James Alverez is a 52 y.o., recently divorced, Hispanic male; a new patient who arrives at the community health clinic for an appointment with a primary care NP. His chief complaint included abdominal pain with vomiting, fatigue, and weight loss. He mentions that although he has experienced overall weight loss, his stomach “looks huge.” As his history is taken, he notes no alcohol use. In speaking with him, the NP notices a yellow tinge to the whites of his eyes. During the examination, the NP indicates organomegaly in the right upper quadrant. He has been diagnosed with nonalcoholic fatty liver disease (NAFLD) based hepatomegaly.
Fatty liver occurs when triglycerides and other fats accumulate in liver cells. There are processes which delivery fats to the liver and remove fats from the liver. There needs to be a proper balance between these two actions in order to prevent the buildup of fats in the liver. It can be associated with hepatic inflammation and hepatomegaly and steatohepatitis. Fatty liver can be due to the breakdown of several different functions. These include decreased mitochondrial fatty acid beta-oxidation, increase in the synthesis of endogenous fatty acids or increased delivery of these fatty acids to the liver, and deficient incorporation or export of triglycerides as very low-density lipoprotein (VLDL). Increased activation of Hedgehog pathways has been found in patients with advanced fatty liver disease. No singular cause or pathophysiology has been found (Sears, 2014).
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Acquired insulin resistance due to obesity, diabetes mellitus, hyperlipidemia, hypothalamic–pituitary dysfunction is associated with the development of NAFLD. It can also be due to genetic/inborn errors of metabolism such as abetalipoproteinemia, galactosemia, Weber–Christian disease, limb lipodystrophy, type 1 glycogen storage disease, Wilson’s disease, tyrosinemia, systemic carnitine deficiency, and Refsum’s syndrome. Intestinal issues can affect the NAFLD as well. They can be surgical issues like jejunoileal bypass, gastroplasty for morbid obesity, biliopancreatic diversion, and extensive small bowel resection or non-surgical such as total parenteral nutrition, starvation and cachexia, rapid weight loss, protein calorie malnutrition found in marasmus and kwashiorkor, inflammatory bowel disease, and jejunal diverticulosis with bacterial overgrowth. Drugs and toxins can cause NAFLD as well, and some which are dangerous include Amiodarone, Methotrexate, Tamoxifen, and Glucocorticoids (Sass, Chang, & Chopra, 2010).
As there is no one particular cause of NAFLD, there is also no one specific treatment. Treating underlying diseases and comorbidities will help to slow the progression of hepatomegaly caused by NAFLD. Obese or overweight patients should lose weight gradually, at the rate of 1 to 2 pounds per week. James has already lost weight and may have done so too quickly. Continuing with his weight loss strategy but at a much slower rate will help to slow down the progression of his disease.
Along with weight loss, increased physical exercise and a more balanced, healthy diet are recommended. Limited caloric intake and quickly digested carbohydrates is best. Foods such as grits, rice, breads, potatoes, corn, and the sugars found in sports drinks are not advantageous for NAFLD and should be avoided (Blahd, 2014). Research indicates that diets with excess fructose are indicative of developing NAFLD and removing these foods can assist in a reversal of the disease. According to Sears “The mechanism appears to be related to the depletion of adenosine triphosphate (ATP), as well as to increased uric acid production from excess fructose.” Eating appropriate portions of healthy foods as well as regularly exercising are leading treatments for James and other NAFLD patients (Sears, 2014). Weight loss and training programs should be developed within the Latin and Asian communities to help these susceptible populations.
The American Association for the Study of Liver Diseases (AASLD), the American Gastroenterological Association (AGA), and the American College of Gastroenterology (ACG) developed recommendations for treatment of NAFLD in 2012. They suggested weight loss to reduce hepatic steatosis, but patients may need to lose up to 10% before improved necroinflammation is noticed. All NAFLD patients should abstain from alcohol. Patients, like James, who are not diabetic, should be prescribed Vitamin E 800 IU/day to improve liver histology. Omega-3 fatty acids should be prescribed to rectify hypertriglyceridemia. Statins should be prescribed to treat dyslipidemia in patients with NAFLD. Long term care should be expected to monitor the increase or decrease of disease (Sears, 2014).
Beyond the guidelines set forth by the AASLD, AGA, and ACG, many experts explore other treatments possibilities. Thiazolidinediones reduce inflammation of the liver while they are being delivered, but they also lead to weight gain which could be counterintuitive for James’ needs. There is some data to suggest that obstructive sleep apnea is linked to NAFLD. More research is required to determine if treatment of sleep apnea results in decreased symptoms of NAFLD. If James does have this comorbidity, it will benefit to treat this issue as well. Also, there has been some research into using N –acetylcysteine and cannabinoid blockers in the treatment of the disease (Sears, 2014).
In short, James should be advised to continue to lose weight at a rate of 1 to 2 pounds per week via the avoidance of carbohydrates and fructose. He should also include additional exercise into his lifestyle. Utilization of weight loss and exercise programs within his community will assist other people in his community which may be susceptible as well. He should continue to abstain from the consumption of alcohol. Vitamin E 800 IU/day, Omega-3 fatty acids, and statins should be prescribed. He should be sent back to his NP for long-term follow-up care and monitoring.
- Blahd, W. (2014, July 9). Fatty Liver Disease. Retrieved from WebMD: http://www.webmd.com/hepatitis/fatty-liver-disease
- Sass, D., Chang, P., & Chopra, K. (2010). Nonalcoholic Fatty Liver Disease: A Clinical Review. Digestive Diseases and Sciences, 171-180.
- Sears, D. (2014, December 14). Fatty Liver. Retrieved from MedScape: http://emedicine.medscape.com/article/175472-overview#aw2aab6b4
