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

Matsuda Kenichi, Hirasawa Hiroyuki, Sugai Takao, Ohtake Yoshio, Oda Shigeto, Shiga Hidetoshi, Kitamura Nobuya

doi:10.3893/jjaam.4.309

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.

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

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