Koike et al. reported a slowly progressive, prevalent sensory polyneuropathy in patients with folate deficiency, which shows some distinctive clinical features with respect to thiamine-deficiency neuropathy. [1,2] However, as the authors mention, the clinical manifestations of folate deficiency may be indistinguishable from that of cobalamin deficiency because of their interaction in one carbon metabolic pathway. [3] In addition, thiamine is poorly absorbed during folate deficiency, because of frequent diarrhea as a result of damaged gastrointestinal mucosa. At the cellular level, a folate deficiency may cause an indirect thiamine deficiency. Even though thiamine is present, it cannot be activated to thiamine pyrophosphate-- its biologically active form--due to a deficient dihydrofolate reductase activity.[4,5] It is possible that the clinical features of a folate-deficiency neuropathy may be partly caused by indirect thiamine deficiency. Even with adequate folate supplementation, the patients in the study showed some residual deficits.[1] Considering these findings, a combined administration of folate, thiamine, and cobalamin, to maximize the therapeutic effect in the early disease phase might have been more beneficial to these patients.
Folate-deficiency neuropathy and indirect thiamine deficiency
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