Issn Print: 0277-2116

Publication Date: 1997/07/01


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Vitamin E Supplementation in Cystic Fibrosis

Brigitte M. Winklhofer-Roob

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To the Editor: I read with interest the article of Peters and Kelly on vitamin E supplementation in cystic fibrosis (CF) (1). During the past decade, vitamin E supplementation has become an established part of the therapeutic regimen for CF patients. A consensus committee recommended in 1992 that, depending on age, vitamin E doses of 25-400 IU/day should be given to CF patients (2). Therefore, the rationale for studying the effect of doses of 15 and 100 mg/day is difficult to understand, particularly in the absence of data on compliance. Drs. Peters and Kelly recommend “that clinicians take care to study the composition of vitamin supplements,” but at no time do they provide information about the vitamin E preparations taken by their study patients. RRR- versus all-racemic α-tocopherol and free versus esterified form (e.g., α-tocopherol acetate) need to be specified (3), so that the dose expressed as milligrams per day can be interpreted regarding biological activity. Particularly at low doses, a possible advantage of the RRR form over the all-racemic form due to discrimination by the α-tocopherol transfer protein (4) may become relevant.
Plasma α-tocopherol concentrations were not standardized for plasma lipids because blood was drawn in the afternoon. Recent data show that plasma cholesterol concentrations are fairly stable, both in CF patients and healthy subjects on an unrestricted diet, with a coefficient of variation of 4.9 and 3.9%, respectively, for five measurements within 12 h (5). This encourages the use of ratios of plasma α-tocopherol to cholesterol (6) even in clinical practice.
The authors claim that erythrocyte (EC) vitamin E concentrations have not previously been studied in CF patients, but an article published in 1992 (7) showed low α-tocopherol concentrations in ECs of CF patients with low plasma α-tocopherol concentrations. Drs. Peters and Kelly used EC α-tocopherol concentrations as a measure of tissue vitamin E, based on “animal studies that showed a good correlation between EC and tissue vitamin E status.” In the article cited (8), however, platelet α-tocopherol concentrations were proposed as a reliable index of tissue vitamin E status, whereas a correlation between EC and tissue vitamin E was not shown. Replacing, in the conclusions, “EC vitamin E,” which was actually measured, with “tissue vitamin E levels” seems to be inappropriate as long as such a correlation has not been shown. The regulatory mechanisms for the α-tocopherol exchange between lipoproteins and ECs may differ substantially from those between lipoproteins, other blood cells, and different tissues and organs.
Data were analyzed using one-way analysis of variance (ANOVA), linear regression analysis, and Mann-Whitney U test, all of which are suitable only for data that are independent of each other. It remains unclear which patients and vitamin E doses were included in the different analyses: Table 1 shows only doses of 0, 15, and 100 mg/day in 32, 32, and 46 patients, respectively, in contrast to Fig. 1A, where doses of 0, 15, 50, 75, 100, 115, 150, and 200 mg are plotted for (approximately) 19, 21, 4, 1, 31, 4, 1, and 6 patients, respectively. Because the study total was 72, some subjects have been entered more than once in Fig. 1A (n = 87) and Table 1 (n = 110), resulting in data that are interdependent. In the text, the authors refer to Fig. 3 in terms of showing the relation between vitamin E dose and the increase in plasma and EC α-tocopherol concentrations, respectively, but actually this figure shows a plot of “change in EC and plasma α-tocopherol concentration pre and post” against the “mean of pre and post concentrations.

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