Print | close window note: large images and tables on this page may necessitate printing in landscape mode. Nonalcoholic fatty liver disease basics description spectrum of diseases with different clinical significance: it is a histological diagnosis: accumulation of large fat droplets in the hepatocytes (macrovescicular steatosis) in absence of excessive alcohol consumption patients are asymptomatic only patients with abnormal lfts during routine testing come to medical attention viral etiology, alcohol abuse and other causes of liver disease must be ruled out nafld includes simple fatty liver, nash and cryptogenic cirrhosis with fatty liver fat in the liver >5â€“10% by weight compatible imaging studies and biopsy nash subset of nafld that may progress to cirrhosis histology: fat, necroinflammatory changes and hepatocellular injury (steatohepatitis) cryptogenic cirrhosis: fatty liver disease most common cause of cryptogenic cirrhosis natural history natural history of the disease is still controversial the progression from steatosis without inflammation to steatohepatitis is debated nash may progress to cirrhosis, although timing and percent of those who progress has not been established. General prevention hyperinsulinemia and diabetes are important predisposing factors: prevention includes weight control, diet and exercise. Epidemiology prevalence parallels obesity epidemic. Good epidemiologic data are lacking. medicaresupplementspecialists.com/pfz-100-mg-generic-viagra-np/viagra for salebuy viagrageneric viagra usa pharmacycheap viagra onlinegeneric viagra onlinehttp://classicmotocrossimages.com/mbs-buy-viagra-online-go/http://classicmotocrossimages.com/mbs-order-cheap-viagra-online-jt/cheap viagrabuy viagra Females represent 60â€“80% of patients in clinical studies common in 3rdâ€“4th decade occurs in 2. 6% of all children and 22â€“52% of children that are obese mexican americans and african americans may have increased prevalence. Incidence unknown prevalence prevalence of nafld in the united states is 20â€“30% as estimated by ultrasound. By autopsy review nafld in 35% of lean patients, and in 70% of obese patients nash in 6. 3% of patients with nafld risk factors obesity in patients with bmi >51: 90% have steatosis and 34% nash niddm hyperlipidemia can occur in nonobese patients genetics family clusters have been described presence of hemochromatosis gene mutations may accelerate the disease process pathophysiology proposed mechanism fatty liver: insulin resistance (ir) causes an increase of free fatty acid (ffa) in the blood stream that overwhelms the liverâ€™s ability to metabolize them causing fatty accumulation in the liver nash: a second hit is required (oxidative stress? Endotoxin? Metabolic syndrome? ) which causes inflammatory cytokines to promote liver damage and fibrosis deposition etiology remains controversial. Metabolic syndrome plays a major role. Metabolic syndrome is an inflammatory condition modulating proinflammatory cytokines. Fat tissue, especially truncal, is metabolically active, secreting some of the key cytokines and neuroendocrine mediators involved in the pathogenesis of nafl.