Monday, February 10, 2020

Non Alcoholic Fatty Liver Disease


Non Alcoholic Fatty Liver Disease





Patients with nonalcoholic steatohepatitis (NASH) are at a higher risk for the progression of hepatic fibrosis.
•Metabolic syndrome and obesity are risk factors associated with the development of nonalcoholic fatty liver disease (NAFLD).
•Nurse practitioners can use diagnostic tools to assess if a patient is at a higher risk for NASH.
•Patients with NAFLD should be counseled on weight loss and the management of medical comorbidities.

Abstract

Nonalcoholic fatty liver disease is the most prevalent liver disease in the world. Metabolic syndrome and obesity are associated risk factors. The inflammatory subtype, nonalcoholic steatohepatitis (NASH), which can progress to cirrhosis, is predicted to become the primary indication for liver transplantation within the next decade. Although there are no approved medications for NASH, there are ongoing multicenter trials aimed at targeting aspects of fat accumulation, inflammation, and fibrosis throughout the disease process. Nurse practitioners should focus on identifying patients at risk for NASH, while using guidelines for the management of nonalcoholic fatty liver disease and the comorbidities contributing to disease progression.

Nonalcoholic fatty liver disease (NAFLD) is the aggregate term defining the disease state that encompasses 1) nonalcoholic fatty liver (NAFL), or ≥ 5% of steatosis (fat) in the hepatocytes, 2) nonalcoholic steatohepatitis (NASH), or fatty infiltration with inflammation and hepatocyte ballooning present with or without fibrosis, and 3) NASH cirrhosis, or end-stage fibrosis of the liver independent of alcohol use or other factors associated with hepatic steatosis.1 NAFLD has become the most prevalent liver disease in the world and is predicted to become the main indication for liver transplantation within the next decade.2 Patients with NASH are at greater risk of developing hepatic fibrosis over time, a precursor for cirrhosis.1
Metabolic syndrome and obesity are the main risk factors that contribute to the development of this disease.2 Patients with metabolic syndrome have 3 or more of the following abnormal measurements: an elevated waist circumference (in men > 40 inches and in women > 35 inches), elevated triglycerides over 150 mg/dL, an elevated systolic blood pressure over 130 mm Hg or an elevated diastolic blood pressure over 85 mm Hg, and/or elevated fasting glucose levels above 100 mg/dL.3
The Food and Drug Administration has not yet approved any pharmacotherapies with an indication for the treatment of NASH; however, several multicenter trials are ongoing with early data supporting promising agents for this patient population.2 These agents target the processes underlying fat accumulation, inflammation, and fibrosis associated with NASH at various points of the disease progression.4 Current clinical guidelines published by the American Association for the Study of Liver Diseases encourage nurse practitioners (NPs) to focus identifying patients at high risk for NASH and the prevention of the progression of fibrosis in these patients through the treatment of liver disease and a patient’s metabolic comorbidities.


Presentation

It is estimated that 25% of the adult population has NAFLD, and 5% to 6% of these patients hold a diagnosis of the inflammatory subtype, NASH (Figure 1).2 A large percentage of NAFLD patients will present with medical comorbidities that increase the risk of the disease including obesity, diabetes, and metabolic syndrome. Regarding patient demographics, the overall incidence of NAFLD and the stage of liver fibrosis increase with age.1 NAFLD prevalence is estimated to be 2 times greater among the male population in comparison with the female population.1 Early analysis of the ethnic differences among this population revealed an increased prevalence of NAFLD among Hispanic individuals in comparison with non-Hispanic whites and an even lower prevalence in the non-Hispanic black population.1 As the field of genomic medicine continues to expand, data suggest genetic differences may play a greater role than previously suspected.1 Patients with polymorphisms in genes such as PNPLA3 and TM6SF2 have been found to have a greater incidence of NAFLD, including progressive disease such as liver cancer.5 Because of the high prevalence of this disease, NPs practicing in all clinical settings will treat patients with NAFLD.

Patients can be characterized on the NAFLD spectrum based on the presence of steatosis, inflammation, ballooning, and hepatic fibrosis.6 These characteristics influence a patient’s clinical course and presentation. Patients with steatosis without inflammation (non-NASH NAFL) generally follow a benign hepatic clinical course, are often asymptomatic, and are at increased risk for diabetes and cardiovascular outcomes.6 In comparison, patients with NASH may experience symptoms and complications of liver disease with the progression of fibrosis (Figure 2).1 Studies estimate one third of NAFL and NASH patients will have disease progression, advancing from one stage of fibrosis to the next at a rate of 7.7 years.6 Although this rate appears relatively slow, the rate of progression in NASH patients is twice as high, with data showing a subset of NASH patients moving from no fibrosis to advanced fibrosis within a 6-year period on average.6 Over time, a subgroup of NASH patients will progress to cirrhosis and liver decompensation.

Diagnosis and Evaluation

In addition to considering a patient’s metabolic risk factors, there are 2 common clinical scenarios that typically increase a provider’s suspicion for NAFLD: 1) the patient presents with abnormal imaging results with evidence of increased echogenicity or hepatic steatosis or 2) the patient has abnormal liver enzymes, particularly aminotransferases (aspartate transaminase [AST] or alanine transaminase [ALT]).7 If an NP encounters a patient with chronically elevated aminotransferases, other potential causes of elevated liver enzymes must be considered. If a patient has a single abnormal laboratory test, the test can be repeated for confirmation.

Non-NASH NAFL can be diagnosed by evidence of hepatic steatosis on imaging.1 If NAFLD is suspected in a patient with abnormal liver tests, an abdominal ultrasound is recommended as the initial cost-effective imaging modality used to evaluate the liver parenchyma for chronic changes, assess hepatic vasculature, and confirm hepatic steatosis (Figure 3).7 Abdominal ultrasound and computed tomographic scans detect steatosis in patients with moderate to massive steatosis and are less specific in detecting NAFLD in a patient with mild steatosis.7 Magnetic resonance imaging has been found to have a greater specificity in detecting steatosis but is not recommended as an initial imaging modality for the evaluation of NAFLD and remains costly.7 Ultrasound, computed tomographic scanning, and general magnetic resonance imaging may reveal steatosis but are limited in accurately detecting hepatic fibrosis.

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2 comments:

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