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Letters
JAMA. 1986;256(19):2677-2678. doi: 10.1001/jama.1986.03380190047021

Oxalosis and the E-Ferol Toxicity Syndrome

  1. Robert A. J. Conyers, MB, BS, DPhil;
  2. Renze Bais, PhD;
  3. Allan M. Rofe, PhD
  1. Institute of Medical and Veterinary Science Adelaide, Australia

Since this article does not have an abstract, we have provided the first 150 words of the full text.

Excerpt

To the Editor.— There is a sense of déjà vu about the description by Bove et al1 of the adverse reactions and deaths that followed the intravenous administration of the vitamin E preparation E-Ferol to low-birth-weight infants. The syndrome of renal dysfunction, hepatic dysfunction, metabolic acidosis, and tissue oxalosis has many similarities to that which occurs in patients who received parenterally large amounts of xylitol.2 When first observed, the xylitol toxicity syndrome was unexpected, and, indeed, it was concluded that the oxalosis was not causally related to the infusion of xylitol.2 However, both animal and biochemical studies have since confirmed that oxalate or oxalate precursors can be formed during the hepatic metabolism of xylitol,2 with the enzymes fructokinase and aldolase playing important roles in the metabolic production of the oxalate precursor glycolaldehyde from xylitol.2,3 In terms of a one-compartment model for the renal elimination of

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