DIAGNOSIS
Initial evaluation
The diagnosis of NAFLD requires
(1) There is hepatic steatosis by imaging or histology;
(2) There is no significant alcohol consumption; (3) No competing etiologies are present for hepatic steatosis; and (4) There are no co-existing causes for chronic liver disease
It is important to rule out common causes of liver injury, such as alcohol, drug use, and viral hepatitis as well as other co-existing etiologies for chronic liver disease including alpha-1 antitrypsin deficiency, hemochromatosis, autoimmune liver disease (types 1 and 2), chronic viral hepatitis, and Wilson’s disease
Elevated alanine aminotransferase and aspartate aminotransferase levels may indicate the presence of hepatic steatosis, inflammation,
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In particular, cytokeratin-18 fragments have shown the most promise in the diagnosis of NASH. It is an indicator of hepatocyte apoptosis, may have clinical utility showing a sensitivity of 66% and specificity of 82% in diagnosing NASH. Currently this assay is not commercially available and there is no established cut-off value. Other serum biomarkers that have been evaluated for the diagnosis of NASH include various cytokines, acute phase proteins, and oxidative stress markers. Two acute phase reactants, C-reactive protein (CRP) and pentatrix-3, have been studied in the diagnosis of NASH.
Radiological evaluation
Ultrasonography (US) is a cheap, fast, and widely available imaging technique with applications for fatty liver. US has been reported to have a sensitivity ranging from 60% to 94% and a specificity of 66% to 95%.
Liver biopsy
Currently, liver biopsy remains the gold-standard for the diagnosis of NASH as it serves as the only means of distinguishing hepatic steatosis from steatohepatitis through examination of liver histology. According to current AGA guidelines, a liver biopsy should only be considered in patients with NAFLD who are at increased risk to have steatohepatitis and advanced fibrosis, such as those who have metabolic
1. What are the common manifestations of alcoholic cirrhosis? Which of these are secondary to
This case study is about Abdul Chidiac, a 51 year old male, married with 4 children. He had a medical history of hypertension, hypercholesterolaemia and cirrhosis with two admissions in the last six months. He is a smoker and drinks beer, 5-6 bottles per day. As Carithers & McClain (2010) explained the patient’s medical history is another indicator of the risk for cirrhosis; the progression to cirrhosis is adaptable and may take time over weeks or many years. Cirrhosis is a liver disease characterized by permanent scarring of the
Cirrhosis is the 11th leading cause of death by disease in the United States. Almost one half of these are alcohol related. About 25,000 people die from cirrhosis each year.
Additionally, many chronic liver diseases can lead to cirrhosis. For example, nonalcoholic fatty liver disease (NAFLD) can lead to cirrhosis and is associated with obesity, hyperlipidemia, metabolic syndrome and type 2 diabetes mellitus. Hereditary metabolic disorders such as hemochromatosis and Wilson disease can also lead to cirrhosis (McCance & Heuther, 2014). It seems the cause of cirrhosis is multifaceted. Additionally, many diseases can lead to cirrhosis and it is understandable why the etiology of cirrhosis has not been parsed out, especially because the cause can differ from a
Alcohol abuse and hepatitis B and C are the most common causes of cirrhosis. Cirrhosis can cause weakness, loss of appetite, jaundice, itching, and fatigue, and can be diagnosed by blood tests, physical examinations, and a liver biopsy. There are many complications of cirrhosis, such as edema and ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, portal vein hypertension, hepatorenal and hepatopulmonary syndrome, hypersplenism, and liver cancer. One of the most common treatments of cirrhosis is a liver transplant. However, alcoholics have to be sober for six months to prove that they are serious about taking care of their new liver and staying sober after the
Symptoms may differ depending on the stage of the disease but some common symptoms are loss of appetite, fatigue, weight loss or gain, jaundice, retaining of fluid, blood in the stool or fever (Digestive Disorders Health Center Cirrhosis of the Liver, 2008). There are other symptoms of Cirrhosis of the Liver but these are the most common. All of these symptoms help in the detection of this horrible disease. The faster Cirrhosis is detected, the better off the person’s chances of survival are. However, there is no cure for Cirrhosis of the Liver and depending on the cause of the disease, some treatments can slow down the progression and minimize damage to liver cells, (Digestive Disorders Health Center Cirrhosis of the Liver, 2008).
Chronic liver diseases and liver biopsy. Chronic liver diseases encompass many different causes, including viral infections, nonalcoholic fatty liver disease (NAFLD), alcohol abuse, primary sclerosing cholangitis, primary hemochromatosis, and autoimmune disease. All of these precipitate chronic damage to the liver via necroinflammation and subsequent cellular injury and accumulation of extracellular matrix (ECM) proteins distorting the hepatic architecture by forming hepatic fibrosis with abnormal collagen deposition. Without treatment, the eventual development of cirrhosis (the end stage of fibrosis) can accelerate to hepatocellular dysfunction, hepatic insufficiency, portal hypertension, and hepatocellular carcinoma (HCC), thus
In the past, the imaging modality of choice has been computed tomography. However, there are growing concerns about radiation exposure. As a result, many doctors are utilizing sonography as the modality of choice to image organs. HCC can take on a variety of appearances when imaged using ultrasound. However, ultrasound images are becoming more advanced which allows the sonographer to more accurately discover irregularities and tumors in the liver. Ultrasound also allows the sonographer to determine to what extent a tumor or cancer has affected the vasculature of the liver.1
The liver is the second most complex organ after the brain and controls critical processes within the body, including detoxification, metabolism, protein synthesis and digestion (Malarkey et al 2005). The liver is also responsible for cholesterol homeostasis and lipoprotein metabolism. The majority of the serum proteins are produced and secreted from the liver including clotting factors, albumin, and hormones. The liver is also responsible for metabolism of endogenous compounds such as ammonia and exogenous compounds like drugs and toxic components. Moreover, the catabolism of amnion acids and glycogen takes place in the liver.
Giving the fact that NAFLD is usually an asymptomatic disorder, it is often unrecognized in everyday clinical practice. Namely, most patients with NAFLD have no symptoms, and aminotransferase levels which are used as a marker of liver damage, are within normal values in almost half of all patients. NAFLD is strongly associated with type 2 diabetes mellitus (T2DM) and has been linked to increased cardiovascular disease (CVD) risk. It is characterized by insulin resistance and mitochondrial dysfunction6. Indeed, there is a gradual increase in the severity of insulin resistance in the range of NAFLD which may contribute to the evolution of liver damage. Also, it is associated with an increased risk of kidney disease in subjects with multiple CVD
Major risk factors for hepatocellular carcinoma include infection with HBV or HCV, alcoholic liver disease, and most probably non-alcoholic fatty liver disease. Less common causes include hereditary hemochromatosis, alpha1-antitrypsin deficiency, autoimmune hepatitis, some porphyrias, and Wilson’s disease, aflatoxin ingestion, exposure to inorganic arsenic through drinking water (Shamseddine et al., 2009). The distribution of these risk factors among patients with hepatocellular carcinoma is highly variable, depending on geographic region and race or ethnic group (El-Serag and Rudolph, 2007). Most of these risk factors lead to the formation and progression of cirrhosis, which is present in 80 to 90% of patients with hepatocellular carcinoma (Chen et al.,2009).
There are three major classifications of drug induced liver injury that occur as a result of both intrinsic and idiosyncratic hepatotoxicity: Hepatocellular injury, cholestatic injury and mixed hepatostatic and cholestatic injury. Hepatocellular injury, as the name suggest, refers to the injury to the liver cell. Cholestatic injury refers to injury to the biliary system. Mixed hepatocellular and cholestatic injury refers to injury to both the liver cells and the biliary system. Other less common types of DILI include chronic hepatitis, chronic cholestatis, granulomatous hepatitis, fibrosis or cirrhosis, and
Choice “E” is the best answer. Ultrasonography is the most widely used imaging technique to help diagnose ADPKD. It can detect cysts from 1-1.5 cm. This study avoids the use of radiation or contrast material, is widely available, and is inexpensive. The sensitivity of ultrasonography for ADPKD1 is 99% for at-risk patients older than 20 years; however, false-negative results are more common in younger patients. Sensitivity for ADPKD2 is lower and is still not well defined. Ultrasonography is also useful for exploring abdominal extrarenal features of ADPKD (e.g., liver cysts, pancreatic cysts). The presence of hepatic or pancreatic cysts supports the diagnosis of ADPKD[1].
Fibroscan is one of the most common, accurate and validated alternative method. It is an ultrasound-based imaging technology, which measures liver stiffness. The degree of liver stiffness directly correlates with the degree of fibrosis (Sandrin et al., 2003).It also allows follow up the progression of fibrosis (Foucher et al., 2006).
Acute liver failure is an unusual but life-threatening critical illness, which arises without preexisting liver disease and always supervenes high mortality. The 30s adults in good condition are main sufferers of acute liver failure. The clinical features commonly include: abnormal liver biochemical values, hepatic dysfunction and coagulopathy. Encephalopathy may also occur with multiorgan failure, which cause 50% of death.