Nutritional Status In Patients With Hepatitis C Virus Biology Essay

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Malnutrition is a recognized complication of chronic liver disease with important prognostic implications. Hepatitis C virus liver disease spans a spectrum from chronic hepatitis C, to compensated cirrhosis, and finally decompensated cirrhosis. Our aim was to assess the nutritional status of patients with hepatitis C virus liver disease.

Methods: Patients were prospectively enrolled from the out-patient clinics, and categorized into 4 distinct populations of 100 patients each: Healthy controls (HC), those with chronic hepatitis C infection (CHC), compensated cirrhotics (CC) and decompensated cirrhotics (DC). The validated subjective global assessment tool was used to assess nutritional status.

Results: A total of 400 patients were enrolled, equally divided amongst the 4 groups. Most of the patients in the HC group were class A (best nutritional status). In contrast the majority (68 %) in the DC group were in the class C (worst status). While 86% of patients in the CHC group had a class A SGA score, only 10% of the CC did. The nutritional status showed a worsening from Class A to C through the 4 groups which was statistically significant (p-value <0.001).

Conclusion: Malnutrition occurs early, and progresses relentlessly throughout the spectrum of HCV disease.

Key words: Malnutrition, nutritional status, hepatitis C virus, liver disease


Malnutrition is an increasingly recognized complication of chronic liver disease that has important prognostic implications. It is found in 65-90% of patients with advanced liver disease and in almost 100% of candidates for liver transplantation.1, 2 . Malnourished patients with cirrhosis have a higher rate of complications and, overall, an increased mortality rate.3, 4 and there is a direct correlation between the progression of the liver disease and the severity of malnutrition.5, 6

The primary etiology of malnutrition is poor oral intake, stemming from multiple factors. Many patients with advanced liver disease have an altered sense of taste, which might be related to vitamin A and/or zinc deficiency.7. The dietary restrictions that are commonly recommended to these patients, such as restriction of sodium, protein, and fluids, can discourage adequate oral intake. In addition, weakness, fatigue, and low-grade encephalopathy can contribute to decreased oral intake8.

Malabsorption is another important factor in the development of malnutrition in this patient population. A number of mechanisms contribute to malabsorption. There might be a reduction in the bile-salt pool in patients with advanced liver disease, leading to fat malabsorption,9 , or bacterial overgrowth resulting from impaired small-bowel motility.10 The presence of portal hypertension has also been implicated as a cause of malabsorption and gastrointestinal protein loss.11, 12 An additional factor is the administration of medications that lead to malabsorption, such as neomycin, which is used in the treatment of hepatic encephalopathy.13 Screening all patients with chronic liver disease for nutritional abnormalities can identify those at risk of developing preventable complications.14

Hepatitis C virus liver disease spans a spectrum from chronic hepatitis c, to compensated cirrhosis, and to finally decompensated cirrhosis. While the overt malnutrition associated with cirrhosis has been documented in literature, there is little data regarding the nutritional status of patients who have simple chronic hepatitis C, with no evidence of severe liver dysfunction, apart from raised transaminases, or the compensated cirrhotic, and how they compare to the normal population.

This data is all the more relevant in the developing world, where lack of education and awareness, and inaccessibility to good health care lead to misinformation. Often faith healers, traditional medicine specialists (hakims), quacks and family members enforce strict and unnecessary dietary restrictions, predominantly of fat and protein, which initiate and worsen nutritional status.

Subjective global assessment (SGA) is a technique that combines multiple elements of nutritional assessment to classify the severity of malnutrition.15 These components are weight loss during the previous 6 months, changes in dietary intake, gastrointestinal symptoms, functional capacity, metabolic demands, signs of muscle wasting, and the presence of presacral or pedal edema. The SGA has been shown to be an excellent tool to assess nutritional status in many diseases, and has an interobserver reproducibility rate of 80%,16 Simple bedside methods like the "Subjective Global Assessment" or anthropometry have been shown to identify malnutrition adequately; the use of more complex scoring systems has not proved superior17.4 M. Plauth, M. Merli, J. Kondrup, P. Ferenci, A. Weimann and M.E.S.P.E.N. Müller, Guidelines for nutrition in liver disease and transplantation, Clin Nutr 16 (1997), pp. 43-55. Abstract | PDF (1653 K) | View Record in Scopus | Cited By in Scopus (163)

Materials and Methods

Patients were enrolled from the out-patient hepatology clinics at the Aga Khan University Hospital in a prospective manner. After a detailed assessment by the physician which included a history and examination, patients were categorized into 4 distinct populations of 100 patients each: Healthy controls (HC), those with chronic hepatitis C infection (CHC), compensated cirrhotics (CC) and decompensated cirrhotics (DC).

Healthy controls were the accompanying house-hold members (gender and closest age matched) of the patients who were assessed to be healthy after a history, examination and a negative HCV antibody screening test. The controls were exposed to the same socio-

economic conditions as the patients, and screening of family members of the index patient is standard practice at our hospital. CHC patients were those who had evidence of HCV viremia, raised transaminases, normal liver synthetic function, and an ultrasound of the liver showing a healthy liver, without evidence of portal hypertension, such as a dilated portal vein, or splenomegaly. Patients were classified as having CC when they had no history of decompensation, and an ultrasound showing features of cirrhosis ± portal hypertension, but no ascites. Finally DC were those who had either a history or physical examination compatible with a diagnosis of decompensation, or a ultrasound demonstrating free fluid in the abdomen.

Decompensation was defined as any episode of variceal bleeding, ascites, or porto-sytemic encephalopathy. The SGA form was filled in all instances by the consultant physician himself. A nutritional history was also noted, with particular reference to any protein or fat restriction. Written, informed consent was taken from all the study participants, and the study was approved by the university ethics committee.


A total of 400 patients were enrolled, equally divided amongst the 4 groups. Age and gender were comparable in all 4 groups (Table 1). Most of the patients in the HC group were class A according to the SGA, and there were none in class C. In contrast the majority (68 %) in the DC group were in the class C, while only 4 % were in the A category. The nutritional status showed a gradual transition from Class A to C, with a third of CC and the majority of DC all scoring a C on the SGA. Fourteen percent of patients with CHC also scored a B on the SGA. (Graph 1)


This is the first study to document the nutritional status of patients across the whole spectrum of hepatitis C virus infection. Most of the literature has been devoted to the nutritional aspects of cirrhotic and pre transplant patients,18, 19 but as our study shows, that the downslide begins much earlier, even before cirrhosis sets in. Even when these patients visit their physicians for other ailments, the nutritional deficiency may not be realized, so the process continues unabated, until frank malnutrition sets in.

The vast majority of patients across all the cohorts were on a diet that was restricted in protein and fat content in varying amounts. This stems from the false but firm belief that when the liver is affected, it should not be "burdened" with calories. This practice, which is endorsed not only by patients and their families, but also unfortunately by ill-informed physicians, is likely the reason why up to 14 % of patients with just CHC are moderately malnourished, and that the majority of CC patients are moderately or overtly malnourished.

The major change in SGS status in our study was seen between the CHC and the CC cohort of patients, and this is where the focus of nutritional intervention should be. Patients with CHC should be expected to have the same level of nutrition as HC, as no significant liver damage has occurred, but this wasn't the case. Up to 14 % of such patients had a moderate nutritional value, most likely a result of caloric and protein restriction. Poor nutritional status contributes to fatigue, anemia, and infection, all of which impair successful HCV treatment, as treatment itself causes cytopenias and profound fatigue. Patients who are in better nutritional health are more likely to tolerate treatment side-effects, require less disruption of treatment, or dose reductions, and therefore have a more successful outcome, as compared to those who are nutritionally depleted20, 21.

The CC group also had a very alarmingly small number of patients who were well nourished (10 %). The vast majority (56 %) were moderately nourished, and a significant number (34 %) were malnourished. The main reason we feel, for such a high number of cirrhotics to be malnourished is PCM, which promotes catabolism, hypoalbuminemia. This is a very delicate group of patients-while they are compensated, they already have extensive hepatic damage. Malnutrition accelerates their slide towards decompensation, as there is a direct correlation between the progression of the liver disease and the severity of malnutrition.5, 20

Patients with cirrhosis who are malnourished have a higher rate of hepatic encephalopathy, infection, and variceal bleeding.18, 22 They are also twice as likely to have refractory ascites.1 All of these events in a cirrhotic have high mortality rates. Numerous studies have found a correlation between poor nutritional status and a decreased survival rate, and malnutrition is an independent predictor of mortality in patients with cirrhosis.3, 23

It is no wonder then, that the nutritionally worst group has the maximum number of patients who have decompensated cirrhosis, followed by CC.

Utilizing modalities such as media campaigns, out-patient counseling, and awareness camps may all serve to fight the disinformation that takes the place of correct information, when it is not supplied by the health care provider. Physicians should also be made aware of not only the importance of nutritional evaluation and counseling in all patients with hepatitis C infection but also its regular assessment at follow up visits.

Patients should be encouraged to take as normal and balanced a diet as possible, including protein, which is routinely restricted in our setting. The institution of a bland, protein and calorie restricted diet is not warranted, and should be counseled against at every encounter with the patient and their attendants. Even in advanced cirrhosis, protein should only be restricted during a period of encephalopathy, and salt should be restricted if there is pedal odema and/or ascites.23, 24


Malnutrition exists throughout the spectrum of HCV disease. It occurs early in the disease process, and is relentless, with important prognostic implications. Etiologies include poor oral intake, malabsorption, but most importantly, protein calorie restriction. It is therefore, of critical importance to assess the nutritional status of all patients with chronic liver disease and to optimize nutritional in these patients. Malnutrition is a potentially reversible condition that, when identified and corrected, can lead to improved patient outcomes. This study documents the baseline nutritional status of a large cohort of patients in our setting, and provides data upon which other nutrition interventional studies may be based.


Faisal Wasim Ismail conceived the study, designed the protocol, recruited patients for the study, carried out the data analyses and drafted the manuscript.

Rustum Khan participated in recruiting patients for the study, and helped in the data analyses and manuscript drafting.

Lubna Kamani participated in the design of the study, recruiting patients for the study and helped in the statistical analysis.

Ashfaq Ahmad participated in recruiting patients for the study and helped to draft the manuscript.

Hasnain Ali Shah helped to draft the manuscript.

Saeed Hamid, helped to draft the manuscript.

Wasim Jafri helped to draft the manuscript.

All authors read and approved the final manuscript.

Source of funding: University research grant

Study sponsors: None

Competing interests: None

Financial disclosures: None

The above is on behalf of all authors.