Malnutrition in Liver Cirrhosis: A Review

Rungta, Sumit; Deep, Amar; Swaroop, Suchit

doi:10.7860/jcdr/2019/38412.12822

Cited by 2 publications

(2 citation statements)

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“…Similar to DRM, in sarcopenia, barriers to adequate calorie and protein intake such as anorexia and nausea are also existent [ 32 ]. In patients with decompensated liver cirrhosis, anorexia contributes up to an 80% prevalence of DRM [ 56 ] while 90% of patients with advanced alcoholic liver disease experience anorexia [ 10 ]. Anorexia may be triggered by an imbalance between orexigenic and anorexigenic hormones, by the chronic increase in circulating proinflammatory cytokines, zinc and vitamin A deficiency, delayed gastric emptying and portal hypertension resulting in gastric and intestinal tissue congestion as well extrinsic compression due to ascites [ 15 , 32 , 44 , 49 , 57 ].…”

Section: Molecular Mechanisms Contributing To Disease-related Malnmentioning

confidence: 99%

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Molecular Mechanism Contributing to Malnutrition and Sarcopenia in Patients with Liver Cirrhosis

Meyer

Bannert

Wiese

et al. 2020

IJMS

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Liver cirrhosis is frequently accompanied by disease-related malnutrition (DRM) and sarcopenia, defined as loss of skeletal muscle mass and function. DRM and sarcopenia often coexist in cirrhotic patients and are associated with increased morbidity and mortality. The clinical manifestation of both comorbidities are triggered by multifactorial mechanisms including reduced nutrient and energy intake caused by dietary restrictions, anorexia, neuroendocrine deregulation, olfactory and gustatory deficits. Maldigestion and malabsorption due to small intestinal bacterial overgrowth, pancreatic insufficiency or cholestasis may also contribute to DRM and sarcopenia. Decreased protein synthesis and increased protein degradation is the cornerstone mechanism to muscle loss, among others mediated by disease- and inflammation-mediated metabolic changes, hyperammonemia, increased myostatin and reduced human growth hormone. The concise pathophysiological mechanisms and interactions of DRM and sarcopenia in liver cirrhosis are not completely understood. Furthermore, most knowledge in this field are based on experimental models, but only few data in humans exist. This review summarizes known and proposed molecular mechanisms contributing to malnutrition and sarcopenia in liver cirrhosis and highlights remaining knowledge gaps. Since, in the prevention and treatment of DRM and sarcopenia in cirrhotic patients, more research is needed to identify potential biomarkers for diagnosis and development of targeted therapeutic strategies.

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Section: Molecular Mechanisms Contributing To Disease-related Malnmentioning

confidence: 99%

“…The liver is the second largest organ in the human body [ 10 ] and primary organ for metabolism [ 11 ]. Its functional integrity is essential for the supply and inter-organ trafficking of macronutrients (proteins, fat and carbohydrates) and their metabolism [ 12 , 13 ].…”

Section: Introductionmentioning

confidence: 99%

Molecular Mechanism Contributing to Malnutrition and Sarcopenia in Patients with Liver Cirrhosis

Meyer

Bannert

Wiese

et al. 2020

IJMS

View full text Add to dashboard Cite

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Risk Factors for Progressive Fibrosis and Cirrhosis in Patients With Chronic Hepatitis C in India

Deep,

Kumari,

Malakar

et al. 2024

Cureus

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Background Liver cirrhosis (LC) caused by chronic hepatitis C (CHC) infection is a major global public health concern. This study will look at the risk factors for progressive fibrosis and cirrhosis in patients with persistent hepatitis C virus (HCV) infection. Methods In this cohort study, a total of 300 patients were included. We collected comprehensive diagnostic records for the entire study group of 200 people with chronic hepatitis C infection. For the comparison, 100 healthy people were recruited and assessed. FibroScan (Echosens, Paris, France) scores were used to categorize liver fibrosis stages: F0-F1 (no or mild fibrosis, <7 kPa), F2 (moderate fibrosis, 7-8.99 kPa), F3 (significant fibrosis, 9-12.49 kPa), and F4 (cirrhosis, ≥12.5 kPa). Their demographic, biochemical, and serological data were evaluated and compared. Results Most patients were males (47% females and 53% males). In the CHC group, the mean age of diagnosis was 37.68±11.57 years, whereas in the chronic hepatitis C-related liver cirrhosis (CHC-LC) group, the mean age was 48.89±12.30 years (p=0.01). Compared to normal individuals, CHC patients had higher body mass index (BMI) (22.37±1.89 versus 21.72±1.95, p=0.01), alanine aminotransferase (ALT) (36.70±7.13 versus 82.78±82.53, p=0.01), and aspartate aminotransferase (AST) (34.96±6.04 versus 80.82±91.77, p=0.01). However, compared to the patients with CHC, the patients with LC have lower platelet (PLT) count (1.51±0.78 versus 1.7±0.41, p=0.01) and higher liver enzymes (AST: 117.7±186.9 versus 80.8±91.7, p=0.01; ALT: 86.71±80.24 versus 82.78±82.53, p=0.01). On regression analysis, higher BMI, older age, low hemoglobin (Hb), and higher bilirubin, ALT, AST, and prothrombin time (PT) were associated with LC. Conclusion It is imperative to shift toward prevention and early intervention as the new approach to managing patients with HCV-related cirrhosis. Cirrhosis should be suspected in older patients with CHC who are obese and have low platelet counts with higher liver enzymes.

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Malnutrition in Liver Cirrhosis: A Review

Cited by 2 publications

References 0 publications

Molecular Mechanism Contributing to Malnutrition and Sarcopenia in Patients with Liver Cirrhosis

Molecular Mechanism Contributing to Malnutrition and Sarcopenia in Patients with Liver Cirrhosis

Risk Factors for Progressive Fibrosis and Cirrhosis in Patients With Chronic Hepatitis C in India

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