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Mechanistically, this is commonly mediated by the prevalent two-hit hypothesis that implies accumulation of TG in hepatocytes (steatosis) in the first hit, followed by triggering progression to inflammation, oxidative stress, and apoptosis in the second hit (37, 38)

In extreme cases this can be followed by hypotension, a rapid, weak, irregular pulse, breathing difficulty, general weakness, circular, and collapse, finally, convulsions