As the primary metabolic organ in the body, liver holds a central role in the regulation of biochemical processes with respect to nutrient intake. Minimal hepatocyte injury in the earlier stages of HCV infection manifests only as subtle nutritional deficits. Only when a significant proportion of hepatocytes have been destroyed, as often seen in chronic liver disease in HCV patients, does the liver function begin to be affected. These alterations in liver function tend to result in poor nutritional intake as well as malabsorption of consumed nutrients and may have significant implications on the body’s nutritional status. Studies have indicated the prevalence of malnutrition to be as high as 60–90% among patients suffering from chronic liver disease (Lautz et al.

 1992; DiCecco et al. 1989)Malnutrition in HCV is a serious complication th?at negatively impacts survival, quality of life, and response to stressors like infections and surgery (Merli et al. 1996). In cirrhotic patients, it manifests not just in the form of Protein-Calorie Malnutrition (PCM) but also Micronutrient deficiencies, particularly in case of an advanced liver disease.

Both PCM and micronutrient deficiencies have been linked with a poorer outcome in patients with compensated as well as decompensated cirrhosis. On the other hand, obesity correlates equally well with a poor prognosis in HCV patients and has been linked to high viral loads and liver damage in patients, particularly the elderly (Petta et al. 2010).PCM in chronic HCV has been linked to an increase in mortality as well as morbidity by predisposing patients to complications like variceal bleeding and ascites. It manifests as Sarcopenia or loss of lean muscle mass which is regarded as the most objective feature of malnutrition in patients with chronic liver disease.Deficiency of micronutrients like vitamins A, C, K, B complexes contributes equally to morbidity by causing skin and vision changes, coagulopathies, and neurological symptoms.HCV patients commonly co-present with obesity and fatty liver, which are thought to potentiate the pro-inflammatory state observed in these patients, as evidenced by the higher circulating and hepatic CRP levels in obese patients with HCV (Jonsson et al. 2008).

In addition, Visceral adiposity is also thought to enhance HCV-induced whole-body Insulin resistance due primarily to the role of free fatty acids released by visceral adipocytes. Furthermore, studies have demonstrated increased levels of ALT in overweight patients, suggesting an increased risk for liver disease (Ruhl and Everhart 2003).Chronic liver diseases like hepatitis C that cause cirrhosis are among the most common indications for liver transplantation worldwide (Mazurak et al. 2017).

The Model for End-Stage Liver Disease or MELD score used by most liver transplant centers for prioritization of organ allocation, despite its innumerable benefits, is limited by its failure to adequately include nutritional status in the evaluation of patients. For this reason, other tools like the Child-Pugh classification that use objective measures of nutritional status such as the International Normalized Ratio (INR) and Serum Albumin levels are deemed superior to the MELD score, further highlighting the importance of nutritional status as a prognostic indicator in patients with chronic HCV.

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