NASH Related Cirrhosis and Hepato-Cellular Carcinoma: A Case Study
Creators: name: Saeed, Aisha
name: Silverman, Rosalind
name: Silverman, Lorelei
Publisher: name: figshare
Year: 2018
Subjects: subject: 110307 Gastroenterology and Hepatology
subject: FOS: Clinical medicine
subject: FOS: Clinical medicine

description: <b>Abstract</b> Non-Alcoholic fatty liver disease (NAFLD) is a condition in which excess fat is stored in the liver in the absence of alcohol consumption. It is one of the most common causes of liver damage in Canada affecting over 7 million people [R-1]. There are two types of NAFLD, non-alcoholic fatty liver (NAFL) and non-alcoholic steatohepatitis (NASH). The former is a benign condition in which there is fat accumulation in the liver but little or no inflammation. However, in NASH there is accumulation of fat in the liver causing inflammation and damage to the liver cells leading to fibrosis and scarring. The prevalence of NASH is 2% to 6% in the general population [R-1] [R-2] [R-5]. NASH causes histological liver damage which is similar to that found in alcoholic hepatitis but occurs in patients who are non alcoholic or have a low level of alcohol consumption. Risk factors of NASH include obesity, dyslipidemia, glucose intolerance and metabolic syndrome. Up to 20% of adults with NASH develop cirrhosis and about 11% may experience liver related deaths [R-1]. Symptoms are usually absent, but some patients may have right upper quadrant discomfort, fatigue, or malaise. Signs of portal hypertension and cirrhosis can eventually occur and may be the first manifestations. Hepato-cellular carcinoma may present as a late complication of NASH-related cirrhosis. Diagnosis of NASH is made by presence of risk factors (obesity, diabetes), abnormal liver function tests (LFT’s), serologic tests to rule out Hepatitis B &amp;C and a liver ultrasound showing steatosis. A liver biopsy is the definitive test to distinguish NASH from other forms of liver disease [R-8]. Management is based on treating liver disease as well as the associated metabolic co-morbidities such as obesity, hyperlipidemia, insulin resistance and type 2 Diabetes Mellitus. Lifestyle modification, weight loss and regular exercise may improve hepatic steatosis [R-3]. Since alcohol is a risk factor for chronic liver disease, it should also be avoided. Currently there is no medication proven effective to treat fatty liver disease. Patients with NASH cirrhosis should be screened for Hepato-cellular carcinoma (HCC) according to AASLD/ACG practice guidelines [R-3] [R-9]. <b>Case Study</b> A 50 year old man presented in the office with complaints of shortness of breath. He also thinks that his abdomen is a little more distended than before. In the year 2016, the patient presented with complaints of fatigue and right upper abdominal discomfort and was diagnosed with NASH induced liver cirrhosis. In early 2017 the patient developed iron deficiency anaemia secondary to oesophageal varices and required banding 3 times. He was also given iron treatment. Due to a suspicious ultrasound, CT abdomen was done in May 2017 and showed cirrhosis, portal hypertension and a 2.2cm hepatic segment 6 lesion keeping with Hepato-cellular carcinoma (HCC). Biopsy confirmed HCC to be well differentiated on background of cirrhotic liver. He successfully underwent radiofrequency ablation for HCC in June 2017. The patient was referred to the transplant team but was unfortunately declined .The current Ontario guidelines requires the tumour (HCC) to be at least 3 cm and above to be accepted to be a transplant candidate. The patient was informed by the transplant team in Ontario that if his tumour recurred he would become a transplant candidate for a live liver donor [R-7]. Follow up CTs showed no recurrence of HCC but did show an increase in ascites. <b><i>Past medical history:</i></b> Diabetes, thyroid nodules, femur/tibia multiple surgeries, 3 variceal banded. <b><i>Medications:</i></b> Victoza, Metformin, Insulin, Lipitor, Pantoprazole <b><i>Allergies:</i></b><b> </b>Penicillin <b><i>Social History:</i></b><b> </b>The patient has past social history of drinking but stopped ever since he was diagnosed with cirrhosis. He was also a smoker, smoked 20 packs per year but quit smoking 14 years ago. <b><i>Examination:</i></b><b> </b>On general examination the patient is in mild distress and there is conjunctival pallor. Abdominal exam shows abdomen to be more distended than before and there is some shifting dullness. <b><i>Investigation:</i></b><b> </b>Recent blood work shows his haemoglobin has fallen from 116mg/dl in last visit to 60mg/dl in this visit. It is possible that he has Gastro Intestinal (GI) bleed again and may need gastroscopy.<b></b> Imaging done again showed possibility of a small area of residual tumour at the margin of ablative site. His INR is 1.26, Albumin 35, creatinine 56 and Sodium138mg\dl. His MELD* score is still not high enough to warrant transplantation. *The Model for End-Stage Liver Disease (MELD) score is frequently used to measure the severity of liver dysfunction in cirrhotic patients. It is also used in predicting likely survival of patients awaiting liver transplant. <br>