkable proportion of CLD patients had hyperlipidemia which varied with the severity of disease on Child-Pugh classification necessitating routine monitoring of lipid profile of such patients for timely identification and management. This would improve the outcome of CLD patients. Our results suggest that lipid profile has an important role in the risk stratification and management planning of CLD patients and warrants further studies in this regard.
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The authors have declared that no competing interests exist.
Human Ethics
Consent was obtained or waived by all participants in this study. Peoples University of Medical and Health Sciences for Women issued approval 35472/45
Animal Ethics
Animal subjects: All authors have confirmed that this study did not involve animal subjects or tissue.
References
- 1.Correlation of fasting lipid profile in patients with chronic liver disease: a descriptive cross-sectional study in tertiary care hospital. Tauseef A, Zafar M, Rashid B, Thirumalareddy J, Chalfant V, Farooque U, Mirza M. Cureus. 2020;12:0. doi: 10.7759/cureus.11019. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.Frequency of venous thromboembolism in patients with liver cirrhosis. Omer Sultan M, Farooque U, Inam Khan M, et al. Cureus. 2020;12:0. doi: 10.7759/cureus.9594. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3.Dyslipidemia; helicobacter pylori infected patients. Karim I, Zardari AK, Shaikh MK, Baloch ZAQ, Shah SZA. http://theprofesional.com/index.php/tpmj/article/view/2529 Professional Med J. 2014;21:956–959. [Google Scholar]
- 4.Dyslipidemia in chronic liver disease. Mehboob F, Ranjha FA. https://www.pjmhsonline.com/2007/july_sep/pdf/gg%20%20%20Dyslipidemia%20in%20Chronic%20Liver%20Disease.pdf Pak J Med Sci. 2007;1:103–105. [Google Scholar]
- 5.Serum lipid profile in alcoholic cirrhosis: a study in a teaching hospital of north-eastern India. Phukan JP, Sinha A, Deka JP. Niger Med J. 2013;54:5–9. doi: 10.4103/0300-1652.108886. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6.Dyslipoproteinaemia of liver disease. Miller JP. Baillieres Clin Endocrinol Metab. 1990;4:807–832. doi: 10.1016/s0950-351x(05)80080-1. [DOI] [PubMed] [Google Scholar]
- 7.Mechanisms of intrahepatic triglyceride accumulation. Ress C, Kaser S. World J Gastroenterol. 2016;22:1664–1673. doi: 10.3748/wjg.v22.i4.1664. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 8.Changes in serum lipid profile among patients suffering from chronic liver disease secondary to hepatitis C. Qazi F, Khan SB, Umar A, Shaikh NS, Choudhry F. https://ecommons.aku.edu/pakistan_fhs_mc_med_gastroenterol/90/ Open J Gastroenterol. 2016;6:333–342. [Google Scholar]
- 9.Changes in the prevalence of the most common causes of chronic liver diseases in the United States from 1988 to 2008. Younossi ZM, Stepanova M, Afendy M, Fang Y, Younossi Y, Mir H, Srishord M. Clin Gastroenterol Hepatol. 2011;9:524–530. doi: 10.1016/j.cgh.2011.03.020. [DOI] [PubMed] [Google Scholar]
- 10.Prevalence of nonalcoholic fatty liver disease and nonalcoholic steatohepatitis among a largely middle-aged population utilizing ultrasound and liver biopsy: a prospective study. Williams CD, Stengel J, Asike MI, et al. Gastroenterology. 2011;140:124–131. doi: 10.1053/j.gastro.2010.09.038. [DOI] [PubMed] [Google Scholar]
- 11.Non-B, non-C hepatitis as a cause of advanced chronic liver disease requiring medical admission at a rural centre in Pakistan. Ali M, Abbas SZ, Sultana F, Akhtar W, Shaw S, Abbas SQ. https://www.pjms.com.pk/issues/aprjun108/article/article18.html Pak J Med Sci. 2008;24:278–282. [Google Scholar]
- 12.Frequency of gallstones in patients with liver cirrhosis. Hussain A, Nadeem MA, Nisar S, Tauseef HA. http://jamc.ayubmed.edu.pk/index.php/jamc/article/view/1502. J Ayub Med Coll Abbott. 2014;26:341–343. [PubMed] [Google Scholar]
- 13.Factors leading to hepatic encephalopathy in patients with liver cirrhosis at a tertiary care hospital in Karachi, Pakistan. Achakazi MS, Shaikh H, Mobin A, et al. http://gjms.com.pk/index.php/journal/article/view/653 Gomal J Med Sci. 2016;14:71–74. [Google Scholar]
- 14.Cirrhosis of liver: etiological factors, complications and prognosis. Almani SA, Memon AS, Memon AI, Shah I, Rahpoto Q, Solangi R. http://www.lumhs.edu.pk/jlumhs/Vol07No02/pdfs/v7n2oa01.pdf J Liaquat Uni Med Health Sci. 2008;7:61–66. [Google Scholar]
- 15.Decreased serum total T3 level in hepatitis B and C related cirrhosis by severity of liver damage. Mansour-Ghanaei F, Mehrdad M, Mortazavi S, Joukar F, Khak M, Atrkar-Roushan Z. Ann Hepatol. 2012;11:667–671. [PubMed] [Google Scholar]
- 16.The influence of end-stage liver disease and liver transplantation on thyroid hormones. Penteado KR, Coelho JCU, Parolin MB, Matias JEF, Freitas ACT. Arq Gastroenterol. 2015;52:124–128. doi: 10.1590/S0004-28032015000200009. [DOI] [PubMed] [Google Scholar]
- 17.Clinical profile of cirrhosis of liver in a tertiary care hospital of Assam, North East India. Bhattacharyya M, Barman NN, Goswami B. https://www.semanticscholar.org/paper/Clinical-profile-of-cirrhosis-of-liver-in-a-care-of-Bhattacharyya-Barman/9e83d99992482b0af0d76a0adaf03c34e3754534 IOSR J Dent Med Sci. 2016;5:21–27. [Google Scholar]
- 18.Prevalence of hypothyroidism in liver cirrhosis among Indian patients. Deepika G, Veeraiah N, Rao PN, Reddy DN. https://www.semanticscholar.org/paper/Prevalence-of-hypothyroidism-in-Liver-Cirrhosis-Deepika-Veeraiah/0f9715651c48ed0ab9873ac88ffa852a1c8c543f Int J Pharm Med Res. 2015;3:4–7. [Google Scholar]
- 19.Serum level of thyroid hormones in patients with chronic hepatitis C virus infection. El-Feki MAF, Abdalla NH, Atta MI, Ibrahim AA. Open J Endocr Metab Dis. 2016;6:126–134. [Google Scholar]
- 20.Frequency of cirrhotic cardiomyopathy in patients with cirrhosis of liver: a tertiary care hospital experience. Shaikh S, Abro M, Qazi I, Yousfani A. https://pjms.com.pk/index.php/pjms/article/view/512 Pak J Med Sci. 2011;27:744–748. [Google Scholar]
- 21.The heart matters when the liver shatters! cirrhotic cardiomyopathy: frequency, comparison, and correlation with severity of disease. Naqvi IH, Mahmood K, Naeem M, Vashwani AS, Ziaullah S. Prz Gastroenterol. 2016;11:247–256. doi: 10.5114/pg.2016.57962. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 22.Impact of diabetes mellitus on frequency and severity of hepatic encephalopathy in liver cirrhosis. Arshad MF, Butt Z, Mushtaq K, Salaria O. Endo Abs. 2016;44:102–103. [Google Scholar]
- 23.Diabetes mellitus is associated with hepatic encephalopathy in patients with HCV cirrhosis. Sigal SH, Stanca CM, Kontorinis N, Bodian C, Ryan E. Am J Gastroenterol. 2006;101:1490–1496. doi: 10.1111/j.1572-0241.2006.00649.x. [DOI] [PubMed] [Google Scholar]
- 24.Liver cirrhosis and diabetes: risk factors, pathophysiology, clinical implications and management. Garcia-Compean D, Jaquez-Quintana JO, Gonzalez-Gonzalez JA, Maldonado-Garza H. World J Gastroenterol. 2009;15:280–288. doi: 10.3748/wjg.15.280. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 25.Patterns and prevalence of dyslipidemia in patients with different etiologies of chronic liver disease. Unger LW, Forstner B, Schneglberger S, et al. Wien Klin Wochenschr. 2019;131:395–403. doi: 10.1007/s00508-019-01544-5. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 26.Albumin-bilirubin score for predicting the in-hospital mortality of acute upper gastrointestinal bleeding in liver cirrhosis: a retrospective study. Zou D, Qi X, Zhu C, et al. Turk J Gastroenterol. 2016;27:180–186. doi: 10.5152/tjg.2016.15502. [DOI] [PubMed] [Google Scholar]
- 27.Serum lipid profile as an indicator of the severity of liver damage in cirrhotic patients. Subhan F, Khan I, Arif R, Khan A, Khan A. https://www.bibliomed.org/?mno=20506 Rawal Med J. 2012;37:387–389. [Google Scholar]
- 28.The relationship between lipid profile and severity of liver damage in cirrhotic patients. Ghadir MR, Riahin AA, Havaspour A, Nooranipour M, Habibinejad AA. http://www.ncbi.nlm.nih.gov/pmc/articles/pmc3271321/ Hepat Mon. 2010;10:285–288. [PMC free article] [PubMed] [Google Scholar]
- 29.Dyslipidemia and fatty liver disease in overweight and obese children. Deeb A, Attia S, Mahmoud S, Elhaj G, Elfatih A. J Obes. 2018;2018:8626818. doi: 10.1155/2018/8626818. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 30.Dyslipidemia and mean lipid profile in patients with liver cirrhosis. Sohail S, Mustafa MI, Shaheen MA, Ali QM, Tariq MS. Int J Res Med Sci. 2020;8:1658–1661. [Google Scholar]