Nonalcoholic fatty liver disease ( NAFLD ) is one type of liver fat that occurs when fat is stored (steatosis) in the liver due to causes other than alcohol use. Non-alcoholic steatohepatitis ( NASH ) is the most extreme form of NAFLD. NAFLD is the most common liver disorder in developed countries.
NAFLD is associated with insulin resistance and metabolic syndrome and may respond to treatments initially developed for other insulin-resistant states (eg type 2 diabetes mellitus) such as weight loss, metformin, and thiazolidinedion. Up to 80% of obese people have the disease. NASH is considered a major cause of cirrhosis of the unknown cause. Most people have good results if the condition is caught at an early stage.
Approximately 12 to 25% of people in the United States have NAFLD, while NASH affects between 2 and 5% of people in the United States.
Video Non-alcoholic fatty liver disease
Signs and symptoms
Most people with NAFLD have little or no symptoms. Patients may complain of fatigue, malaise, and discomfort of the dull right-up-quadrant stomach. Mild jaundice may be noted, although this is rare. More commonly NAFLD is diagnosed following abnormal liver function tests during routine blood tests. By definition, alcohol consumption of more than 20 g/day (about 25 ml/day of net ethanol) excludes the condition.
NAFLD is associated with insulin resistance and metabolic syndrome (obesity, hyperlipidemia combined, diabetes mellitus (type II), and high blood pressure). Recent research has shown that NAFLD increases the risk of cardiovascular disease, such as cardiac arrhythmias.
Maps Non-alcoholic fatty liver disease
Cause
Common risk factors for NAFLD are hypertriglyceridemia, obesity and type II diabetes. Increasing age causes higher levels of severity and NAFLD levels.
Diet
Soft drinks have been associated with NAFLD because of high fructose concentrations, which may be present either in high fructose corn syrup or, in the same amount, as a metabolite of sucrose. The amount of fructose delivered by a soft drink can cause a buildup of increased fat in the abdomen. Central obesity has the most association with NAFLD.
Genetics
The genetic risk factors of NAFLD are also known. 66.67% of T2DM families report more than one family member has NAFLD. In addition, Hispanics have a higher prevalence of NAFLD than whites and blacks. Indigenous American men have higher levels of non-alcoholic fatty liver disease. Two genetic mutations for this vulnerability have been identified, and these mutations provide guidance on NASH mechanisms and related illnesses.
Polymorphism (genetic variation) in single nucleotide polymorphism (SNP) T455C and C482T in APOC3 is associated with fatty liver disease, insulin resistance, and possibly hypertriglyceridemia. 95 healthy Asian Indian men and 163 healthy non-Asian Indian men around New Haven, Connecticut genotype for polymorphism in the SNP. 20% homogenous wild good locus. The T-455C, C-482T, or both (non-additive) operators experienced a 30% increase in fasting plasma of apolipoprotein C3, a 60% increase in fasting plasma triglyceride and retinal fatty acid ester, and a 46% reduction in plasma triglyceride clearance. The prevalence of non-alcoholic fatty liver disease was 38% in the career, 0% wild (normal). Subjects with fatty liver disease have marked insulin resistance.
Drugs
NAFLD can also be caused by some drugs (drug-induced illness):
- Amiodarone
- Antiviral drugs (nucleoside analogs)
- Aspirin is rare as part of Reye's syndrome in children
- Corticosteroids
- Methotrexate
- Tamoxifen
- Tetracyclines
Pathophysiology
NAFLD is considered to cover the spectrum of disease activity. This spectrum begins as the accumulation of fat in the liver (liver steatosis). The liver can remain fatty without impairing liver function, but with various mechanisms and possible insults to the liver, it can also develop into non-alcoholic steatohepatitis (NASH), a condition in which steatosis is combined with inflammation and fibrosis (steatohepatitis). NASH is a progressive disease: over a 10-year period, up to 20% of patients with NASH will develop liver cirrhosis, and 10% will suffer from liver-related death. Cigarette smoking is not associated with an increased risk of developing NASH.
The exact cause of NAFLD is still unknown. However, obesity and insulin resistance may play a powerful role in the disease process. The exact reason and mechanisms in which the disease progresses from one stage to the next is unknown.
One contested mechanism proposes a "second punch", or further injury, enough to cause a change that leads from liver steatosis to liver inflammation. Oxidative stress, hormonal imbalances, and mitochondrial abnormalities are potential causes for this "second hit" phenomenon.
Diagnosis
A common finding is elevated liver enzymes and liver ultrasound suggests steatosis. Ultrasound can also be used to exclude gallstone problems (cholelithiasis). Liver biopsy (tissue examination) is the only widely accepted test as a definitive NASH that differentiates from other forms of liver disease and can be used to assess the severity of inflammation and fibrosis produced.
Non-invasive diagnostic tests have been developed, such as FibroTest, which estimates liver fibrosis, and SteatoTest, which estimates steatosis, but its use has not been widely adopted. Apoptosis has been indicated as a potential mechanism of hepatocyte injury as caspase-cleaved cytokeratin 18 (M30-Apoptosense ELISA) in serum/plasma is often elevated in patients with NASH and tests based on these parameters have been developed; However, because the role of oncotic necrosis has not been examined, it is unknown how much apoptosis acts as a major form of injury.
More diagnostic tests are available. Relevant blood tests include levels of erythrocyte sedimentation, glucose, albumin, and kidney function. Since the liver is important for making proteins used in coagulation, some coagulation-related studies are often done primarily INR (international normalized ratio). In people with a fatty liver with a related inflammatory injury test (steatohepatitis) is usually used to exclude viral hepatitis (hepatitis A, B, C and herpes virus such as EBV or CMV), rubella, and autoimmune related diseases. Hypothyroidism is more common in NASH patients to be detected by determining TSH.
It has been suggested that in cases involving overweight patients whose blood tests do not improve on weight loss and exercise that a further search of other underlying causes is done. This will also apply to those who have very young liver or are not overweight or insulin resistant. In addition to those whose physical appearance suggests a possible congenital syndrome, have a family history of liver disease, have abnormalities in other organs, and those present with moderate or advanced fibrosis or cirrhosis.
Management
No pharmacologic treatment has been approved by 2015. Several studies have shown that diet, exercise, and antiglycemic drugs can change the course of the disease. Common recommendations include increasing metabolic risk factors and reducing alcohol intake. While many treatments appear to increase biochemical markers such as alanine transaminase levels, most have not been proven to reverse histologic abnormalities or reduce clinical endpoints.
Bariatric surgery may also be effective.
Nutrition
NAFLD treatment usually involves counseling to improve nutrition and consequently weight and composition. Dietary changes have shown significant histologic improvement. In particular, avoiding foods containing high fructose corn syrup and trans fats is recommended. A systematic review and meta-analysis found that supplementation of omega-3 fatty acids in those with NAFLD/NASH using doses closer to or higher than 1 gram daily (median dose of 4 grams/day with median duration of 6 months of treatment) has been associated with improvement in fatty liver. The best dose of omega-3 fatty acids for individuals with NAFLD/NASH is unclear.
Epidemiological data suggest that coffee consumption may be associated with a reduced incidence of NAFLD and may reduce the risk of liver fibrosis in those who already have NAFLD/NASH. Consumption of olive oil, as part of the Mediterranean diet, is also a reasonable dietary intervention; the optimal dose of olive oil supplementation for people with NAFLD/NASH is not well established. Several studies have been conducted to evaluate the impact of each diet rich in avocados, red wine, tree nuts, or tea in people with NAFLD/NASH. However, limited evidence suggests that avocados can increase other areas of cardiovascular health (ie, lipid profiles) and their addition to a balanced diet is reasonable. The consumption of red wine (in moderation) may be safe and may increase insulin resistance but definitive studies are lacking.
Exercise
Gradual weight loss may improve the process in obese patients; rapid loss can aggravate NAFLD. In particular, walking or some form of aerobic exercise at least 30-45 minutes daily is recommended. The negative effects of rapid weight loss are controversial: the results of the meta-analysis show that the risk of progression is very low.
Medication
Insulin sensitizers (metformin and thiazolidinediones) are commonly used for insulin resistance in those with NAFLD. Improvements in liver biochemistry and histology in patients with NAFLD through treatment with statins have been observed in many cases, although this study was conducted on relatively small patient samples. Statins have also been recommended for use in treating dyslipidemia for patients with NAFLD. Treatment with pentoxifylline has shown improvement in the histologic appearance of fatty liver tissue under a microscope in many small trials.
Surgery
Weight loss surgery leads to an increase and/or NASH resolution in about 80% of people.
Epidemiology
The percentage of people with non-alcoholic fatty liver disease ranged from 9 to 36.9% in different parts of the world. Approximately 20% of the population of the United States has non-alcoholic fatty liver, and the number of affected people increases. This means that about 75 to 100 million people in the United States are affected.
Levels of nonalcoholic fatty liver disease are higher in Hispanics, which can be attributed to high rates of obesity and type 2 diabetes in the Hispanic population. Nonalcoholic fatty liver disease is also more common among men than women in all age groups up to age 60, where the prevalence of sex equates. This is because of the protective properties of estrogen. Fatty liver and NASH occur all ages, with the highest number in the age group of 40 to 49 years. This is the most common liver disorder in children aged 2 to 19 years.
History
The cases now understood as NAFLD were first described in Japanese literature in the mid-1970s, followed by case reports in English. The term "nonalcoholic steatohepatitis" was first published by Jurgen Ludwig and co-authors of the Mayo Clinic in 1980, and the wider NAFLD began to be used around 2002.
The 1980 paper was largely ignored at the time but was later seen as an important paper, and beginning in the mid-1990s conditions began to be studied intensively, and a series of international meetings were held on topics beginning in 1998.
Diagnostic criteria are commenced; in 2005 the Pathology Committee of NIH NASH Clinical Research Network proposed a scoring system that in 2006 has not been validated.
Children
Nonalcoholic child fatty liver disease (NAFLD) was first reported in 1983. It is currently the leading form of liver disease among children. NAFLD has been linked to the metabolic syndrome, which is a group of risk factors that contribute to the development of cardiovascular disease and type 2 diabetes mellitus. Studies have shown that abdominal obesity and insulin resistance are particularly considered to be key contributors to NAFLD development. Because obesity is becoming an increasingly common problem worldwide, the prevalence of NAFLD has increased simultaneously. In addition, boys were more likely to be diagnosed with NAFLD than girls with a ratio of 2: 1. Studies have shown that progression toward a more advanced disease stage among children depends on age and the presence of obesity. These findings are consistent with previous studies in adults showing similar relationships between age and obesity, and liver fibrosis. Early diagnosis of NAFLD in children can help prevent the progression of liver disease during adulthood. This is challenging because most children with NAFLD show no symptoms with little to show abdominal pain. Currently, liver biopsy is considered the gold standard for diagnosing NAFLD. However, these methods are invasive, costly and have a greater risk for children, and noninvasive screening and diagnosis methods will have significant public health implications for children with NAFLD. The only treatment that is proven to be truly effective in childhood NAFLD is weight loss.
See also
- Alcoholic liver disease
- Fatty liver (including non-alcoholic and alcoholic liver disease)
References
Further reading
- Hassan K, Bhalla V, Ezz El Regal M, A-Kader HH (September 2014). "Nonalcoholic fatty liver disease: A comprehensive review of the growing epidemic". World Journal of Gastroenterology (review). 20 (34): 12082-12101. doi: 10.3748/wjg.v20.i34.12082. PMCÃ, 4161796 . PMIDÃ, 25232245. Ã,
External links
- Medscape article on NASH.
- MEDICINENET articles on Steatosis.
- NIH page on Nonalcoholic Steatohepatitis
- The British Medical Journal article on the diagnosis and early management of non-alcoholic fatty liver disease
Source of the article : Wikipedia
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