부산대학교 도서관

A 67-year-old man had been under hemodialysis since June 2010 because of chronic renal failure with unproven etiology. He had drunk alcohol at about 80 g/day. He had experienced appetite loss since March 2011. In mid-April, his fatigue had gotten worse and blood gas analysis showed remarkable hypoglycemia (30 mg/dL) and acidemia (pH 7.19) at an outpatient clinic. Although hemodialysis was started, it was stopped and he was injected with 20 g of glucose and transported to our hospital. Blood gas analysis at our hospital revealed pH 7.351, pCO2 29.1 torr, pO2 104.4 torr, HCO3− 16.1 mmol/L, and high anion-gap metabolic acidosis (anion-gap 23.9 mmol/L). Recognizing his disorientation and ataxia with anamnesis indicating that he could not have had a sufficient diet, we diagnosed Wernicke’s encephalopathy. Regarding the metabolic acidosis, we considered that alcoholic acidosis from an excessive intake of alcohol and lactic acidosis from a lack of vitamin B1 (thiamine) had synergistically induced it. After admission, supplying glucose and vitamin B1, his symptoms and metabolic acidosis clearly improved. We compared the serum vitamin B1 level of 20 patients under maintenance hemodialysis in our hospital before and after hemodialysis. However, there was no significant difference (30.4±6.7 ng/mL and 30.2±7.2 ng/mL, respectively). On the other hand, a study has demonstrated a case that underwent 40% decrease in the serum vitamin B1 level, so the possibility of removing vitamin B1 with hemodialysis has been indicated. In addition, several cases of Wernicke’s encephalopathy in non-alcoholic patients on hemodialysis have been reported. We should consider the lack of vitamin B1 and Wernicke’s encephalopathy when we recognize consciousness disturbance or metabolic acidosis in patients on maintenance hemodialysis, whether they are drinkers or not.