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Volume 86, Issue 11
Displaying 1-19 of 19 articles from this issue
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Fumio WatanabeArticle type: Article
2012 Volume 86 Issue 11 Pages 597-611
Published: November 25, 2012
Released on J-STAGE: October 10, 2017
JOURNAL FREE ACCESSVitamin B_<12> (B_<12>) is the largest and most complex compound among all vitamins, and synthesized only in certain bacteria. B_<12> is concentrated mainly in the bodies of higher predatory organisms in the natural food chain system. As animal foods, but not plant foods, are considered to be the major dietary sources of B_<12>, strict vegetarians and/or elderly persons have a great risk of developing B_<12>-deficiency. When corrinoid compounds were purified and characterized from various B_<12>-rich foods, inactive corrinoid compounds including pseudovitamin B_<12> predominated in certain shellfish and edible cyanobacteria. Significant losses of B_<12> occur in various foods during cooking and preservation. The underlying cause(s) for the link between B_<12>-deficiency and its symptoms (developmental disorder, metabolic abnormalities, and neuropathy) are poorly understood. The molecular mechanisms of these metabolic disorders were investigated using B_<12>-deficient animal models, and physiological functions of B_<12> and/or pseudo-B_<12> were also evaluated using many prokaryotic and eukaryotic organisms.View full abstractDownload PDF (1647K) -
Shigenobu NakamuraArticle type: Article
2012 Volume 86 Issue 11 Pages 612-619
Published: November 25, 2012
Released on J-STAGE: October 10, 2017
JOURNAL FREE ACCESSWernicke's encephalopathy was first described by Wernicke in 1881. However, the disease is often overlooked in our daily clinical activities, since Wernicke's encephalopathy can not be definitely diagnosed in an emergency room. If Wernicke's encephalopathy is not treated properly with vitamin B_1, patients will usually suffer from Korsakoff syndrome or sometimes fall into death. Vitamin B_1 deficiency has been thought to be overcome by an abundant food supply or effective vitamin B_1 treatment. Increased alcohol consumption or unbalanced diet has introduced a new aspect of vitamin B_1 deficiency, especially Wernicke's encephalopathy which often leads to dementia. To prevent dementia due to Wernicke's encephalopathy, it has been recommended that a large dose of vitamin B_1 is administered to patients with consciousness disturbance. This article summarizes the pathophysiology, diagnosis and symptoms of Wernicke's encephalopathy as well as the dose of vitamin B_1 administered to patients with Wernicke's encephalopathy and the side effect of the vitamin B_1 therapy.View full abstractDownload PDF (981K) -
Katsushi KoyamaArticle type: Article
2012 Volume 86 Issue 11 Pages 620-624
Published: November 25, 2012
Released on J-STAGE: October 10, 2017
JOURNAL FREE ACCESSSymptoms of vitamin B_1 deficiency are diverse. Wernicke's encephalopathy, which is developed by vitamin B_1 deficiency, has a poor prognosis. This disease is preventable, but cure of this disease is difficult. Therefore, factors defining the developing process of Wernicke's encephalopathy and background factors of this disease should be taken into consideration for evaluation of this disease.View full abstractDownload PDF (520K) -
Hiroaki MiyajimaArticle type: Article
2012 Volume 86 Issue 11 Pages 625-629
Published: November 25, 2012
Released on J-STAGE: October 10, 2017
JOURNAL FREE ACCESSWe report on two previously healthy Japanese brothers with a newly discovered recessively inherited syndrome similar to Wernicke's encephalopathy that developed in the second decade of life; this syndrome was manifested clinically as thiamine-responsive diplopia, ptosis, gait ataxia, and disturbance of consciousness without serum thiamine deficiency. The administration of high-dose thiamine improved the symptoms within a few weeks. There was no history of chronic alcoholism in either patient. Magnetic resonance imaging of the brain showed high-intensity signals in the bilateral medial thalamus and periaqueductal region on fluid-attenuated inversion recovery images; these signals were characteristic of findings in Wernicke's encephalopathy. Genomic analysis of SLC19A3 encoding human thiamine transporter 2 (hTHTR2) revealed that the patients were compound heterozygotes for the K44E and E320Q mutations. Gene-expression analyses of mammalian culture cells showed intracellular thiamine uptake activity was decreased significantly. The identification of this syndrome showed a thiamine-dependent state and provides insight into the thiamine metabolism associated with Wernicke's encephalopathy in humans.View full abstractDownload PDF (3372K) -
Toshifumi Matsui, Hideki Sakurai, Tomomi Tohyama, Atsushi Yoshimura, S ...Article type: Article
2012 Volume 86 Issue 11 Pages 630-635
Published: November 25, 2012
Released on J-STAGE: October 10, 2017
JOURNAL FREE ACCESSWernicke's encephalopathy (WE) is the best known acute neurologic complication of vitamin B_1 (B_1) deficiency and often occurs in chronic alcoholism. The plausible causes of B_1 deficiency in alcoholics depend on the underlying mechanisms, such as a low dietary intake of B_1, inadequate absorption of B_1 from the intestine due to the gastrointestinal tract damage, and coexistent alcoholic liver disease altering the capacity of B_1 storage and the metabolism of biologically important nutrients. Because the use of the classic triad of WE may overlook a mild form of WE that can be detected as inactive WE pathology, Caine and colleagues have proposed the clinical criteria for diagnosis of WE in chronic alcoholics based on the clinical-neuropathological correction. The Caine criteria include dietary deficiency, oculomotor abnormalities, cerebellar dysfunction and either altered mental status or mild memory impairment, two of which are required for diagnosis of clinical WE. In our cohort, 13 alcoholic patients who fulfilled the Caine criteria were followed up and CSF-tau levels increased at the acute stage of the disease and then decreased at the chronic stage, suggesting that the patients have a transient neuronal damage. The Caine criteria enabled an immediate intravenous administration of B_1 and provided a favorable prognosis. For the therapy of WE, parenteral treatment with a high dose of B_1 is now recommended. A typical regimen is that 500 mg of B_1 is intravenously administered three times daily for two consecutive days and 500 mg of B_1 is intravenously administered once daily for additional five days, in combination with other B vitamins. After establishment of a sufficiently low threshold for parenteral B_1 treatment, the B_1 treatment should be conducted in all alcoholic patients with altered mental status, oculomotor disorders or ataxia.View full abstractDownload PDF (5121K) -
Masaru KuriyamaArticle type: Article
2012 Volume 86 Issue 11 Pages 636-639
Published: November 25, 2012
Released on J-STAGE: October 10, 2017
JOURNAL FREE ACCESSWernicke's encephalopathy is an acute neuropsychiatric syndrome resulting from vitamin B_1 (thiamin) deficiency. Criteria for diagnosing Wernicke's encephalopathy requires the presence of three clinical signs, i.e., oculomotor abnormalities, cerebellar dysfunction, and confusion. However, it has often been reported that most patients do not fulfill all of the three criteria. Autopsy-based studies indicate that 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's encephalopathy has not been established in Japan. Patients with Wernicke's encephalopathy should be treated empirically with a minimum of 500 mg thiamin (dissolved in 100 ml of physiological saline) for 2〜3 days. In this treatment, thiamin is infused to the patients over a period of 30 min three times per day. In a case of no response, thiamin supplementation should be discontinued after a few days. Other vitamins including vitamin B_2, vitamin B_6, nicotinamide, and vitamin C should be additionally given to the patients, because multivitamin could be deficient in the patients. The clinical manifestations in the patients may be iatrogenically precipitated by glucose loading. To avoid this complication, thiamin must be administered prior to glucose loading.View full abstractDownload PDF (469K) -
Midori NaruseArticle type: Article
2012 Volume 86 Issue 11 Pages 640-646
Published: November 25, 2012
Released on J-STAGE: October 10, 2017
JOURNAL FREE ACCESSVitamin B_1 (thiamin) has been clinically used in prophylaxis of Wernicke's encephalopathy. It is recognized that the parenteral vitamin B_1 administration is almost safe. However, the administration of usual amounts of vitamin B_1 occasionally causes life-threatening abnormality such as anaphylaxis. In this review, I introduce the previously reported data about the unexpected abnormalities after the parenteral administration of vitamin B_1. Moreover, I also introduce an available report which suggested that a non-toxic vitamin B_1 derivative with a benzoyl group may be converted into a toxic compound, O-benzoylthiamin, in animal body.View full abstractDownload PDF (588K) -
Kazuto Nosaka, Hiroyoshi EsakiArticle type: Article
2012 Volume 86 Issue 11 Pages 647-649
Published: November 25, 2012
Released on J-STAGE: October 10, 2017
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[in Japanese]Article type: Article
2012 Volume 86 Issue 11 Pages 650-651
Published: November 25, 2012
Released on J-STAGE: October 10, 2017
JOURNAL FREE ACCESSDownload PDF (318K) -
[in Japanese]Article type: Article
2012 Volume 86 Issue 11 Pages 651-
Published: November 25, 2012
Released on J-STAGE: October 10, 2017
JOURNAL FREE ACCESSDownload PDF (194K) -
[in Japanese], [in Japanese], [in Japanese], [in Japanese], [in Japane ...Article type: Article
2012 Volume 86 Issue 11 Pages 651-652
Published: November 25, 2012
Released on J-STAGE: October 10, 2017
JOURNAL FREE ACCESSDownload PDF (341K) -
[in Japanese]Article type: Article
2012 Volume 86 Issue 11 Pages 652-653
Published: November 25, 2012
Released on J-STAGE: October 10, 2017
JOURNAL FREE ACCESSDownload PDF (348K) -
[in Japanese], [in Japanese], [in Japanese], [in Japanese], [in Japane ...Article type: Article
2012 Volume 86 Issue 11 Pages 653-654
Published: November 25, 2012
Released on J-STAGE: October 10, 2017
JOURNAL FREE ACCESSDownload PDF (337K) -
[in Japanese], [in Japanese], [in Japanese], [in Japanese], [in Japane ...Article type: Article
2012 Volume 86 Issue 11 Pages 654-655
Published: November 25, 2012
Released on J-STAGE: October 10, 2017
JOURNAL FREE ACCESSDownload PDF (329K) -
[in Japanese], [in Japanese], [in Japanese], [in Japanese], [in Japane ...Article type: Article
2012 Volume 86 Issue 11 Pages 655-
Published: November 25, 2012
Released on J-STAGE: October 10, 2017
JOURNAL FREE ACCESSDownload PDF (190K) -
[in Japanese], [in Japanese], Ardiansyah, [in Japanese], [in Japanese ...Article type: Article
2012 Volume 86 Issue 11 Pages 655-656
Published: November 25, 2012
Released on J-STAGE: October 10, 2017
JOURNAL FREE ACCESSDownload PDF (330K) -
[in Japanese]Article type: Article
2012 Volume 86 Issue 11 Pages 656-657
Published: November 25, 2012
Released on J-STAGE: October 10, 2017
JOURNAL FREE ACCESSDownload PDF (346K) -
[in Japanese], [in Japanese], [in Japanese], [in Japanese], [in Japane ...Article type: Article
2012 Volume 86 Issue 11 Pages 657-658
Published: November 25, 2012
Released on J-STAGE: October 10, 2017
JOURNAL FREE ACCESSDownload PDF (331K) -
[in Japanese], [in Japanese], [in Japanese]Article type: Article
2012 Volume 86 Issue 11 Pages 658-
Published: November 25, 2012
Released on J-STAGE: October 10, 2017
JOURNAL FREE ACCESSDownload PDF (172K)
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