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The literature reports that carnitine can promote the excretion of excess organic or fatty acids in patients with defects in fatty acid metabolism and/or specific organic acidopathies that bioaccumulate acylCoA esters.1-6 Secondary carnitine deficiency can be a consequence of inborn errors of metabolism

LPL activity is stimulated by apoCII and suppressed by apoC-III

Treatment with peginterferon alfa-2a monotherapy at a dose of 135g SQ/week for patients on hemodialysis may be considered, with close monitoring for interferon toxicity