Letter To The Editor: “Is There Any Benefit from Oral A-Tocopherol Administration in Hemodialysis Patients?”

Dear Sirs,

We read the recently published study by Hodkova et al., which failed to detect any beneficial effect of oral a‐tocopherol administration on several markers of micro-inflammation.[1] The authors conclude that a daily oral dose of 400 mg of vitamin E for five weeks does not seem to be able to reduce enhanced oxidative stress and micro-inflammation in chronic hemodialysis (HD) patients. In the discussion, they referred to the pro-oxidative effects of a-tocopherol in co-antioxidant-depleted HD patients.[2]

We also studied the effect of oral a-tocopherol administration at a dose of 500mg/d on oxidative stress in HD patients. The period of administration was longer (i.e., one year) and we too failed to detect any beneficial effect too. In contrary, in 36 stable HD patients, plasma total antioxidant status got worse after a-tocopherol administration, from 1.624 ± 0.179 to 1.421 ± 0.263 mmol/L (p < 0.05). Red cell's superoxide dismutase activity decreased after a-tocopherol administration from 1433 ± 657 to 1172 ± 374 u/grHb (p < 0.05), whereas red cell's glutathione peroxidase activity remained unaffected (34.95 ± 11.7 vs. 27.32 ± 14.99 u/grHb, p = ns).[3] We also examined the effect of one-year oral a-tocopherol administration at the same dose on serum anticardiolipin IgG antibodies (ACA-IgG) and IgM antibodies (ACA-IgM) levels, as oxidative stress has been implicated in ACA formation. ACA-IgG levels were higher in HD patients compared with control. This was not the case for ACA-IgM levels. A-tocopherol administration resulted in a further increase in ACA-IgG (26.7 ± 14.7 GPL/mL vs. 13.3 ± 6.64 GPL/mL, p < 0.001) and ACA-IgM levels (8.17 ± 1.95 MPL/mL vs. 2.96 ± 4.18 MPL/mL, p < 0.001) in HD patients.[4]

Our studies, like that by Hodkova et al., failed to detect any beneficial effect of oral a-tocopherol administration on oxidative stress markers or on one of the oxidative stress consequences (ACA) in HD patients. In contrary, one-year oral a-tocopherol deteriorated most of the examined factors, raising questions about the usefulness or even the safety of its administration in HD patients, who are not a-tocopherol depleted, as Hodkova[1] and other investigators confirmed previously. The most possible explanation, which Hadkova et al. also support, is that a-tocopherol plays a pro-oxidative role in HD patients due to the depletion of other co-antioxidant factors.[2] The co-administration of a-tocopherol with these factors, like ascorbate, could reverse its action to the beneficial way. Another possible explanation that also needs evaluation is that a-tocopherol is not the only form of vitamin E. Another form is the γ-tocopherol, which has distinct and very important biologic effects.[5] Interestingly, oral a-tocopherol administration decreases plasma and tissue γ-tocopherol levels with consequences that have not yet been evaluated in HD patients.[6] The differences in patients' selection in the duration of a-tocopherol administration, in the route of administration (intravenously in the case of vitamin E-coated dialyzers or orally), and finally in diet regarding the adequacy for the several antioxidant substances could be responsible for the conflicted results of different studies. In our opinion, the current bibliographic data do not lead to a definite conclusion about the worth and safety of oral a-tocopherol administration in HD patients.