On the occasion of publication of the feature on diagnosis and assessment of nonalcoholic fatty liver disease/nonalcohol
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SPECIAL FEATURE: EDITORIAL Diagnosis and assessment of nonalcoholic fatty liver disease / nonalcoholic steatohepatitis using ultrasound elastography
On the occasion of publication of the feature on diagnosis and assessment of nonalcoholic fatty liver disease/nonalcoholic steatohepatitis using ultrasound elastography Kazushi Numata1
© The Japan Society of Ultrasonics in Medicine 2020
It is now possible to eliminate the hepatitis C virus and inhibit proliferation of the hepatitis B virus, leading to a downward trend in carcinogenesis subsequent to viral hepatitis in Japan, but the occurrence of hepatocellular carcinoma subsequent to non-B, non-C hepatitis is increasing year by year, with non-B, non-C hepatitis being the cause in about one-third of hepatic carcinoma cases [1]. The primary origins of non-B, non-C hepatitis are alcoholic liver disease in individuals with a history of excessive alcohol intake (defined in Japan as 60 g/day (ethanol equivalent)) and nonalcoholic fatty liver disease (NAFLD) in individuals without a history of alcohol intake or who drink little. NAFLD, which is primarily associated with metabolic syndrome, is a condition in which fatty liver is found on histological examination or diagnostic imaging. The prevalence of NAFLD is increasing as the number of obese and diabetic patients increases. NAFLD is classified as nonalcoholic fatty liver (NAFL), which is considered to be an almost non-progressive entity, and nonalcoholic steatohepatitis (NASH), which is a form of NAFLD with the progression of fibrosis. NAFL and NASH are differentiated by means of liver biopsy, in principle. According to the Clinical Practice Guideline for NAFLD/ NASH 2020 (revised 2nd edition), NAFLD is defined as follows: (1) Fatty deposition in the liver histologically ≥ 5% is considered significant. (2) NASH is characterized by steatosis, inflammation, and hepatocellular damage (ballooning degeneration) according to pathological diagnosis. (3) Intertransition of NAFL and NASH is seen, with the progression * Kazushi Numata kz‑[email protected]‑cu.ac.jp 1
Gastroenterological Center, Yokohama City University Medical Center, Urafune‑cho 4‑57, Minami‑ku, Yokohama, Kanagawa 232‑0024, Japan
of fibrosis sometimes occurring despite a slow progression rate in some cases of NAFL. (4) The upper limit of alcohol intake is 30 g/day for men and 20 g/day for women (ethanol equivalent). (5) Drug-induced fatty liver disease is fundamentally regarded as drug-induced hepatic injury. (6) Disorders that present so-called microvesicular degeneration such as Reye syndrome and acute fatty liver of pregnancy are excluded from NAFLD. (7) In some cases of NASH liver cirrhosis, the characteristics of NASH such as steatosis and ballooning degeneration disappear as it progresses, resulting in burned-out NASH. Furthermore, the pathological finding most associated with the vital prognosis is liver fibrosis; therefore, the degree of fibrosis should be considered when selecting the method of follow-up observation and treatment. There are some i
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