Diagnosis and management of chronic liver disease in older people

Fox, Mark; Fox, Jenny; Davies, Mervyn H.

doi:10.1017/s0959259810000365

Cited by 9 publications

(3 citation statements)

References 152 publications

(144 reference statements)

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“…Hepatic fibrosis is a significant pathology that occurs in most types of chronic liver disease, such as alcoholic liver disease, nonalcoholic fatty liver disease (NAFLD)/nonalcoholic steatohepatitis (NASH), viral hepatitis infection, cholestasis, and hemochromatosis, among others (Friedman, 2003). Advancing age has been shown to accelerate liver injury and increase the severity of fibrosis associated with alcohol abuse, NAFLD/NASH and hepatitis C infection (Martin‐Carbonero et al, 2004; Seitz and Stickel, 2007; Davis et al, 2010; Frith and Newton, 2010; Fox et al, 2011; Gan et al, 2011). We have recently reported a high prevalence of liver fibrosis in elderly cadavers (mean age, 82.1 ± 10.4 years) with diverse causes of death (Mak et al, 2012).…”

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confidence: 99%

Liver Fibrosis in Elderly Cadavers: Localization of Collagen Types I, III, and IV, α‐Smooth Muscle Actin, and Elastic Fibers

Mak

Chu

Lau

et al. 2012

The Anatomical Record

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We have shown a high prevalence of liver fibrosis in elderly cadavers with diverse causes of death by Sirius red stain; however, the various collagen types in these samples have yet to be evaluated. To further characterize the histopathology of the fibrotic lesions in the livers of these elderly cadavers, this study used immunohistochemistry and histochemistry to identify the principal collagens produced in liver fibrosis, fibrogenic cells and elastic fibers. Collagen I and III immunoreactions were found to colocalize in collagen fibers of fibrotic central veins, perisinusoidal fibrotic foci, portal tract stroma, and fibrous septa. a-Smooth muscle actinexpressing perisinusoidal hepatic stellate cells (HSCs), as well as perivenular, portal, and septal myofibroblasts, were closely associated with collagen fibers, reflecting their fibrogenic functions. HSCs and myofibroblasts were also noted to express collagen IV, which may contribute to production of basal lamina-like structures. In fibrotic livers, the sinusoidal lining showed variable immunostaining for collagen IV. Collagen IV immunostaining revealed vascular proliferation and atypical ductular reaction at the portal-septal parenchymal borders, as well as capillarylike vessels in the lobular parenchyma. While elastic fibers were absent in the space of Disse, they were found to codistribute with collagens in portal tracts, fibrous septa and central veins. Our combined assessment of collagen types, HSCs, myofibroblasts, and elastic fibers is significant in understanding the histopathology of fibrosis in the aging liver.

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confidence: 99%

Liver Fibrosis in Elderly Cadavers: Localization of Collagen Types I, III, and IV, α‐Smooth Muscle Actin, and Elastic Fibers

Mak

Chu

Lau

et al. 2012

The Anatomical Record

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“…Older livers regenerate less effectively and undergo cellular senescence (Tomaszewski & Wong, 2019). Advancing age has been shown to accelerate liver injury in people with alcoholic liver disease, nonalcoholic fatty liver disease (NAFLD)/steatohepatitis (NASH), and hepatitis C virus (HCV) infection (Floreani, 2007; Fox et al, 2011; Frith et al, 2009; Gan et al, 2011; Jansen, 2002; Martín‐Carbonero et al, 2004; Noureddin et al, 2013), which are the most common chronic liver disorders among young adults worldwide. These liver diseases are complicated by steatosis, fibrosis, cirrhosis, cancer, and inflammation, but there are little data on the incidence of these histopathologies in older adults of the general population.…”

Section: Introductionmentioning

confidence: 99%

A review of hepatic fibrosis‐associated histopathology in aged cadavers

Mak

Kee

Cheng

2022

The Anatomical Record

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This article reviews hepatic fibrosis-associated histopathology of aged cadavers (mean age 82 years). A study of 68 livers identified steatosis in 35.5%, central vein fibrosis in 49.2%, perisinusoidal fibrosis in 63.2%, portal tract fibrosis in 47.7%, septa formation in 44.1%, bridging fibrosis in 30.8%, and cirrhosis in 4.4% of the samples as well as one hepatocellular carcinoma and six metastatic tumors. Other studies have revealed that collagens I, III, IV, V, and VI and fibronectin constitute the matrices of fibrous central veins, perisinusoidal space, portal tracts, and septa. Elastin is rich in portal tracts and fibrous septa but absent from the perisinusoidal space. Hepatic stellate cells are ubiquitous in the liver parenchyma while myofibroblasts localize in fibrotic foci. Factor VIII-related antigen expression signals sinusoidal to systemic vascular endothelium transformation while collagen IV and laminin codistribution indicates formation of perisinusoidal membranes. Their coincidence reflects focalized capillarization of sinusoids in the aged liver. In response to fibrogenesis, hepatic progenitor cells residing in the canal of Hering in the periportal parenchyma undergo expansion and migration deep into the lobule. Concomitantly, intermediate hepatocyte-like cells increase in advanced fibrosis stages, which is possibly related to hepatic regeneration. Metabolic zonation of glutamine synthetase expands from the perivenous to non-perivenous parenchyma in fibrosis progression but its expression is lost in cirrhosis, while cytochrome P-4502E1 expression is maintained in centrilobular and midlobular zones in fibrosis progression and expressed in cirrhosis. Hence, cadaveric livers provide a platform for further investigation of hepatic histopathologies associated with the aging liver.

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“…After reaching maximum size in early adulthood, the liver steadily decreases in both size and the amount of blood flow it receives, leading to decreased function and efficiency over time [10] . Also, increased ammonia production and bacterial overgrowth are common in older adulthood, both of which are thought to play a key role in development of hepatic encephalopathy [11] .…”

Section: Introductionmentioning

confidence: 99%

Protein Recommendations for Older Adults with Cirrhosis: A Review

Iiames

Logomarsino

2015

Journal of Gastroenterology and Hepatology Research

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Protein intake has a key role in liver cirrhosis in older adults. However, types and amounts of protein intake in cirrhosis have been controversial. The aim of this paper is to investigate the optimal protein intake for management of cirrhosis and prevention of hepatic encephalopathy in older adults. Protein restriction of 0.6 g/kg/d has traditionally been used as medical nutrition therapy in liver cirrhosis. However, recent evidence has shown that protein restrictions have many negative consequences for older adults with cirrhosis. Current research indicates protein intakes of 1.2-1.5 g/ kg/d in liver cirrhosis; however, many older adults do not consume this amount. Strategies to help increase protein intake and manage cirrhosis include ensuring adequate protein at every meal through either regular intake or supplementation, protein supplementation prior to bedtime or overnight, and supplementation with branchedchain amino acids. An emphasis on vegetable protein versus animal protein is probably not an advantageous treatment option because of lack of conclusive evidence regarding benefits and potential negative side effects. and progression of chronic liver disease and cirrhosis.There are several different factors that naturally occur in older adulthood that help contribute to the development of chronic liver disease and cirrhosis. After reaching maximum size in early adulthood, the liver steadily decreases in both size and the amount of blood flow it receives, leading to decreased function and efficiency over time [10] . Also, increased ammonia production and bacterial overgrowth are common in older adulthood, both of which are thought to play a key role in development of hepatic encephalopathy [11] . Older adults tend to have chronic constipation, intestinal dysmotility, and increased colonic transit time, which predisposes them to increased ammonia production [12] . Finally, older adulthood is associated with a higher incidence of diabetes, which is strongly correlated to progression of liver cirrhosis [13] . Pathogenesis of malnutrition in older adults with cirrhosisIt is estimated that 20% of patients with compensated cirrhosis and 60% of patients with decompensated cirrhosis have malnutrition [14] . In older adults, protein energy malnutrition is associated with high health care costs, increased frequency of infection and bedsores, increased morbidity and mortality, and poor physical functioning [4,5] . In canine trials, poor nutritional status has been shown to encourage the development of hepatic encephalopathy [15] . In addition, malnutrition in cirrhosis is positively associated with old age [14] . Multiple factors help contribute to the development of malnutrition in older adults with cirrhosis, including inadequate intake, altered absorption, sarcopenia, and altered metabolism. All causes must be explored and taken into consideration when developing treatment and prevention strategies.In older adults, food intake naturally decreases over time [16] , which promotes the development of malnutri...

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Diagnosis and management of chronic liver disease in older people

Cited by 9 publications

References 152 publications

Liver Fibrosis in Elderly Cadavers: Localization of Collagen Types I, III, and IV, α‐Smooth Muscle Actin, and Elastic Fibers

Liver Fibrosis in Elderly Cadavers: Localization of Collagen Types I, III, and IV, α‐Smooth Muscle Actin, and Elastic Fibers

A review of hepatic fibrosis‐associated histopathology in aged cadavers

Protein Recommendations for Older Adults with Cirrhosis: A Review

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