Evaluation of the Diagnosis and Management of Non-Alcoholic

Fatty Liver Disease, Non-Alcoholic Fatty Liver (NAFL) and Non-

Alcoholic Steatohepatitis (NASH) Guideline

Marlene Feron-Rigodon

The Guideline: Diagnosis and management of non-alcoholic fatty liver disease, including non-

alcoholic fatty liver (NAFL) and non-alcoholic steatohepatitis (NASH) (May, 2015).

The goal of the guideline is to prevent, treat and diagnose the disease with a focus on children

and adults who seem to have risk factors that put them at risk to developing NAFL (May,

2015).

NASH is a common liver disease, it affects two to five percent of Americans, it

resembles alcoholic liver disease, but in people who ingest little or no alcohol (May, 2015). The

major effect of NASH is fat in the liver associated with inflammation and damage.

Introduction

. Nash can lead to cirrhosis, where the liver is permanently damaged and not able to function properly (May, 2015). NAFL is

having fat in the liver which by itself causes little harm or can also cause permanent damage. If a liver biopsy is performed, it can

determine if someone might have NASH or just a fatty liver. NASH and NAFL are becoming common possibly because of a

greater number of Americans with obesity. In the past 10 years, the rate of obesity has doubled in adults and tripled in children

(May, 2015). Obesity also contributes to diabetes and high blood cholesterol which can further complicate an individual’s health

that has NASH (May, 2015). NASH is usually first suspected in a person who is found to have elevations in liver enzymes, when

further evaluation shows no apparent reason for liver disease (such as medications, viral hepatitis, or excessive use of alcohol) and

when x rays or imaging studies of the liver show fat, NASH is suspected( May,2015).

The review of the literature

From the article The Hunt for Treatment Options of Fatty Liver Continues: Effects of Retinoic Acid on Hepatic Steatosis Reveal

Novel Transcriptional Interactions of Nuclear Receptors, NAFL is characterized by hepatic steatosis, which may progress to

nonalcoholic steatohepatitis (NASH) with or without fibrosis (May, 2014). Without fibrosis already existing, it may develop into

hepatocellular carcinoma. Insulin resistance and hepatic fatty acid turnover are important features of metabolic syndrome and

contribute to NASH progression (May, 2014). Specific activation of Retinoic acid receptors (RAR) adds a novel aspect to the

nuclear receptor interaction to the field of NAFL disease research. It gives emerging data supporting the importance of bile acids as

mediators in glucose and lipid metabolism (May, 2014). In the article Does Interleukin-17 Play the Villain in Nonalcoholic

Steatohepatitis, Interleukin (IL-17) is a member of the Th17 family of cytokines comprised of IL-17A, IL-17F, IL-17B, IL-17C,

and IL-17E (May, 2014). IL-17 plays a critical role in mediating autoimmunity, such as the autoimmune inflammatory diseases

psoriasis and rheumatoid arthritis that respond to anti-IL-17 biological therapies. More recently, IL-17 has been implicated in liver,

lung, and skin fibrosis, and in tumorgensis (May, 2014).

Within the article Poly (ADP-Ribose) Polymerase-1 Is a Key Mediator of Liver Inflammation

and Fibrosis, Poly (ADP-Ribose) (PAR-1) is expressed primarily nuclear enzyme, it

functions as a DNA damage censor (May, 2014). It binds to a damaged DNA and forms long

branches of ADP-Ribose proteins (May, 2014). The findings of the pathogenic role of the

PARP-1 in liver inflammation shows a beneficial use of the PARP inhibitors for liver disease

and fibrosis (May, 2014). “These results indicate that oxidative stress and PARP1 plays

important pathogenic roles in liver injury, metabolism, inflammation and fibrosis “(May,

2014, p. 2007).

It is concluded that PARP1 indicates a key checkpoint in liver fibrosis and its inhibition can

be of therapeutic potential.

Research has shown us the importance in diagnosing and treatment of NAFL and NASH. It is important

for nurses to educate their patients at risk for NAFL and NASH on the importance of diet and exercise.

These lifestyle modification are the primary steps that we need to teach stress to our patients. We also

must understand the importance of research in the development of new treatments. In educating the

patients on the disease process of NAFL and NASH, it can lead to a better understanding of new

therapeutic solutions that on the horizon. My literature review on this guideline demonstrated on the

many ways that research is progressing to identify and treat NAFL and NASH.

It is important that when teaching patients life style modifications if the progressive

approach isn’t taken in preventing liver fibrosis progression, it can lead to liver cirrhosis which

ultimately leads to liver cancer.

Recommendations for Practice

There is new research on the horizon to help treat patients with NAFL and NASH. When pathways that lead to liver injury are well

known, safe and effective ways can be developed to reverse these pathways. Recent breakthroughs in identifying the human

genome and uncovering the individual pathways by which insulin and other hormones regulate blood glucose and fat could provide

necessary clues in NASH progression (May, 2015).

Conclusion

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Guichelaar,M.M.,Charlton,M.R.(2014,May). Decreased Muscle Mass in Nonalcoholic Fatty Liver Disease: New Evidence of a Link

Between Growth Hormone and Fatty Liver Disease? Hepatology59(5) 1668-1669.

Kisseleva, T.(2014,May).Does Interleukin-17 Play the Villain in Nonalcoholic Steatohepatitis?Hepatology 59(5)1671-1672.

Harley,I.T.,Stankiewicz,T.E., Giles,D.A., Softic,S., Flick,L.M.,Cappelletti,M., Sheridan,R.,Xanthakos,S.A.,

Steinbrecher,K.A.,Sartor,R.B., Kohli,R.,Karp,C.L.,Divanovic,S. IL-17 Signaling Accelerates the Progression of NONalcoholic Fatty Liver Disease

in Mice. Hepatolgy 59(5)1830-1839.

Gutscher,T.,Hammerle,M.,Pazaitis,N.,Bley,N.,Fiskin,E.,Uckelmann,H.,Heim,A.,Grob,M.,Hofmann,N.,Geffers,R.,Skawran,B.,

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an Important Protumorigenic Factor in Hepatocellular Carcinoma.(2014,May).Hepatology59(5) 1900-1911.

Mukhopadhyay,P. Rajesh,M., Cao,Z., Horvath,B., Park,O.Wang,H.,Erdelyi,K., Holovac,E.,Wang,Y.,Liaudet,L.,Hamdaoui,N.,

Lafdil,F.,Hasko,G.,Szabo,C.,Boulares,A.H., Gao,B.,Pacher,P.(2014,May).Poly(ADP-Ribose) Polymerase-1 Is a Key Mediator of Liver

Inflammation and Fibrosis. Hepatology 59(5)1998-2010.Agency for Healthcare and Research (2002) https://jhuccs1.us/nash (May, 2015).

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