We report a 66-year-old man who developed vitamin B1 deficiency polyneuropathy long after a gastrectomy. After a preceding bronchial infection, the patient noticed numbness and weakness in his extremities, followed by generalized edema and exertional dyspnea. He had undergone subtotal gastrectomy due to duodenal ulcer at age 19. His daily oral intake of food was normal without any alcoholic abuse. He was admitted to our hospital with rapidly progressive gait disturbance due to muscle weakness, and sensory disturbance. Neurological examination showed peripheral polyneuropathy with distal dominant muscular weakness and sensory disturbance. Chest X-ray film showed marked cardiomegaly and pleural effusion. Nerve conduction studies showed decreases in the action potentials of both the motor and sensory nerves, with the sensory nerves being more severely affected than the motor nerves. Sural nerve biopsy demonstrated severe axonal degeneration without any inflammatory change. The blood concentration of thiamine (vitamin B1) was slightly decreased below the normal range (19 ng/ml; normal, 20-50), and the serum vascular endothelial growth factor (VEGF) was high (890 pg/ml; normal < 200 pg/ml). Intravenous administration of vitamin B1 (50 mg per day) dramatically improved his symptoms in a few days and the level of VEGF returned to nearly normal. In this gastrectomized patient many years ago, vitamin B1 deficiency neuropathy is warranted in view of a prompt response to thiamine administration. This case suggests that VEGF is involved in the pathogenesis of vitamin B1 deficiency polyneuropathy.