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9 10 During this  study we have never recorded any side effect. The presence of manifestations of a mild thiamine deficiency even in patients with normal concentrations of thiamine and TPP in the blood could be explained if referred to a form of thiamine deficiency due to a dysfunction of the vitamin B1 active intracellular transport, or to structural enzymatic abnormalities.9 11 We deem that the concentration of thiamine in the blood before and after the therapy has higher relevance in understanding the action of vitamin B1 in these cases because, it is known that thiamine is converted into TPP within the cells and thus, TPP concentration in the blood may not be related to improvement of the diffusion [http://www.selleckchem.com/products/byl719.html Alpelisib] mechanism throughout the organism.12 On the other hand, the much higher content of thiamine in the blood after the high-dose therapy leads to an increment of the intracellular TPP and to an improvement of the manifestations as shown in our observations. In the 1950s and 1960?s, several authors treated MS using TPP without any result.13 We deem that if the aforementioned early studies focused on administration of thiamine rather than TPP, they might have witnessed an improvement of the fatigue due to the action of thiamine at cellular level in favouring the production of TPP. Unfortunately, for the current study we were not in the position to measure the TPP levels in the cells. However,  whatever be the kind of dysfunction taking place in our patients, the symptoms were responsive to administration of large quantities of thiamine. The administration of large quantities of thiamine orally or parenterally increases its concentration in the blood to the levels which  the passive transport restores the normal glucose metabolism. According to literature, the dysfunction of active intracellular transport or enzymatic abnormalities could be overcome by diffusion mediated at supranormal thiamine concentrations.9 11 Other mechanisms have been thought to be responsible of the efficacy of high doses of thiamine, but we reckon these are less likely.11 The doses employed in this study were calculated empirically based on previous studies on inflammatory bowel diseases and they may be defined with higher accuracy as a result of further studies, in order to improve the efficiency of the therapy. As of today, there is only one non-alcoholic case report of Wernicke��s encephalopathy manifesting with symptoms of thiamine deficiency with normal blood concentrations of thiamine level, caused by vomiting and severe diarrhoea secondary to Clostridium difficile colitis.14 Clinical improvements are documented following administration of pharmacological doses of thiamine in patients with inborn errors of metabolism such as thiamine-responsive megaloblastic anaemia and Wernicke��s like encephalopathy.9 11 In addition, recently, improvement of fatigue with high doses of thiamine was observed in a case of Spinocerebellar Ataxia type 2.