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Intravenous vitamin E (E-Ferol) in premature infants was linked to fatalities. Researchers found polysorbates, not vitamin E, suppressed immune cell responses, indicating a potential cause for infant complications.
Area of Science:
- Neonatal Medicine
- Immunology
- Toxicology
Background:
- Intravenous vitamin E (E-Ferol) use in low birth weight, premature infants is associated with fatalities.
- An unusual syndrome has been observed in neonatal intensive care units following E-Ferol administration.
Purpose of the Study:
- To investigate the in vitro effects of E-Ferol on human lymphocyte response to phytohemagglutinin (PHA).
- To identify the specific component within E-Ferol responsible for observed immune suppression.
Main Methods:
- In vitro testing of human lymphocytes' response to PHA with E-Ferol, alpha-tocopherol acetate, polysorbate 80, and polysorbate 20.
- Analysis of T11 lymphocyte percentages concurrently with PHA response.
Main Results:
- E-Ferol significantly suppressed the PHA response in human lymphocytes, particularly at low PHA doses.
- Alpha-tocopherol acetate alone did not suppress, and sometimes enhanced, the PHA response.
- Polysorbate 80 and polysorbate 20, used as E-Ferol carriers, were identified as the suppressive agents, with polysorbate 80 being particularly potent.
Conclusions:
- The observed immune suppression associated with E-Ferol is attributed to its polysorbate carriers, not vitamin E itself.
- Polysorbate-induced suppression of PHA response correlates with a decrease in T11 lymphocytes.
- Findings suggest a need to re-evaluate the safety and formulation of intravenous vitamin E preparations for vulnerable infant populations.
Abstract:
The relatively recent introduction and use of an intravenous form of a vitamin E preparation (E-Ferol) has been associated with the development of an unusual syndrome and fatalities among low birth weight (less than 1,500 g), premature infants in neonatal intensive care units. We have observed an inhibitory effect by this vitamin E preparation on the in vitro response of human lymphocytes to phytohemagglutinin (PHA). E-Ferol suppressed the expected response to low doses of PHA. However, this suppression was not due to the alpha-tocopherol acetate (vitamin E) component, because alpha-tocopherol acetate by itself was not inhibitory; in fact, it often enhanced the PHA response. Because a mixture of polysorbate 80 and polysorbate 20 is used as a carrier in E-Ferol, these components were also tested and were found to be responsible for the suppression, especially the polysorbate 80. Concurrent with this suppression of PHA-induced mitogenesis was a decrease in the percentage of T11 lymphocytes.