With an overall prevalence exceeding 50% in women and around 25% in men, anaemia remains a major public health issue in India, contributing significantly to morbidity and impaired quality of life among affected populations¹,². The World Health Organization (WHO) defines anaemia as a decrease in haemoglobin (Hb) concentration and/or red blood cell (RBC) count, resulting in insufficient oxygen-carrying capacity to meet physiological demands, thereby leading to tissue hypoxia³,⁴. Conceptually, any pathological process that disrupts normal blood homeostasis can culminate in anaemia. From foetal life, where the liver is the primary hematopoietic organ, to postnatal life, where it maintains haematological stability, the liver plays a central role in blood homeostasis⁵,⁶. It serves as a storage depot for iron, folic acid, and vitamin B12, while also synthesizing transferrin, ferritin, and hepcidin—proteins crucial for iron homeostasis⁵,⁶. Consequently, chronic liver disease (CLD) is accompanied by a broad spectrum of biochemical and haematological disturbances⁶. CLD is defined as a hepatic disease persisting for six months or longer, characterized by chronic inflammation, progressive destruction of hepatic parenchyma, architectural distortion, and fibrosis, ultimately resulting in cirrhosis and functional decompensation⁶,⁷. Its etiological spectrum is wide, including alcohol-related liver disease (ALD), nonalcoholic steatohepatitis (NASH), autoimmune liver disease, genetic conditions such as Wilson’s disease, vascular causes like Budd–Chiari syndrome, chronic viral hepatitis B and C, hepatocellular carcinoma (HCC), metastatic involvement, and cryptogenic cirrhosis⁷⁻⁹. The development of anaemia in CLD is multifactorial. In ALD, ethanol exerts direct marrow toxicity, suppressing erythropoiesis, while concomitant malnutrition contributes to macrocytic anaemia due to vitamin B12 and folate deficiencies⁵,⁷,¹⁰. Portal hypertension with secondary hypersplenism promotes red cell sequestration and hemolysis, exacerbating cytopenias¹⁰,¹¹. Therapeutic interventions may also induce anaemia; for instance, patients with hepatitis C virus (HCV) infection receiving ribavirin and pegylated interferon often develop treatment-related anaemia¹⁰. Invasive procedures and surgeries, including liver transplantation, may further lead to perioperative blood loss and clinically significant anaemia¹⁰,¹². The clinical implications of anaemia in CLD are considerable. It is not only a marker of hepatic decompensation but also an independent risk factor for adverse outcomes, including increased mortality¹³,¹⁴. Furthermore, anaemia limits eligibility for invasive diagnostic and therapeutic procedures such as liver biopsy, as pre-existing anaemia predisposes to poor outcomes after haemorrhagic episodes¹³. Beyond hepatology, anaemia significantly worsens cancer-related fatigue, further diminishing quality of life in patients with hepatocellular carcinoma or metastatic liver disease¹⁴⁻¹⁶. The management of anaemia in CLD remains challenging due to its complex and often overlapping aetiologies. Addressing the underlying cause is essential, but clinical decision-making is hampered by the absence of standardized guidelines specifically tailored to anaemia in CLD. This results in suboptimal diagnostic evaluation and inconsistent management practices¹³,¹⁷,¹⁸. Additionally, since most patients have multifactorial aetiologies—ranging from nutritional deficiencies and bleeding to inflammation and marrow suppression—laboratory findings may be difficult to interpret in isolation¹⁸⁻²⁰. For example, a single etiological factor can manifest with multiple anaemia subtypes, while multiple concurrent mechanisms may converge to produce a single haematological phenotype. Globally, cirrhosis accounts for a substantial share of morbidity and mortality, with nearly one million deaths attributed to cirrhosis in 2010 alone²⁴. Anaemia, though frequently under-recognized, contributes to this burden by worsening clinical severity, impairing functional capacity, and limiting therapeutic options⁹,¹³,²⁶,³⁶. In India, multicentric data highlight the diverse aetiologies of CLD, predominantly alcohol and viral hepatitis, yet anaemia often remains an underestimated comorbidity²³,³⁰. Given these challenges, it is imperative to elucidate the clinicopathological correlates of anaemia in CLD. A comprehensive understanding of the interplay between hepatic dysfunction and haematological abnormalities is essential for developing effective interventions. Large, multidisciplinary centers with expertise in hepatology, liver transplantation, and oncology provide the ideal setting for such studies, offering insights into the multifactorial nature of anaemia and its impact on patient outcomes. This review synthesizes current evidence on anaemia in CLD, with a focus on its underlying mechanisms, epidemiology, clinical manifestations, prognostic significance, diagnostic challenges, and management strategies. By highlighting anaemia as both a reflection of disease severity and an independent contributor to adverse outcomes, this review underscores the need for early recognition and tailored therapeutic approaches in patients with CLD.

Study Design and Setting After obtaining approval from the Institutional Ethics Committee, a case-only observational study was conducted in the Department of Pathology of a tertiary-care multispecialty hospital over a three-year period (January 2019 – December 2022). The cohort comprised 100 adult patients with chronic liver disease (CLD) of any aetiology, with or without anaemia as defined by the World Health Organization (WHO) criteria3,4. Inclusion and Exclusion Criteria Consecutive adults (≥18 years) with biopsy- and/or imaging-confirmed CLD of ≥6 months’ duration were enrolled. Exclusion criteria were: pregnancy, acute hepatitis, congenital bleeding disorders, and incomplete medical records. Data Collection Cases were identified from the total pool of CLD patients reported during the study period. Data were collected prospectively using a pre-designed case study proforma. Detailed clinical information was recorded, including age, sex, clinical features, drug history, addictions, and imaging findings. Haematological Assessment Anaemia workup included: • Complete blood count and indices: Haemoglobin, red blood cell indices, reticulocyte count (K3 EDTA, Automated cell counter ALINITY Hq – Abbott). • Peripheral blood smear examination for morphological classification of anaemia. Biochemical Assessment Additional biochemical investigations were performed to evaluate the aetiology of anaemia: • Iron studies, serum vitamin B12, high-sensitivity C-reactive protein (hsCRP), lactate dehydrogenase (LDH), serum haptoglobin, D-dimer, and INR. • Automated analyzers used included: VITROS XT-7600, Alinity ci (Abbott), and ACL TOP 750 Analyzer (Werfen). • Reference ranges were standardized as per Wallach’s Interpretation of Diagnostic Tests, 9th edition45. Etiology of CLD The underlying CLD aetiology in each case was determined by histopathology (core biopsy and/or explant specimen) and correlated with clinical history, imaging findings, and laboratory investigations. These included viral markers (HBV, HCV, HIV, EBV), autoimmune hepatitis markers, liver and renal function tests. Disease Severity Scoring Severity of liver disease was assessed using the Model for End-Stage Liver Disease (MELD) score, calculated as7,44: MELD = 9.57 × ln(creatinine in mg/dL) + 3.78 × ln(total bilirubin in mg/dL) + 11.2 × ln(INR) + 6.43. With serum sodium included, “MELD-Na” score was calculated as follows[7,8,56]: MELD-Na score = MELD score – Serum Na – (0.025*MELD score*(140- Serum Na)) +140 With serum sodium included, the MELD-Na score was calculated as7,8,44: MELD-Na score = MELD score – Serum Na – (0.025*MELD score*(140- Serum Na)) +140 Statistical Analysis Data analysis was performed using IBM SPSS Statistics Version 20. • Categorical variables: expressed as frequencies and percentages; associations tested using Chi-square or Fisher’s exact test. • Continuous variables: expressed as mean, median, and standard deviation; non-parametric tests applied (as normality assumption was not met). Kruskal–Wallis test was used for >2 groups, and Mann–Whitney U test for two independent groups. • Correlations: assessed using Pearson’s correlation coefficient, and visualized with scatter plots. • Significance threshold: p < 0.05 considered statistically significant, and p < 0.01 highly significant.

Patient Demographics and Clinical Features A total of 100 patients with histopathologically confirmed CLD were included. The age range was 18–82 years with a male-to-female ratio of 1.44:1. Jaundice was the most common clinical feature (53%), followed by loss of weight and appetite (46%). Decompensated liver disease was observed in 45% of patients. Statistically significant differences were noted in the distribution of most clinical features across aetiologies, except for loss of weight and appetite (P = 0.137). Figure 1: Clustered heatmap: Demographics, Clinical features, Anaemia profiles across CLD Aetiologies: The heatmap displays demographic variables, clinical features, and anaemia profiles (rows) mapped against CLD aetiologies (columns: hepatic metastasis, hepatocellular carcinoma, alcoholic liver disease [ALD], non-alcoholic steatohepatitis [NASH], and autoimmune CLD). Colour intensity denotes relative frequency or severity, with cell annotations indicating exact values. Clustering highlights distinct patterns, such as male predominance and more severe anaemia in ALD, higher jaundice and weight loss in HCC, metabolic associations in NASH, and autoimmune-specific trends. Aetiologies and Histopathological Findings Hepatic metastasis was the most common aetiology (28%), followed by hepatocellular carcinoma (16%) and ALD (15%). Overall, cirrhosis was present in 47% of cases, most commonly micronodular (46.8%). No significant correlation was observed between type of cirrhosis or hepatitis severity and anaemia severity. Figure 2: CLD Aetiologies Distribution of CLD aetiologies: Pie chart showing the frequency distribution of chronic liver disease (CLD) etiologies in the study cohort. Hepatic metastasis was the most common cause, followed by hepatocellular carcinoma (HCC), alcoholic liver disease (ALD), non-alcoholic steatohepatitis (NASH), and autoimmune CLD. Table 3: Clinical features stratified by aetiology of chronic liver disease (n = 100) Corelation with Biochemical Parameters A significant negative correlation was found between haemoglobin levels and serum iron, TIBC, LDH, D-Dimer, hsCRP, and biochemical parameters used in MELD-Na calculation (urea, creatinine, bilirubin, INR, sodium). This indicates worsening anaemia with increasing disease severity. Figure 4. Correlation matrix heatmap of biomarkers with haemoglobin in patients with chronic liver disease The heatmap demonstrates Pearson’s correlation coefficients between haemoglobin and key biochemical parameters. Strong negative correlations were observed with MELD-Na score, bilirubin, INR, creatinine, LDH, D-dimer, and hsCRP, indicating that worsening anaemia parallels advancing liver dysfunction, haemolysis, and systemic inflammation. Positive correlations were seen with serum iron and transferrin saturation, reflecting preserved iron availability. The color gradient represents the strength and direction of correlations (red = negative, blue = positive), and numerical values in each cell denote the correlation coefficient. Figure 5: Clinical Feature and Anaemia Severity by Aetiology • Blue shades = lower prevalence/frequency. • Red shades = higher prevalence/frequency. • Columns = anaemia aetiologies. • Rows = clinical features + anaemia severity (WHO categories) Comparison Between Severity of Anaemia and CLD A strong negative correlation (P = 0.0609) was observed between MELD-Na score and haemoglobin. Higher MELD-Na scores were associated with lower haemoglobin levels, reflecting increased severity of anaemia with progressive liver disease. Figure 6. Correlation of MELD-Na with Haemoglobin Regression plot illustrating the negative correlation between MELD-Na score and haemoglobin levels. Higher MELD-Na scores were associated with lower haemoglobin concentrations, reflecting greater anaemia severity in advanced CLD. Patient Outcomes During six-month follow-up, mortality was 4% and 8% of patients were lost to follow-up. Surgical intervention was required in 60% of patients, including liver transplant (29%) and partial hepatectomy (31%), with one post-operative death. Among the remainder, 22% required repeated hospitalization for complications, while only 7% could be managed medically on an outpatient basis, highlighting the significant morbidity in this cohort. Figure 7: Patient Management and Outcomes at 6-Month Follow up Pie chart depicting proportions of management and clinical outcomes in CLD patients. Interventions included liver transplant, partial hepatectomy, repeated hospitalizations, and outpatient management. Loss to follow-up and mortality are also represented. The chart highlights the high proportion of patients requiring surgical management and the morbidity associated with CLD.

Chronic liver disease (CLD) remains a major public health problem in India and worldwide, characterized by progressive hepatic injury that leads to fibrosis, cirrhosis and organ dysfunction. CLD significantly impairs patients' quality of life and is associated with considerable morbidity and mortality. The high burden of anaemia in the general Indian population and in CLD underscores the clinical importance of systematic screening and management. Population and community studies have reported very high anaemia prevalence among women and men in India. 1,2 In our cohort of 100 histopathologically confirmed CLD patients, anaemia prevalence was 79%, with the majority classified as moderate severity (haemoglobin 8.0–10.9 g/dL). The multifactorial aetiopathogenesis of anaemia in CLD—encompassing nutritional deficiencies (vitamin B12, folate), iron deficiency, anaemia of chronic disease (ACD), hypersplenism, haemolysis, gastrointestinal blood loss and treatment‑related effects—makes accurate phenotyping essential for targeted therapy. Foundational definitions and diagnostic thresholds for anaemia and haemoglobin concentrations follow internationally accepted criteria. 3,4 The liver has numerous roles relevant to haematological homeostasis: it stores iron and B vitamins, synthesizes proteins critical for iron metabolism such as transferrin, ferritin and hepcidin, and modulates erythropoiesis indirectly through systemic inflammation and renal interactions. Accordingly, chronic hepatic dysfunction precipitates derangements in iron handling, inflammatory signaling, and coagulation, all of which contribute to abnormal blood indices in CLD. 5,6 The clinical and histopathological spectrum in our cohort was heterogeneous: malignant aetiologies (hepatic metastases and hepatocellular carcinoma) accounted for 44% of cases, while alcoholic liver disease (ALD), NASH, viral hepatitis and cryptogenic cirrhosis comprised the remainder. Cirrhosis was present in 47% of patients, predominantly showing a micronodular pattern, consistent with prior tertiary‑center series. 7,30,31 We observed a robust negative correlation between MELD‑Na score and haemoglobin concentration, indicating that anaemia severity parallels liver disease progression. This aligns with prior reports that show anaemia correlates with portal hypertension, hepatic decompensation and worse clinical outcomes in advanced chronic liver disease. 9,26,27 Detection: Given the high prevalence and varied mechanisms, routine screening should include a complete blood count with red cell indices and peripheral smear, iron studies (serum iron, ferritin, transferrin saturation, TIBC), vitamin B12 and folate assays, and haemolysis markers (LDH, haptoglobin, reticulocyte count) where indicated. Additionally, measurement or consideration of hepcidin and the hepcidin: ferritin ratio may aid discrimination between true iron deficiency and iron‑restricted erythropoiesis in the inflammatory milieu of CLD. Recent systematic reviews and meta‑analyses document altered hepcidin dynamics across CLD etiologies, reinforcing its diagnostic utility. 18,20,42 Treatment and management principles: Therapeutic strategies must be individualized according to the specific cause(s) of anaemia. For iron‑deficiency states, intravenous iron is often preferred in CLD due to oral malabsorption, intolerance, and inflammation‑mediated sequestration. A recent randomized controlled trial in patients with cirrhosis and iron‑deficiency anemia following variceal bleeding demonstrated significantly greater haemoglobin recovery, normalization of iron stores, and improvements in quality‑of‑life domains with intravenous ferric carboxymaltose compared with oral iron, without a difference in liver‑related adverse events. 39 Correction of vitamin B12 and folate deficiency is simple, low‑risk, and frequently efficacious in macrocytic anaemias often seen in alcohol‑related CLD; early repletion can expedite haematological recovery and improve symptoms such as fatigue. 10,11 Anaemia of chronic disease (ACD) and mixed anaemias require treatment of the underlying liver disease and management of systemic inflammation. In select patients with persistent symptomatic anaemia despite correction of deficits, erythropoiesis‑stimulating agents (ESAs) have been used as adjuncts, though evidence in CLD is limited and risks (thromboembolism, hypertension) must be balanced against potential benefits. 17,18 Haemolytic anaemia—in our series disproportionately represented among severe anaemia cases—should prompt evaluation for hypersplenism, autoimmune hemolysis, drug‑induced mechanisms, and microangiopathic processes. Management is cause‑directed, and in refractory cases may necessitate hematology input and consideration of interventional approaches. 11,19 Transfusion considerations: Blood transfusion remains essential for hemodynamic instability or acute large volume loss but carries risks in CLD patients (volume overload, alloimmunization, infection transmission, and potentially increased portal pressures). Contemporary guidance favors restrictive transfusion thresholds where clinically appropriate, and interventions that restore iron stores (especially IV iron) can reduce transfusion dependence. 51,39,12 Quality of life and morbidity: Anaemia substantially worsens health‑related quality of life (HRQoL) in CLD—through fatigue, exercise intolerance, and cognitive impairment—and contributes to higher hospitalization rates and perioperative morbidity. Interventional studies and care‑bundle approaches in recent years indicate that addressing anaemia and nutritional deficits improves patient‑reported outcomes and reduces resource utilization. 14,15,41 Implementation and systems approaches: Standardized protocols for screening, investigation, and stepwise management of anaemia should be integrated into hepatology practice. Multidisciplinary care involving hepatology, hematology, nutrition and nursing improves detection, facilitates timely iron and vitamin repletion, and supports perioperative optimisation for patients undergoing transplant or hepatic resections. Recent narrative and systematic reviews emphasize proactive, team‑based management of hematologic complications in cirrhosis. 40,41 Limitations: This study is limited by its single‑center design, moderate sample size, and six‑month follow‑up. Some confounders (socioeconomic status, dietary intake, prior outpatient therapies) were not fully captured. Despite these limitations, the integration of histopathology with comprehensive biochemical profiling strengthens the clinical relevance of our findings. Conclusions: Anaemia is highly prevalent in CLD and is closely associated with disease severity. Early detection using a structured diagnostic algorithm and targeted therapy (IV iron for iron deficiency, vitamin B12/folate repletion, treatment of underlying inflammation, and judicious use of ESAs and transfusion) can improve haemoglobin levels, reduce transfusion needs, enhance quality of life, and potentially decrease CLD‑related morbidity. Incorporation of routine anaemia screening and treatment pathways into hepatology services is recommended. 13,39,42

Chronic liver disease (CLD) continues to represent a major clinical and public health burden due to its progressive nature, multisystem involvement, and frequent association with anaemia. In this study, hepatic malignancies—particularly metastatic disease—emerged as the leading cause of CLD, followed by hepatocellular carcinoma and Alcoholic Liver Disease, highlighting a shift from traditionally predominant non-malignant etiologies. Nearly half of all patients had cirrhosis, most often micronodular in morphology. Anaemia was highly prevalent, predominantly of moderate severity, with vitamin B12 deficiency, anaemia of chronic disease, and iron deficiency being the most frequent underlying causes. A significant negative correlation was observed between haemoglobin levels and disease severity as measured by the MELD-Na score, reinforcing f’r as an important prognostic marker in CLD. Furthermore, biochemical markers of haemolysis, inflammation, and renal dysfunction were also significantly associated with the severity of anaemia, suggesting their potential role in risk stratification. Outcomes over six months underscored the considerable morbidity in this cohort, with a majority requiring surgical interventions such as transplantation or partial hepatectomy, while only a minority could be managed conservatively. Mortality remained relatively low, largely due to timely surgical management. These findings emphasize the need for routine screening and comprehensive management of anaemia in CLD patients. Early detection and targeted treatment of anaemia may improve quality of life, reduce hospitalization, and enhance overall outcomes. Future multicentric prospective studies are warranted to establish standardized guidelines for diagnosis and management of anaemia in CLD, ensuring better integration of haematological care into hepatology practice.

1. Panyang R, Teli A, Saikia S. Prevalence of anemia among the women of childbearing age belonging to the tea garden community of Assam, India: A community-based study. J Family Med Prim Care. 2018;7(4):734. 2. Singh A, Ram S, Singh S, Tripathi P. Prevalence and determinants of anaemia among men in rural India: Evidence from a nationally representative survey. PLOS Global Public Health. 2022 Dec 1;2(12):e0001159. 3. Kumar V, Abbas AK, Aster JC, Perkins JA. Robbins basic pathology. 935 p. 4. Vmnis. Haemoglobin concentrations for the diagnosis of anaemia and assessment of severity. 5. Rappai M, Rao PS, Ilanthodi S. A STUDY OF VARIATION IN HAEMATOLOGICAL PARAMETERS IN CHRONIC LIVER DISEASE. J Evol Med Dent Sci. 2019 Jun 17;8(24):1949–52. 6. Tara V. A Comparative Study of Variations in Haemotological Parameters in Chronic Liver Disease. IOSR Journal of Dental and Medical Sciences (IOSR-JDMS) e-ISSN [Internet]. 2019;18:1–05. Available from: www.iosrjournals.org 7. Sharma A, Shivaraj ;, Affiliations N. Chronic Liver Disease Continuing Education Activity [Internet]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK554597/?report=printable 8. Acharya G, Kaushik RM, Gupta R, Kaushik R. Child-Turcotte-Pugh Score, MELD Score and MELD-Na Score as Predictors of Short-Term Mortality among Patients with End-Stage Liver Disease in Northern India. Inflamm Intest Dis. 2020 Feb 1;5(1):1–10. 9. Scheiner B, Semmler G, Maurer F, Schwabl P, Bucsics TA, Paternostro R, et al. Prevalence of and risk factors for anaemia in patients with advanced chronic liver disease. Liver International. 2020 Jan 1;40(1):194–204. 10. Gonzalez-Casas R, Jones EA, Moreno-Otero R. Spectrum of anemia associated with chronic liver disease. Vol. 15, World Journal of Gastroenterology. Baishideng Publishing Group Co; 2009. p. 4653–8. 11. Simbrunner B, Beer A, Wöran K, Schmitz F, Primas C, Wewalka M, et al. Portal hypertensive gastropathy is associated with iron deficiency anemia. Wien Klin Wochenschr. 2020 Jan;132(1–2):1–11. 12. Tan TCH, Crawford DHG, Franklin ME, Jaskowski LA, Macdonald GA, Jonsson JR, et al. The serum hepcidin:ferritin ratio is a potential biomarker for cirrhosis. Liver Int. 2012 Oct;32(9):1391–9. 13. Paternostro R, Kapzan L, Mandorfer M, Schwarzer R, Benedikt S, Viveiros A, et al. Anemia and iron deficiency in compensated and decompensated cirrhosis: Prevalence and impact on clinical outcomes. J Gastroenterol Hepatol. 2020 Sep;35(9):1619–27. 14. Dicato M, Plawny L, Diederich M. Anemia in cancer. Ann Oncol. 2010 Oct;21 Suppl 7:vii167-72. 15. Stasi R, Abriani L, Beccaglia P, Terzoli E, Amadori S. Cancer-Related Fatigue: Evolving Concepts in Evaluation and Treatment. Vol. 98, Cancer. 2003. p. 1786–801. 16. J J Caro 1 MSAWGG. Anemia as an independent prognostic factor for survival in patients with cancer: a systemic, quantitative review. Cancer . 2001; 17. Stein J, Connor S, Virgin G, Ong DEH, Pereyra L. Anemia and iron deficiency in gastrointestinal and liver conditions. Vol. 22, World Journal of Gastroenterology. Baishideng Publishing Group Co; 2016. p. 7908–25. 18. Intragumtornchai T, Rojnukkarin P, Swasdikul D, Israsena S. The role of serum ferritin in the diagnosis of iron deficiency anaemia in patients with liver cirrhosis. J Intern Med. 1998 Mar;243(3):233–41. 19. Özatli D, Köksal AS, Haznedaroglu IC, Simsek H, Karakus S, Büyükasik Y, et al. Erythrocytes: Anemias in Chronic Liver Diseases. Hematology. 2000;5(1):69–76. 20. Gkamprela E, Deutsch M, Pectasides D. Iron deficiency anemia in chronic liver disease: etiopathogenesis, diagnosis and treatment. Ann Gastroenterol. 2017;30(4):405–13. 21. Williamson M, Snyder M. Wallach’s Interpretation of Diagnostic Tests . Ninth Edition. New Delhi: Wolter Kluwer(India) Pvt Ltd; 2013. 71–381 p. 22. Kamath PS, Kim WR. The model for end-stage liver disease (MELD). Hepatology. 2007 Mar;45(3):797–805. 23. Mondal D, Das K, Chowdhury A. Epidemiology of Liver Diseases in India. Vol. 19, Clinical Liver Disease. John Wiley and Sons Inc; 2022. p. 114–7. 24. Mokdad AA, Lopez AD, Shahraz S, Lozano R, Mokdad AH, Stanaway J, et al. Liver cirrhosis mortality in 187 countries between 1980 and 2010: a systematic analysis. BMC Med. 2014 Sep 18;12:145. 25. Frijo Jose A, Jayaraj PM, Chethan G. Anemia in Chronic Liver Disease and Liver Failure in Adults - A Clinical Study. International Journal of Contemporary Medical Research [IJCMR]. 2020 Feb;7(2). 26. Manrai M, Dawra S, Srivastava S, Kapoor R, Singh A. Anemia in cirrhosis: An underestimated entity. World J Clin Cases. 2022;10(3):777–89. 27. Mallik S, Sarkar K, Rahman M, Haldar SN. Clinical and Etiological Study on Chronic Liver Diseases. International Journal of Contemporary Medicine, Surgery and Radiology. 2018 Jul;3(2). 28. Wang TE, Chang CW, Liu CY, Chen MJ, Chu CH, Lin SC, et al. Clinical Characteristics of Hepatocellular Carcinoma in Elderly Patients. Int J Gerontol. 2013 Jun;7(2):85–9. 29. Horn SR, Stoltzfus KC, Lehrer EJ, Dawson LA, Tchelebi L, Gusani NJ, et al. Epidemiology of liver metastases. Cancer Epidemiol. 2020 Aug;67:101760. 30. Mukherjee PS, Vishnubhatla S, Amarapurkar DN, Das K, Sood A, Chawla YK, et al. Etiology and mode of presentation of chronic liver diseases in India: A multi centric study. PLoS One. 2017;12(10):e0187033. 31. Griscom JT, Patrick ;, Wolf S. Liver Metastasis Continuing Education Activity [Internet]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK553118/ 32. Ho CH, Yu YB, Wu PH. The prevalence of iron deficiency anemia and its clinical implications in patients with colorectal carcinoma. J Chin Med Assoc. 2008 Mar;71(3):119–22. 33. Cai Q, Zhu M, Duan J, Wang H, Sheng J. Establishment of prognostic scoring models for different etiologies of acute decompensation in hospitalized patients with cirrhosis. Journal of International Medical Research. 2019 Sep 31;47(9):4492–504. 34. Mathurin SA, Agüero AP, Dascani NA, Prestera JA, Gianserra C, Londero E, et al. [Anemia in hospitalized patients with cirrhosis: prevalence, clinical relevance and predictive factors]. Acta Gastroenterol Latinoam. 2009 Jun;39(2):103–11. 35. Jain D, Aggarwal H, Rao A, Dahiya S, Singla S. Hematological spectrum in patients with alcoholic liver cirrhosis: a model of end-stage liver disease score based approach. International Journal of Advances in Medicine. 2016;234–40. 36. Singh S, Manrai M, Parvathi VS, Kumar D, Srivastava S, Pathak B. Association of liver cirrhosis severity with anemia: Does it matter? Ann Gastroenterol. 2020 May 9;33(3):272–6. 37. Kim WR, Biggins SW, Kremers WK, Wiesner RH, Kamath PS, Benson JT, et al. Hyponatremia and Mortality among Patients on the Liver-Transplant Waiting List. New England Journal of Medicine. 2008 Sep 4;359(10):1018–26. 38. Ala A WAAKDJSM. Wilson’s disease. Lancet. 2007 Feb 3;369(9559):397–408. 39. Tabish M, Agarwal S, Gopi S, Rana R, Ahmed S, Gunjan D, Sharma S, Saraya A. Randomized Controlled Trial of Intravenous Ferric Carboxymaltose vs Oral Iron to Treat Iron Deficiency Anemia After Variceal Bleed in Patients With Cirrhosis. Am J Gastroenterol. 2024;119(10):2061-2069. doi:10.14309/ajg.0000000000002775. 40. Fierro-Angulo OM, González-Regueiro JA, Pereira-García A, Ruiz-Margáin A, Solis-Huerta F, Macías-Rodríguez RU. Hematological abnormalities in liver cirrhosis. World J Hepatol. 2024;16(9):1229-1244. doi:10.4254/wjh.v16.i9.1229. 41. Tantia P, Aggarwal P, Acharya S, Kumar S, Kothari M, Kadam A, Patil R. Exploring Haematological Complications in Cirrhosis of the Liver: A Comprehensive Review. Cureus. 2024;16(7):e65319. doi:10.7759/cureus.65319. 42. Sharma R, Zhao W, Zafar Y, Murali AR, Brown KE. Serum hepcidin levels in chronic liver disease: a systematic review and meta-analysis. Clin Chem Lab Med. 2023;62(3):373-384. doi:10.1515/cclm-2023-0540. 43. Iolascon A, Andolfo I. Recommendations for diagnosis, treatment, and prevention of iron deficiency and iron deficiency anemia. HemaSphere. 2024;8:e108.