Thiamine diphosphate is the active form and serves

as a co‐factor to several enzymes involved primarily in carbohydrate catabolism. Those enzymes are important in the biosynthesis of a number of cell constituents, including neurotransmitters, and for the production of reducing equivalents used in oxidant stress defenses and in biosyntheses and for synthesis of pentoses used as nucleic acid precursors. The major manifestations of thiamine deficiency in humans involve the cardiovascular (wet beriberi) and nervous (dry beriberi, neuropathy and Wernicke–Korsakoff syndrome) systems.7 WE is a devastating acute or subacute neurological disorder and remains the most important encephalopathy due to a single vitamin deficiency. The disease is rare, catastrophic in onset, clinically complex and often delayed in diagnosis. The reported prevalence of WE in autopsy studies ranges from 0.4% to 2.8%, accounting on average

AZD0530 molecular weight for 1.3% of all autopsies, and seems to be much higher in alcoholics than in non‐alcoholics.8 The clinical diagnosis of WE requires two of the following four signs: dietary deficiencies, eye signs, cerebellar dysfunction, and either altered mental state or mild memory impairment.8 Whenever possible, direct measurement of thiamine and its phosphate esters in human blood by Dapagliflozin order high‐performance liquid chromatography should be performed before thiamine administration and MRI should be used to support the diagnosis of acute WE.8 According to European Federation of Neurological Societies (EFNS)

guidelines published in 2010, 600 cases of WE were reported in non‐alcoholic patients. WE was typically associated with malignant pathologies, gastrointestinal diseases and previous surgeries, or resulting from vomiting due to hyperemesis gravidarum.8 There are few reports in the literature of patients with IBD developing WE. Hanh et al. reported a case of a female patient with CD that was on chronic total parenteral nutrition and developed WE after a shortage of multivitamin infusion in the United States and recovered after thiamine replacement.9 In Larnaout et al. report, a patient with CD died due to the lack of thiamine replacement.10 In another report, a patient with CD, submitted to intestinal resection, presented with neurological manifestations and decreased thiamine levels and a significant improvement after vitamin B1 infusion was observed.11 oxyclozanide Similar to this case study, Mattioli et al. reported the occurrence of WE in a patient with complicated UC and total parenteral nutrition, despite the administration of the usually recommended doses of vitamin B1.12 Another unusual finding in our patient was the complaint of dysphagia and the gastric stasis that developed before other neurologic findings and recovered after thiamine infusion. Dysphagia is an unusual finding in WE, especially as presenting symptom. Karaiskos13 described this same clinical presentation in an alcoholic man and Truedsson14 in a non‐alchoolic patient.