VITAMINS

Homocysteine (Hcy) itself is considered to have neurotoxicity and it has been reported that Hcy has a relation with neurodegenerative diseases such as Parkinson's disease. In addition, it has also been reported that the L-DOPA preparation has an effect to increase the blood Hcy concentrations, and the presence of hyperhomocysteinemia in Parkinson's disease and its influences on clinical symptoms are attracting attention. In this study, we investigated the rate of patients with parkinsonism in 98 patients with hyperhomocysteinemia showing their blood Hcy concentrations exceeding 20 μmol/L and also investigated the therapeutic effect of a vitamin B preparation (vitamin B_<12> and, folic acid). As a result, parkinsonism was detected in 30 of the 98 patients (30.6%). When the vitamin B preparation was administered to hyperhomocysteinemia patients with parkinsonism, their blood Hcy concentrations decreased significantly from 29.4±2.9μmol/L to 12.8±1.7 μmol/L. In addition, parkinsonian symptoms were improved by administration of the vitamin B preparation alone in 4 patients. It is therefore considered that parkinsonism would possibly be improved by administration of the vitamin B preparation when the blood concentrations of Hcy, vitamin B_<12> and folic acid are determined in patients with parkinsonism and thereby hyperhomocysteinemia is recognized.

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Recently the number of patients with vitamin B_1 deficiency including Wernicke encephalopathy has increased were mainly in the aged population. The new problems of nutritional, medical and social backgrounds have to be studied. Wernicke encephalopathy is an acute neuropsychiatric syndrome resulting from vitamin B_1 deficiency. Criteria for diagnosing Wernicke encephalopathy requires the presence of three clinical signs, oculomotor abnormalities, cerebellar dysfunction, and confusion. However, it has often been reported that most patients do not fulfill all three criteria. According to autopsy-based studies, the disorder is still underdiagnosed. Even diagnosing the disorder, an insufficient treatment is followed by mental sequelae such as Korsakoff syndrome. The guideline of treatment of Wernicke encephalopathy is not established in Japan. The patients should be treated empirically with a minimum of 500mg thiamine (dissolved in 100 ml of normal saline), given by infusion over a period of 30 min, three times per day for 2〜3 days. In cases of no response, supplementation may be still continued for a few day. The clinical manifestations may be iatrogenically precipitated by glucose loading in the patients. To avoid this complication, thiamine must be administered prior to glucose infusion. Other vitamins including B_2, B_6, nicotinamide, and C should be additionally given, because multivitamin could be deficient in the patients.

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In 1882-3, many Japanese sailors suffered from beriberi and some died in warships. Japanese government started a committee to prevent beriberi. A parallel controlled trial for beriberi was carried out in 1884 by Kanehiro Takagi who had studied at St Thomas Hospital in London and noticed a remarkable difference in the frequency of beriberi between Japan and London. He determined the ratio of nitrogen to carbon content of food taken by the crew of warship Rhujo which sailed from Japan to Hawaii via Chile and resulted in a miserable occurrence of beriberi. Carbon content in the food was higher during the voyage from Chile to Hawaii than that from Hawaii to Japan, the latter of which brought about beriberi much less frequently. These data prompted Dr. Takagi a trial voyage under similar conditions except partially replacing polished rice with meat in crew's diet. Dr. Takagi postulated the Emperor on importance of diet during the trial voyage. Warship Tsukuba set out on the trial voyage in February, 1884 and arrived at Hawaii without any beriberi patient. The success in preventing beriberi led to taking food without polished rice in Japanese navy, while Japanese army and professors in Tokyo Imperial University neglected these data due to an erroneous assumption that beriberi might be infectious. A mistaken trust in polished rice had prevailed in Japan until 1923 when vitamin B_1 deficiency derived from polished rice was revealed as a cause of beriberi. Thereafter, the incidence of beriberi has decreased dramatically.

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