"The most significant factor recognized in this study was that of alcohol intake," said Dr. Zein. "Our study supports emerging data that alcohol intake, even in 'social' quantities, may potentially increase the risk of HCC development in NASH- and HCV-cirrhotic patients compared with non-drinkers."
The Cleveland Clinic study established that NASH-induced cirrhosis is a much greater risk factor for HCC than previously thought. A related study offers an explanation as to why NASH often progresses to liver cancer.
Researchers at Duke University hypothesized that natural killer T (NKT) cells modulate the liver's response to damage related to fat deposition. NKT cells are specialized types of T lymphoctyes (white blood cells) that reside in healthy livers and regulate immune responses that control tissue inflammation, fibrosis, and cancer progression.
Earlier studies from the Duke group and other researchers have demonstrated that the livers of animals and humans with mild forms of nonalcoholic fatty liver disease (NAFLD) were relatively depleted of NKT cells and Th1 cytokines were abundant. In the current study, Anna Mae Diehl, M.D., and colleagues examined the possibility that excessive accumulation of NKT cells in the liver would tip the cytokine balance in the opposite direction, resulting in liver fibrosis.
Results showed that the Hedgehog (Hh) pathway became activated and NKT cells accumulated excessively in the livers of wild type mice that developed NASH-related liver fibrosis. "Hh pathway activation leads to hepatic enrichment with NKT cells that contribute to fibrosis progression in NASH," concluded Dr. Diehl. "Our study proves that activation of liver NKT cells generates soluble factors that promote fibrogenesis via a mechanism invo
|Contact: Dawn Peters|