ビタミンＢ１欠乏に起因したショック時の糖質・脂質代謝動態の検討

DOI 被引用文献4件 オープンアクセス

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  • Carbohydrate and lipid metabolism in shock due to vitamin B1 deficiency.

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Shock due to vitamin B1 deficiency was previously known as “shoshin beriberi”. The disease was caused by derangement in carbohydrate metabolism. From the viewpoint of the metabolic disturbances, the disease in similar to multiple organ failure (MOF), which is induced by cellular damage. The present study investigated carbohydrate and lipid metabolism in 3 patients with shock due to vitamin B1 deficiency. Lactate, pyruvate pyruvate/lactate and ketone body concentration {KBC (β-hybroxybutyrate+acetoacetate)} were compared between the 3 patients and septic MOF patients. The patients in shock due to vitamin B1 deficiency were found to have markedly high lactate (297±78.7mg/dl) and pyruvate concentrations (8.55±1.69mg/dl) and low pyruvate/lactate (0.030±0.003) compared with septic MOF patients, indicating derangement in the tricarboxylic acid cycle. Two of the patients were found to have high KBC (822, 481μmol/l) due to hypermetabolism of lipid to compensate for depressed glucose metabolism. Furthermore, 2 patients were found to have remarkably high NH3 concentrations due to energy deficiency for NH3 metabolism. One patient had the highest lactate, pyruvate and NH3 concentrations, and normal KBC. The patient was considered to have not only impairment in the tricarboxylic acid cycle for vitamin B1 deficiency but also in lipid metabolism caused by the overloading of carbohydrate. On the other hand, in the septic MOF patients, lactate and pyruvate concentrations and pyruvate/lactate were 56.3±67.6mg/dl, 2.90±1.73mg/dl and 0.078±0.033, respectively. KBC was 104±76.9μmol/l and had a significant correlation with lactate in the septic MOF patients. The patients in shock due to vitamin B1 deficiency had higher lactate and pyruvate concentrations, higher KBC and lower pyruvate/lactate than the septic MOF patients. These results indicate that in vitamin B1 deficiency the metabolic impairment is partial and that the other metabolic mechanisms support the energy deficiency caused by the metabolic derangement. In conclusion, if a patient in shock has high lactate, high pyruvate and high KBC, one must consider vitamin B1 deficiency and must give thiamine as soon as possible. We believe that by early diagnosis and treatment we can save the life of patients in shock or with MOF due to vitamin B1 deficiency.

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