• Archives of Pharmacal Research
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• v.3 no.1
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• pp.51-55
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• 1980

Thiamine, in the form of its diphosphate (TDP), is well known to act as a coenzyme, and during the early stage in the study of thiamine it had been believed that the symptoms of thiamine-deficiency were resulted secondarily from the disturbance of metabolic processes in which TDP participated as a coenzyme. However, the neurological symptoms in thiamine deficiency are now separated from the metabolic disturbances in thiamine deficiency. On the other hand, the specific involvement of phosphorylated thiamine in nerve conduction has been suggested by von Muralt, but nature of this involvement has not been elucidated at a molecular level. Recently the possible significance of thiamine triphosphate (TTP) in nervous tissue was suggested by the demonstration that TTP is not present in the brain of patients with subacute necrotizing encephalomyelitis, a fatal disease associated with an abnormality in thiamine metabolism. Furthermore, the studies using membrane fragments of rat brain strongly indicated that ion movement across the nerve membrane is associated with dephosphorylation of phosphorylated thiamine.

• The Korean Journal of Food & Health Convergence
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• v.5 no.6
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• pp.1-4
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• 2019

Wernicke korsakoff syndrome is caused by thiamine deficiency in the body. Thiamine not available in the body, is a substance to be taken from outside with foods. There are some conditions that reduce the metabolism of thiamine taken from the body and cause a vital risk. The most important factor is alcoholism. Wernicke Korsakoff syndrome produces both neurological and vestibular symptoms. At the same time, the damage of these symptoms to the patient psychology cannot be ignored. The aim of this study is to investigate the damage and mechanism of the syndrome in the vestibular system. In this study, we investigated vestibular symptoms of Wernicke Korsakoff syndrome due to thiamine deficiency, differences of vestibular system according to individuals and mechanism of damage caused by syndrome in vestibular system. Thiamine deficiency is caused by Wernicke Karsokoff syndrome with some external factors. This syndrome shows the most important effects of alcoholism. It causes neurological, vestibular and psychological symptoms. In this context, we can say that thiamine deficiency is a disease that causes damage in the vestibular system due to nystagmus formation and imbalance. The most important detail in the treatment stage is the detailed evaluation of symptoms associated with each other.

• Journal of Audiology & Otology
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• v.25 no.1
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• pp.55-58
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• 2021

Sensorineural hearing loss (SNHL) is seldom associated with Wernicke encephalopathy (WE) or thiamine deficiency. While thiamine deficiency and repletion are often considered prior to dextrose infusions in patients with chronic alcohol abuse to prevent WE, they are often overlooked in non-alcoholic patients who are also at risk for malnutrition. In this paper we describe a case of a non-alcoholic 28-year-old female status post-sleeve gastrectomy who developed SNHL in the setting of thiamine deficiency and WE, with ongoing hearing impairment requiring hearing aids despite thiamine repletion.

• Korean Journal of Audiology
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• v.25 no.1
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• pp.55-58
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• 2021

Sensorineural hearing loss (SNHL) is seldom associated with Wernicke encephalopathy (WE) or thiamine deficiency. While thiamine deficiency and repletion are often considered prior to dextrose infusions in patients with chronic alcohol abuse to prevent WE, they are often overlooked in non-alcoholic patients who are also at risk for malnutrition. In this paper we describe a case of a non-alcoholic 28-year-old female status post-sleeve gastrectomy who developed SNHL in the setting of thiamine deficiency and WE, with ongoing hearing impairment requiring hearing aids despite thiamine repletion.

• Journal of Yeungnam Medical Science
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• v.31 no.1
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• pp.38-42
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• 2014

Cardiovascular beriberi is caused by thiamine deficiency and usually presents as high cardiac output failure associated with predominantly right-sided heart failure and rapid recovery after treatment with thiamine. Because of its rarity in developed countries, the diagnosis can often be delayed and missed. We recently experienced a case of cardiovascular beriberi with pulmonary hypertension which successfully treated with thiamine infusion. A 50-year-old man with chronic heavy alcoholics was refered to our department for dyspnea with mental change. Echocardiography showed marked right ventricular (RV) dilatation and flattening of the interventricular septum with a D-shaped deformation of the left ventricle. Moderate tricuspid valve regurgitation was found and estimated RV systolic pressure was 52 mm Hg. Because of his confused mentality and history of chronic alcohol intake, neurological disorder due to thiamine deficiency was suspected and intravenous thiamine was administered and he continuously received a daily dose of 100 mg of thiamine. Follow up echocardiography showed marked reduction of RV dilatation and improvement of a D-shaped deformation of the left ventricle. He finally diagnosed as cardiovascular beriberi on the basis of dramatic response to intravenous thiamine. Thiamine deficiency can cause reversible pulmonary hypertension, and can still be encountered in the clinical setting. Thus high index of suspicion is critically needed for diagnosis.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.22 no.5
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• pp.493-499
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• 2019

Thiamine (vitamin $B_1$) is a water-soluble vitamin that is not endogenously synthesized in humans. It is absorbed by the small intestine, where it is activated. Its active form acts as a coenzyme in many energy pathways. We report a rare case of thiamine deficiency in a 3.5-year old boy with short bowel syndrome secondary to extensive bowel resection due to necrotizing enterocolitis during his neonatal age. The patient was parenteral nutrition-dependent since birth and had suffered from recurrent central catheter-related bloodstream infections. He developed confusion with disorientation and unsteady gait as well as profound strabismus due to bilateral paresis of the abductor muscle. Based on these and a very low thiamine level he was diagnosed and treated for Wernicke encephalopathy due to incomplete thiamine acquisition despite adequate administration. He fully recovered after thiamine administration. After 1999 eight more cases have been reported in the PubMed mostly of iatrogenic origin.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1995.04a
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• pp.96-96
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• 1995

It was recognized that lead intoxication reduces thiamine content in the brain of rat and this change produces the alterations of thiamine-related biochemical reactions. In the present study, it was tested whether the changes of myelin composition as well as seizure threshold induced by lead intoxication in rats may be related to these changes of thiamine status and thiamine related biochemical factors. Wistar rats were divided into five groups: Control group, Lead-treated group, Lead plus Thiamine-treated group, Thiamine-deficient group, Pyrithiamine-treated group. Each group was divided into three subgroups: 3, 7 and 16 week old group. Myelin protein and phospholipid, one of the compositions of myelin lipid, were measured in the myelin isolated from rat brain. Threshold of electric shock seizure was tested in each group. The amount of each myelin composition in lead-treated group and thiamine-deficient group was significantly lower than those of all the brains in control group, but recovery by supplementation with thiamine during lead intoxication was occurred only in the cerebellum of 3 week old animal. Thresholds of the electric shock seizure of lead treated group and thiamine deficient group in 3 and 7 week old rats were significantly lower than those of control group, while those of lead plus thiamine treated group were similar to those of control group.

• Annals of Clinical Neurophysiology
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• v.16 no.1
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• pp.27-31
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• 2014

Thiamine deficiency can cause peripheral polyneuropathy and Wernicke's encephalopathy. Wernicke's encephalopathy is characterized by ataxia, ophthalmoplegia, nystagmus, and confusion, and typically presents acute and rapidly progressive course, whereas peripheral neuropathy associated with thiamine deficiency manifests chronic and slowly progressive one. However, acute and rapidly progressive axonal polyneuropathy combined with Wernicke's encephalopathy is quite rare and unusual. Here, we describe a patient with Wernicke's encephalopathy who presented with acute bilateral axonal neuropathy.

• Proceedings of the Korean Society of Veterinary Clinics Conference
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• 2009.04a
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• pp.232-232
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• 2009

• Proceedings of the Korean Society of Applied Pharmacology
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• 1995.10a
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• pp.137-146
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• 1995

In this study, it was tested whether lead intoxication could change thiamine content and the thiamine related biochemical factor such as activity of transketolase in the brain, and whether the changes of the myelin composition :s well as the seizure threshold induced by lead intoxication in rats be related to these changes of thiamine status and thiamine related biochemical factors. In addition, it was also tested whether administration of excessive thiamine can reverse the toxic manifestation of lead in lead intoxicated animals. Five groups of Wistar rats were prepared: 1)Control group, 2)lead treated group, 3)thiamine treated group, 4)lead plus thiamine treated group and 5)thiamine deficiency group. Each group of animals was divided into three subgroups based on ages: 3, 7 and 10 weeks of age subgroups. Lead concentration, thiamine content, the activity of transketolase and myelin composition in brain areas and threshold of electric shock seizure were tested in each group. Lead concentrations in all brain regions of lead treated group were higher than those of control group, and those of lead plus thiamine treated group were significantly lower than those of lead treated group. Thiamine contents in the brain regions of lead treated group were significantly lower than those of control group, and those of lead plus thiamine treated group were recovered back to those of control group. Activities of transketolase of lead treated group were significantly lower than those of control group, while those of lead plus thiamine treated group were recovered back to those of control group. The cases of which was observed with the concomitant changes of thiamine content and transketolase activity in myelin content or constituent of all the brain regions tested were total amount of myelin protein in the cerebellum of 3 week old rats, and phospholipid in the cerebellum of 3 week old rats and the telencephalon of 16 week old rats. Thresholds of the electroshock seizure of lead-treated group and thiamine-deficient group in 3, 7 week old rats were significantly lower than those of control group, while those of the lead plus thiamine-treated group were similar to those of control group. Changes of the electroshock seizure threshold induced by lead intoxication were observed in 3 week and 7 week old animals with the concomitant decrement of thiamine content in all the brain regions tested. These observations were reversed by the supplementation with thiamine to those animals. However, the changes of seizure threshold induced by lead intoxication corelated with the changes of thiamine contents as well as. transketolase due to lead intoxication. The changes of myelin phospholipid as one of myelin composition and those of myelin Protein content only in the cerebellum of 3 week old rats correlated with the changes of the seizure threshold as well as thiamine content due to lead intoxication. The results from the present study may indicate that neurotoxicity of lead in rats may be mediated at least in part through the changes of thiamine status. Such changes of thiamine status may induce the changes of myelin composition such as myelin phospholipid and those of myelin protein content especially in the cerebellum of 3 week old rats which may eventually affect the threshold of seizure.