Journal articles: 'Thiamine deficiency'

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Pan, Xiaohua, Xuemei Nan, Liang Yang, Linshu Jiang, and Benhai Xiong. "Thiamine status, metabolism and application in dairy cows: a review." British Journal of Nutrition 120, no. 5 (July 10, 2018): 491–99. http://dx.doi.org/10.1017/s0007114518001666.

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AbstractAs the co-enzyme of pyruvate dehydrogenase andα-ketoglutarate dehydrogenase, thiamine plays a critical role in carbohydrate metabolism in dairy cows. Apart from feedstuff, microbial thiamine synthesis in the rumen is the main source for dairy cows. However, the amount of ruminal thiamine synthesis, which is influenced by dietary N levels and forage to concentrate ratio, varies greatly. Notably, when dairy cows are overfed high-grain diets, subacute ruminal acidosis (SARA) occurs and results in thiamine deficiency. Thiamine deficiency is characterised by decreased ruminal and blood thiamine concentrations and an increased blood thiamine pyrophosphate effect to >45 %. Thiamine deficiency caused by SARA is mainly related to the increased thiamine requirement during high grain feeding, decreased bacterial thiamine synthesis in the rumen, increased thiamine degradation by thiaminase, and decreased thiamine absorption by transporters. Interestingly, thiamine deficiency can be reversed by exogenous thiamine supplementation in the diet. Besides, thiamine supplementation has beneficial effects in dairy cows, such as increased milk and component production and attenuated SARA by improving rumen fermentation, balancing bacterial community and alleviating inflammatory response in the ruminal epithelium. However, there is no conclusive dietary thiamine recommendation for dairy cows, and the impacts of thiamine supplementation on protozoa, solid-attached bacteria, rumen wall-adherent bacteria and nutrient metabolism in dairy cows are still unclear. This knowledge is critical to understand thiamine status and function in dairy cows. Overall, the present review described the current state of knowledge on thiamine nutrition in dairy cows and the major problems that must be addressed in future research.

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Richter, Catherine A., Allison N. Evans, Maureen K. Wright-Osment, James L. Zajicek, Scott A. Heppell, Stephen C. Riley, Charles C. Krueger, and Donald E. Tillitt. "Paenibacillus thiaminolyticus is not the cause of thiamine deficiency impeding lake trout (Salvelinus namaycush) recruitment in the Great Lakes." Canadian Journal of Fisheries and Aquatic Sciences 69, no. 6 (June 2012): 1056–64. http://dx.doi.org/10.1139/f2012-043.

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Thiamine (vitamin B1) deficiency is a global concern affecting wildlife, livestock, and humans. In Great Lakes salmonines, thiamine deficiency causes embryo mortality and is an impediment to restoration of native lake trout ( Salvelinus namaycush ) stocks. Thiamine deficiency in fish may result from a diet of prey with high levels of thiaminase I. The discoveries that the bacterial species Paenibacillus thiaminolyticus produces thiaminase I, is found in viscera of thiaminase-containing prey fish, and causes mortality when fed to lake trout in the laboratory provided circumstantial evidence implicating P. thiaminolyticus. This study quantified the contribution of P. thiaminolyticus to the total thiaminase I activity in multiple trophic levels of Great Lakes food webs. Unexpectedly, no relationship between thiaminase activity and either the amount of P. thiaminolyticus thiaminase I protein or the abundance of P. thiaminolyticus cells was found. These results demonstrate that P. thiaminolyticus is not the primary source of thiaminase activity affecting Great Lakes salmonines and calls into question the long-standing assumption that P. thiaminolyticus is the source of thiaminase in other wild and domestic animals.

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Skelton, William P., and Nadine K. Skelton. "Thiamine deficiency neuropathy." Postgraduate Medicine 85, no. 8 (June 1989): 301–6. http://dx.doi.org/10.1080/00325481.1989.11700760.

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GOMES, Marleide da Mota, and Marcos Raimundo Gomes de FREITAS. "Probable first report of a motor deafferentation syndrome in the Paraguayan War." Arquivos de Neuro-Psiquiatria 79, no. 6 (June 2021): 554–56. http://dx.doi.org/10.1590/0004-282x-anp-2020-0479.

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ABSTRACT The Paraguayan War ended 150 years ago. Back then, there were outbreaks of combatants’ limb weakness and tingling related to "palustrian cachexia", not clearly funded at the time on nutritional deficiency, the use of native flora to feed troops, and alcoholism. We report a case of a soldier with ascending paralysis, mental confusion and finally tetraplegia with preserved oculomotricity. This would probably be a case of locked-in syndrome (LIS) due to Gayet-Wernicke's encephalopathy consequent to thiamine deficiency. The role of thiamine in the peripheral or central nervous system expression was shown decades later to be related to poor diet, or use of foods containing thiaminase or thiamine antagonists, worsened by the fact that the bodily stores of thiamine are restricted, and deficits may grow fast.

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Lonsdale, Derrick. "A Review of the Biochemistry, Metabolism and Clinical Benefits of Thiamin(e) and Its Derivatives." Evidence-Based Complementary and Alternative Medicine 3, no. 1 (2006): 49–59. http://dx.doi.org/10.1093/ecam/nek009.

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Thiamin(e), also known as vitamin B1, is now known to play a fundamental role in energy metabolism. Its discovery followed from the original early research on the ‘anti-beriberi factor’ found in rice polishings. After its synthesis in 1936, it led to many years of research to find its action in treating beriberi, a lethal scourge known for thousands of years, particularly in cultures dependent on rice as a staple. This paper refers to the previously described symptomatology of beriberi, emphasizing that it differs from that in pure, experimentally induced thiamine deficiency in human subjects. Emphasis is placed on some of the more unusual manifestations of thiamine deficiency and its potential role in modern nutrition. Its biochemistry and pathophysiology are discussed and some of the less common conditions associated with thiamine deficiency are reviewed. An understanding of the role of thiamine in modern nutrition is crucial in the rapidly advancing knowledge applicable to Complementary Alternative Medicine. References are given that provide insight into the use of this vitamin in clinical conditions that are not usually associated with nutritional deficiency. The role of allithiamine and its synthetic derivatives is discussed. Thiamine plays a vital role in metabolism of glucose. Thus, emphasis is placed on the fact that ingestion of excessive simple carbohydrates automatically increases the need for this vitamin. This is referred to as high calorie malnutrition.

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Bourassa, Megan, and Gilles Bergeron. "Advances from the International Thiamine Alliance." Current Developments in Nutrition 4, Supplement_2 (May 29, 2020): 814. http://dx.doi.org/10.1093/cdn/nzaa053_019.

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Abstract Objectives Thiamine deficiency disorders, including beriberi, remain a pressing public health problem. Without rapid recognition of symptoms and treatment, it is often fatal, especially in infants, and can have lasting neurological effects for survivors. Thus our objective is to create an alliance of country representatives, public health professionals, physicians and researchers who can quantify the prevalence of thiamine deficiency disorders globally and create control and prevention strategies. Methods The first meeting of this international thiamine alliance was held in November 2019 to discuss the prevalence of thiamine deficiency disorders and devise strategies to improve thiamine status in at-risk populations. Results This alliance creates the first community of practice for thiamine deficiency. As a result of this meeting and recent data, there is growing recognition that thiamine deficiency is not localized to small areas within Southeast Asia, but covers a much broader area to include much of South and Central Asia, including areas of Kashmir and Assam in India and Bhutan. Challenges in diagnosing thiamine deficiency based on symptoms or biomarkers have been major barriers to recognizing thiamine deficiency disorders. Conclusions This group is now working to improve assessments of thiamine deficiency and raising awareness among the public health and medical professionals in areas where the diets are low in thiamine to ensure that its diagnosis is not overlooked. In areas with a known prevalence of thiamine deficiency, efforts are underway to increase dietary intake of thiamine, provide supplements especially to pregnant and lactating women, and fortify foods to improve thiamine status. Funding Sources Bill & Melinda Gates Foundation.

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van Snippenburg, Wouter, Mariet G. J. Reijnders, Jose G. M. Hofhuis, Rien de Vos, Stephan Kamphuis, and Peter E. Spronk. "Thiamine Levels During Intensive Insulin Therapy in Critically Ill Patients." Journal of Intensive Care Medicine 32, no. 9 (July 20, 2016): 559–64. http://dx.doi.org/10.1177/0885066616659429.

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Introduction: Thiamine is an essential cofactor in carbohydrate metabolism, and deficiency can therefore cause various organ dysfunctions. Little is known about the prevalence and possible worsening of thiamine deficiency in critically ill patients. In this study, we investigated the prevalence of thiamine deficiency at admission to the intensive care unit (ICU) and hypothesized that intensive insulin therapy, aimed at regulating glucose levels, increases thiamine utilization and therefore might cause or worsen deficiency in patients with limited thiamine stores. Materials and Methods: An observational prospective cohort study was carried out in a medical–surgical ICU in a general teaching hospital in Apeldoorn, the Netherlands. All adults who were treated during that time with intensive insulin therapy were included. Deficiency was defined as a thiamine level <100 nmol/L. No thiamine supplementation was administered except for normal amounts present in standard enteral feeding. Results: A total of 58 patients were available for analysis. Median thiamine level at admission was 111 nmol/L. Deficiency was present in 39.7% of patients and was significantly associated with the presence of gastrointestinal pathology and with recent surgery. Thiamine levels increased a median of 14 nmol/L in 48 hours. Only 3.4% of patients showed a predefined relevant decline in thiamine levels. Conclusion: Intensive insulin therapy does not appear to cause or worsen thiamine deficiency. However, based on the high prevalence of deficiency at admission, it might be warranted to supplement thiamine in all patients admitted to the ICU, especially when there is an underlying gastrointestinal disease or recent surgery.

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Sweet, Rebecca L., and Jason A. Zastre. "HIF1-α-Mediated Gene Expression Induced by Vitamin B1 Deficiency." International Journal for Vitamin and Nutrition Research 83, no. 3 (June 1, 2013): 188–97. http://dx.doi.org/10.1024/0300-9831/a000159.

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It is well established that thiamine deficiency results in an excess of metabolic intermediates such as lactate and pyruvate, which is likely due to insufficient levels of cofactor for the function of thiamine-dependent enzymes. When in excess, both pyruvate and lactate can increase the stabilization of the hypoxia-inducible factor 1-alpha (HIF-1α) transcription factor, resulting in the trans-activation of HIF-1α regulated genes independent of low oxygen, termed pseudo-hypoxia. Therefore, the resulting dysfunction in cellular metabolism and accumulation of pyruvate and lactate during thiamine deficiency may facilitate a pseudo-hypoxic state. In order to investigate the possibility of a transcriptional relationship between hypoxia and thiamine deficiency, we measured alterations in metabolic intermediates, HIF-1α stabilization, and gene expression. We found an increase in intracellular pyruvate and extracellular lactate levels after thiamine deficiency exposure to the neuroblastoma cell line SK-N-BE. Similar to cells exposed to hypoxia, there was a corresponding increase in HIF-1α stabilization and activation of target gene expression during thiamine deficiency, including glucose transporter-1 (GLUT1), vascular endothelial growth factor (VEGF), and aldolase A. Both hypoxia and thiamine deficiency exposure resulted in an increase in the expression of the thiamine transporter SLC19A3. These results indicate thiamine deficiency induces HIF-1α-mediated gene expression similar to that observed in hypoxic stress, and may provide evidence for a central transcriptional response associated with the clinical manifestations of thiamine deficiency.

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Mohamed, Ragaa Abd-Elsalam, Ibrahim Mohamed Abu Farag, Marwa Elhady, and Radwa Saeed Ibrahim. "Myocardial dysfunction in relation to serum thiamine levels in children with diabetic ketoacidosis." Journal of Pediatric Endocrinology and Metabolism 32, no. 4 (April 24, 2019): 335–40. http://dx.doi.org/10.1515/jpem-2018-0320.

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Abstract Background Thiamine deficiency is commonly reported in patients with diabetes especially during diabetic ketoacidosis (DKA) that could attribute to myocardial dysfunction in those patients. However, there is limited data regarding its relation to myocardial function among those patients. This study aimed to explore the association between myocardial function and serum thiamine levels in children with type 1 diabetes mellitus (DM). Methods This cross-sectional comparative study included 25 patients with DKA. Clinical data assessment, echocardiographic examination and measurement of serum high-sensitive troponin T (hs-cTnT) and thiamine levels were done. We also assessed the association between troponin levels, echocardiographic ventricular systolic and diastolic function and serum thiamine. Results Twenty-four percent of children with DKA had thiamine deficiency. DKA children with thiamine deficiency had significant acidosis and higher serum troponin levels and significant impairment of diastolic function than those without thiamine deficiency. The serum thiamine level had a significant positive correlation with the echocardiographic indices of diastolic function but negative correlation with troponin levels. Conclusions Thiamine deficiency is a common finding during the treatment of children with DKA, and this deficiency may be associated with myocardial dysfunction.

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Buranasakda, Marturod, and Ratrawee Pattanarattanamolee. "Thiamine Level in Out-of-hospital Cardiac Arrest Patients." Open Access Macedonian Journal of Medical Sciences 10, B (April 2, 2022): 1037–41. http://dx.doi.org/10.3889/oamjms.2022.8015.

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BACKGROUND: Thiamine deficiency is more common in critically ill patients. Administration of thiamine in cardiac arrest mice has improved survival and neurological outcomes. Evidence for thiamine deficiency in cardiac arrest humans is insufficient to support routine use of thiamine in cardiac arrest patients. AIM: This study aimed to determine thiamine blood levels in cardiac arrest patients to understand whether the presence of thiamine deficiency is common in cardiac arrest patients. METHODS: A prospective descriptive study from April 2017 to March 2018, on 24 adult out-of-hospital cardiac arrest patients. We used the high-performance liquid chromatography technique to determine whole blood thiamine pyrophosphate levels in cardiac arrest patients who arrived at the emergency department within 1 h of the onset of a cardiac arrest. RESULTS: The mean thiamine pyrophosphate level within 1 h of the onset of a cardiac arrest was 170.9 ± 56.7 nmol/L. Only one participant had thiamine deficiency according to the cut-off level for thiamine pyrophosphate in whole blood of <70 nmol/L. Fourteen patients had spontaneous return of circulation. Thiamine pyrophosphate levels were not different between the two groups of patients who had and did not have the return of spontaneous circulation at the emergency department. CONCLUSION: Little evidence was found to support thiamine deficiency as a feature among our cardiac arrest patients. A study with a larger population is required for more meaningful statistical analysis. As there is no consensus on cut-off level for thiamine deficiency diagnosis, the level of thiamine pyrophosphate in specific populations should be evaluated to establish reference values.

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Millichap, J. Gordon, and John J. Millichap. "Thiamine Deficiency in Infancy." Pediatric Neurology Briefs 28, no. 10 (October 1, 2014): 76. http://dx.doi.org/10.15844/pedneurbriefs-28-10-4.

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Holz, Peter H., James R. Phelan, and Ron Slocombe. "Thiamine Deficiency in Honeyeaters." Journal of Avian Medicine and Surgery 16, no. 1 (March 2002): 21–25. http://dx.doi.org/10.1647/1082-6742(2002)016[0021:tdih]2.0.co;2.

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Suzuki, Takahiro. "Treatable Dementia: Thiamine Deficiency." Journal of Nihon University Medical Association 77, no. 5 (October 1, 2018): 309–12. http://dx.doi.org/10.4264/numa.77.5_309.

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Pritchard, Peter. "Thiamine deficiency in cats." Veterinary Record 180, no. 10 (March 10, 2017): 256.4–257. http://dx.doi.org/10.1136/vr.j1202.

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Keyset, A., and B. de Bruijn. "Thiamine deficiency and epilepsy." Clinical Neurology and Neurosurgery 90, no. 3 (January 1988): 303. http://dx.doi.org/10.1016/0303-8467(88)90083-2.

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Butterworth, RogerF, Christiane Gaudreau, Jean Vincelette, Anne-Marie Bourgault, François Lamothe, and Anne-Marie Nutini. "Thiamine deficiency in AIDS." Lancet 338, no. 8774 (October 1991): 1086. http://dx.doi.org/10.1016/0140-6736(91)91948-t.

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Reed, Aimee N., Freya E. Rowland, Jennifer A. Krajcik, and Donald E. Tillitt. "Thiamine Supplementation Improves Survival and Body Condition of Hatchery-Reared Steelhead (Oncorhynchus mykiss) in Oregon." Veterinary Sciences 10, no. 2 (February 14, 2023): 156. http://dx.doi.org/10.3390/vetsci10020156.

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Early rearing of steelhead (Oncorhynchus mykiss) in Oregon hatcheries is often problematic; fry can become emaciated and die during the period between hatch and first feed. Thiamine (vitamin B1) deficiency has caused early mortality in salmonids; however, the thiamine status of Oregon’s steelhead populations is unknown, to date. Of the 26 egg samples from three Oregon hatcheries in 2019, 20 (77%) had thiamine levels < 10 nmol/g, and 13 of those samples (50%) had levels <6.5 nmol/g, suggesting the thiamine deficiency of adult, female steelhead. To investigate if thiamine deficiency was causally related to fry survival, females were injected with buffered thiamine HCl 50 mg/kg prior to spawning; additionally, a subset of eggs were supplemented via bath treatment with thiamine mononitrate (1000 ppm) at spawning. Cumulative fry mortality at 8 weeks post-hatch from thiamine-injected females was 2.9% compared to 13.8% mortality of fry without thiamine supplementation. Fry treated only with the thiamine via bath as eggs had a mortality rate of 6.9%. There were no additional improvements for the survival of fry from injected females that also received a thiamine bath. Furthermore, condition factors were greater in thiamine-supplemented fry than in those that received no thiamine. These data identify thiamine deficiency in Oregon steelhead and suggest supplementation with thiamine can mitigate early rearing mortality.

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Pacei, Federico, Antonella Tesone, Nazzareno Laudi, Emanuele Laudi, Anna Cretti, Shira Pnini, Fabio Varesco, and Chiara Colombo. "The Relevance of Thiamine Evaluation in a Practical Setting." Nutrients 12, no. 9 (September 13, 2020): 2810. http://dx.doi.org/10.3390/nu12092810.

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Thiamine is a crucial cofactor involved in the maintenance of carbohydrate metabolism and participates in multiple cellular metabolic processes. Although thiamine can be obtained from various food sources, some common food groups are deficient in thiamine, and it can be denatured by high temperature and pH. Additionally, different drugs can alter thiamine metabolism. In addition, the half-life of thiamine in the body is between 1 and 3 weeks. All these factors could provide an explanation for the relatively short period needed to develop thiamine deficiency and observe the consequent clinical symptoms. Thiamine deficiency could lead to neurological and cardiological problems. These clinical conditions could be severe or even fatal. Marginal deficiency too may promote weaker symptoms that might be overlooked. Patients undergoing upper gastrointestinal or pancreatic surgery could have or develop thiamine deficiency for many different reasons. To achieve the best outcome for these patients, we strongly recommend the execution of both an adequate preoperative nutritional assessment, which includes thiamine evaluation, and a close nutritional follow up to avoid a nutrient deficit in the postoperative period.

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Kloss, Olena, N. A. Michael Eskin, and Miyoung Suh. "Thiamin deficiency on fetal brain development with and without prenatal alcohol exposure." Biochemistry and Cell Biology 96, no. 2 (April 2018): 169–77. http://dx.doi.org/10.1139/bcb-2017-0082.

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Adequate thiamin levels are crucial for optimal health through maintenance of homeostasis and viability of metabolic enzymes, which require thiamine as a co-factor. Thiamin deficiency occurs during pregnancy when the dietary intake is inadequate or excessive alcohol is consumed. Thiamin deficiency leads to brain dysfunction because thiamin is involved in the synthesis of myelin and neurotransmitters (e.g., acetylcholine, γ-aminobutyric acid, glutamate), and its deficiency increases oxidative stress by decreasing the production of reducing agents. Thiamin deficiency also leads to neural membrane dysfunction, because thiamin is a structural component of mitochondrial and synaptosomal membranes. Similarly, in-utero exposure to alcohol leads to fetal brain dysfunction, resulting in negative effects such as fetal alcohol spectrum disorder (FASD). Thiamin deficiency and prenatal exposure to alcohol could act synergistically to produce negative effects on fetal development; however, this area of research is currently under-studied. This minireview summarizes the evidence for the potential role of thiamin deficiency in fetal brain development, with or without prenatal exposure to alcohol. Such evidence may influence the development of new nutritional strategies for preventing or mitigating the symptoms of FASD.

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Iimura, Yohei, Shohei Andoh, Toyotaka Kawamata, Aki Sato, Kazuaki Yokoyama, Yoichi Imai, Arinobu Tojo, Masanori Nojima, Munetoshi Sugiura, and Seiichiro Kuroda. "Thiamine Deficiency and Neurological Symptoms in Patients with Hematological Cancer Receiving Chemotherapy: A Retrospective Analysis." Journal of Neurosciences in Rural Practice 12, no. 04 (September 28, 2021): 726–32. http://dx.doi.org/10.1055/s-0041-1735825.

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Abstract Objectives Patients with hematological cancer receiving chemotherapy have a high risk of thiamine deficiency due to accelerated thiamine usage by tumor cells. Mild or severe thiamine deficiency can lead to varying degrees of neurological symptoms. We evaluated the relationship between thiamine deficiency and neurological symptoms, including mild or nonspecific symptoms, and the influence of chemotherapy on thiamine serum levels in patients with hematological cancer receiving chemotherapy. Materials and Methods We retrospectively identified 42 patients diagnosed with hematological cancer at our hospital, using electronic medical records collected from March 2019 to March 2020. We evaluated the risk factors associated with neurological symptoms (mild-to-severe cognitive impairment, attention impairment, and mood or emotional disorder), the relationship between the presence of neurological symptoms and thiamine serum levels, and changes in thiamine serum levels after chemotherapy. Results Thiamine deficiency was significantly associated with neurological symptoms. The thiamine serum levels in the group with neurological symptoms were significantly lower than those in the group without neurological symptoms. The Wilcoxon rank-sum test showed that thiamine serum levels after chemotherapy were significantly lower than those before administration of chemotherapy. Conclusion Thiamine serum levels in patients with hematological cancer may be used as a reference to maintain neurological status during chemotherapy.

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Hassan, Mahmuda, Hamidur Rahman, BH Nazma Yasmeen, Afsana Mukti, Hakimul Haque, Masuma Khan, Marium Begum, et al. "Thiamine deficiency - Beriberi – A forgotten disease." Northern International Medical College Journal 10, no. 1 (December 20, 2018): 351–54. http://dx.doi.org/10.3329/nimcj.v10i1.39331.

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Thiamine (vitamin B1) was the first B vitamin which has been identified. It serves as a cofactor for several enzymes involved in energy metabolism. The thiamine-dependent enzymes are important for the biosynthesis of neurotransmitters and for the production of reducing substances used in oxidant stress defenses, as well as for the synthesis of pentose used as nucleic acid precursors. Thiamine also plays a central role in cerebral metabolism. There are 2 major manifestations of thiamine deficiency(TD): cardiovascular disease (wet beriberi) and nervous system disease (dry beriberi and Wernicke–Korsakoff syndrome). In wet beriberi, cardiomyopathy with edema and lactic acidosis and in dry beriberi, peripheral neuropathy occurs. Manifestations of Wernicke–Korsakoff syndrome, consist of nystagmus, ophthalmoplegia and ataxia evolving into confusion, retrograde amnesia, cognitive impairment and confabulation. Thiamine deficiency is now very rare in developed countries, but still common in South East Asia specially in developing countries like Bangladesh. It is an important public health problem with potentially fatal consequences. Now a days highly polished rice (Minicut rice) is a popular staple food and other primary dietary sources of thiamine are in short supply. In wet beriberi myocardial disease is prominent which causes a high cardiac output with peripheral vasodilation and warm extremities. Before heart failure, tachycardia, a wide pulse pressure, sweating, warm skin and lactic acidosis develop leading to salt and water retention by the kidneys. The resulting fluid overload leads to edema of the dependent extremities. If it is left untreated the severity of potential outcome will be increased even up to death. Therefore, makes it essential for physician, cardiologists and Paediatrician to have an understanding of this condition and its optimal treatment. Patients on a strict thiamine-deficient diet display a state of severe depletion within 18 days. The most common cause of thiamine deficiency in affluent countries is either alcoholism or malnutrition in nonalcoholic patients especially in children. Treatment by thiamine supplementation is beneficial for diagnostic and therapeutic purposes. Northern International Medical College Journal Vol.10(1) Jul 2018: 351-354

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Zhao, Yanling, Yiying Wu, Haolu Hu, Jinghui Cai, Min Ning, Xiushi Ni, and Chunjiu Zhong. "Downregulation of Transketolase Activity Is Related to Inhibition of Hippocampal Progenitor Cell Proliferation Induced by Thiamine Deficiency." BioMed Research International 2014 (2014): 1–9. http://dx.doi.org/10.1155/2014/572915.

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In animal experiments, hippocampal neurogenesis and the activity of thiamine-dependent transketolase decrease markedly under conditions of thiamine deficiency. To further investigate the effect of thiamine deficiency on the proliferation of hippocampal progenitor cells (HPCs) and the potential mechanisms involved in this effect, we cultured HPCs in vitro in the absence of thiamine and found that proliferation and transketolase activity were both significantly repressed. Furthermore, specific inhibition of transketolase activity by oxythiamine strongly inhibited HPC proliferation in a dose-dependent manner. However, thiamine deficiency itself inhibited the proliferation to a greater degree than did oxythiamine. Taken together, our results suggest that modulation of transketolase activity might be one of the mechanisms by which thiamine regulates the proliferation of hippocampal progenitor cells.

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Todurov, I. M., O. O. Kalashnikov, O. V. Perekhrestenko, S. V. Kosiukhno, G. C. Chervyts, and O. I. O. I. Mytsak. "Thiamine deficiency after sleeve gastrectomy." Clinical Endocrinology and Endocrine Surgery, no. 2 (October 8, 2021): 52–59. http://dx.doi.org/10.30978/cees-2021-2-52.

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The prevalence of morbid obesity has risen to global epidemic proportions. Bariatric surgery has been proven to be a safe and effective treatment for obesity with weight reduction, resolution of obesity-related co-morbidities, improved quality of life and an increased life expectancy. Sleeve gastrectomy (SG) is the most commonly performed bariatric procedure worldwide. Obesity is associated with micronutrient deficiencies that results in the high prevalence of deficient vitamins status prior to bariatric surgery. After bariatric surgery, these micronutrient and vitamins deficiencies increase or occur de novo, and they may be threatening when left unattended. This presented clinical case demonstrates the clinical features of thiamine deficiency as well as the principles of laboratory and instrumental diagnostics. Electromyography is an informative method for diagnostic of muscle weakness. The lower serum thiamine level, neurological symptoms and electromyography results are the most important for the diagnosis of thiamine deficiency. Pathogenetic treatment can improve the patient’s condition in a short period of time. Although the SG is a purely restrictive procedure with no malabsorptive component, microelement or vitamin deficiency can occur in patients after procedure. The presented clinical case demonstrates the importance of timely thorough diagnosis and correct treatment of thiamine deficiency in patients after SG. Thus, patients after the LRS in deficiency of vitamin B1 may cause the development of neurological complications of varying severity, in particular dysmetabolic polyneuropathy. This condition is reversed and administration of an adequate and timely substitution therapy in patients with thiamine insufficiency allows be avoided the development of fatal complications.

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Ton, Angie Nu, Trisha Jethwa, Greta C. Stamper, and Ashley Yenior. "Sensorineural Hearing Loss and Wernicke Encephalopathy: A Case Report and Literature Review." Journal of Audiology and Otology 25, no. 1 (January 10, 2021): 55–58. http://dx.doi.org/10.7874/jao.2020.00045.

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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.

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Ushakova, H. O., O. Z. Brazaluk, and O. Yu Yevstafieva. "THIAMINE DEFICIENCY IN EXTREMELY PREMATURE NEWBORNS." Medical and Clinical Chemistry, no. 2 (July 10, 2019): 18–23. http://dx.doi.org/10.11603/mcch.2410-681x.2019.v.i2.10289.

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Introduction. The critical state of extremely premature newborns is accompanied by significant oxidative stress, which leads to an increase in anaerobic metabolism; impaired oxygen utilization in mitochondrial oxidation may occur due to thiamine deficiency. The aim of the study – to learn the thiamine status of extremely premature new-borns in the neonatal period follow-up. Research Methods. The study involved 55 of premature newborns with birth weight less than 1000 g and 35 healthy full-term newborns. The indicated children’s blood tests were made in the first day of life and at the end of the neonatal period. The lactate and magnesium were determined by colorimetric method; the pyruvate content was determined enzymatically; the concentration of vitamin B1 was studied using a fluorimeter. Results and Discussion. In the first days of life, all premature infants have a significantly lower level of thiamine in the blood than the normal one, with the low limit of the norm of mature infants, due to the greatest intensity of adaptive reactions and the redistribution of nutrients in fasting. The deficiency of thiamine of extremely premature infants is accompanied by hypomagnesemia. The defining factor of thiamine deficiency of premature infants is morphofunctional immaturity. Deficiency of thiamine of premature infants is correlated with hyperlactatemia throughout the neonatal period. The metabolic features of an organism of a newborn with an extremely low birth weight reflect hypoxic disturbances (increased lactate and pyruvate level, changes in their ratio), which indicates the activation of glycolysis. The highest level of pyruvate was observed in premature infants in the first day of life and significantly exceeded the reference values with subsequent decrease during the first month of life, but remained beyond the norm, resulting in the development of secondary acidosis and persistent decrease in aerobic metabolism. Thiamine deficiency contributes to the pathogenesis of suppression of the pyruvate-dehydrogenase complex, bypassing pyruvate towards lactate overproduction and the development of metabolic acidosis. Conclusion. Deficiency of thiamine in premature newborns may lead to a deeper critical condition.

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Shehab-Eldin, Mohamed. "The role of thiamine as a resuscitator in patients with nonalcoholic medical and CNS disorders." Southwest Respiratory and Critical Care Chronicles 5, no. 19 (May 5, 2017): 11. http://dx.doi.org/10.12746/swrccc.v5i19.398.

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Thiamine (vitamin B1), a water-soluble vitamin, is an essential factor in cellular metabolismand fundamental cofactor in important biochemical cycles. Thiamine deficiency is a wellknowncause of neurological and cardiologic disorders, especially in patients with alcoholdependence. Recently, several researchers have studied the role of thiamine deficiency incritically ill patients and the link between thiamine supplementation and changes in lactatelevels in septic shock patients. The role of thiamine in this group of patients is still unclear;however, thiamine supplementation does not cause toxic side effects or increase morbidityor mortality. In this review, we discuss the most common conditions associated with thiaminedeficiency and the limited literature available on thiamine supplementation in critically illpatients.

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Bahat, Hilla, Gad Reisler, Nurit Brandriss, Adina Bar-Chaim, and Michael Goldman. "Thiamine Deficiency in Adolescents with Eating Disorders: A Prospective Cohort Study." Nutrients 12, no. 5 (May 13, 2020): 1396. http://dx.doi.org/10.3390/nu12051396.

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Background: Pediatric eating disorders (PED) patients are prone to nutritional deficiencies. Thiamine deficiency is well described in other malnutrition states but is not routinely screened for in PED. In the current study we evaluated the prevalence of thiamine deficiency among PED patients on their first admission to an outpatient day hospital for eating disorders (DH). Methods: In this prospective cohort study, we measured whole blood thiamine pyrophosphate concentrations (TPP) in addition to a routine laboratory workup in 69 girls on their first admission to DH. Two subgroup analyses were performed: (I) Patients with a previous dietary intervention (“diet” group, n = 30) or naïve-to-treatment patients (“naïve” group, n = 39) and (II) Type of PED: Restrictive (group R, n = 44) or binge-eating/purging (group BP, n = 25). Results: Thiamine deficiency was identified in four girls (6%), all in the “naïve” group. Three of them had BP, and one had R. Patients in the “diet” group had a significantly higher TPP compared to the “naïve” group (55.5 µg/L vs. 46.7 µg/L, p = 0.004). TPP levels returned to normal after two weeks of the treatment program in all deficient patients. Conclusion: Thiamine deficiency was uncommon among PED patients and was easily replenished. Screening for deficiency should be performed among treatment-naïve patients. Keynotes: Whole blood thiamine pyrophosphate concentrations (TPP) are seldom screened for among PED patients. In the current study, we detected thiamine deficiency in only 6% of patients on their first admission to an outpatient day hospital for eating disorders. All deficient patients did not have a recent dietary intervention. We recommend considering screening for thiamine deficiency in treatment-naïve PED patients.

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Venkat, Cuddapah Gaurav, Vallivedu Chennakesavulu Pujitha, Kanchan S. Channawar, and Vadde Vasavi. "Thiamine responsive pulmonary hypertension: case series." International Journal of Contemporary Pediatrics 8, no. 6 (May 25, 2021): 1102. http://dx.doi.org/10.18203/2349-3291.ijcp20212056.

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Pulmonary hypertension (PH) is most commonly related either to a cardiac or a pulmonary cause. But less commonly various hematological, hepatic, genetic causes are also associated. Infantile PH due to vitamin deficiencies is very rare though few cases with thiamine deficiencies causing PH have been reported lately. Lack of awareness and late recognition of thiamine deficiency may result in high mortality. A high index of suspicion is required for early diagnosis and management to decrease the severity and morbidity and thereby preventing long term implications on neurological development. Here, we described three cases of infants admitted to Kamineni academy of medical sciences diagnosed with PH who responded dramatically to thiamine supplements. The lack of rapid diagnostic capacity and the severe outcome of thiamine deficiency justify the use of a therapeutic thiamine challenge in cases with high clinical suspicion. Increased awareness about thiamine deficiency and low threshold for thiamine use should guide clinicians in their practice.

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Hilal Ahmad, Sheikh, S. Bashir Ahmad, and Asma Jan. "Thiamine deficiency related peripheral neuropathy in peripartum women of Kashmir, India: a hospital based study." International Journal of Advances in Medicine 6, no. 3 (May 24, 2019): 662. http://dx.doi.org/10.18203/2349-3933.ijam20191498.

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Background: Beri Beri is still seen in Asian countries due to the large-scale consumption of thiamine depleted polished rice. Thiamine deficiency related disorders are increasingly being reported from Kashmir from last two decades. Specifically, a sensorimotor axonal neuropathy occasionally develops from thiamine deficiency and may occur even without associated Wernicke’s encephalopathy.Methods: This study is a retrospective observational study. All peripartum females referred to our departments from January 2016 to December 2017 with complaints of generalized weakness and or sensory symptoms in form of paresthesias /numbness in limbs were enrolled. Clinical features, electrophysiological features, course in hospital and response to treatment in suspected thiamine deficiency related neuropathy patients were recorded.Results: Forty-three cases were included in the study. Twenty-nine patients were suspected to have nutritional neuropathy because of thiamine deficiency at the time of admission. Out of these 27 showed improvement on treatment with thiamine.Conclusions: Thiamine responsive neuropathy is common in peripartum women of this part of world. Diagnosis is usually made clinically, in at risk individuals presenting with characteristic clinical features.

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Bell, D., C. E. Robertson, and A. L. Muir. "Carbonated Drinks, Thiamine Deficiency and Right Ventricular Failure." Scottish Medical Journal 32, no. 5 (October 1987): 137–38. http://dx.doi.org/10.1177/003693308703200505.

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A 69 year old male presented with clinical features of right ventricular failure. A dilated poorly contracting right ventricle was confirmed by echocardiography and radionuclide ventriculography, with subsequent improvement following thiamine replacement. Wet beriberi is a result of thiamine deficiency and is uncommon in Europe and North America except in association with chronic alcohol abuse. We report a patient with beriberi presenting unusually with severe right-sided cardiac failure, with documented impairment of right ventricular function, which improved with thiamine replacement. His dietary intake of thiamine was low because of excess intake of carbonated drinks and carbohydrates.

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Sharma, Anupama, and Renu Bist. "Alteration in MDA, GSH level and hematological changes due to thiamine deficiency in Mus musculus." Interdisciplinary Toxicology 11, no. 4 (December 1, 2018): 321–25. http://dx.doi.org/10.2478/intox-2018-0032.

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Abstract It is known that thiamine deficiency may lead to Alzheimer’s diseases in humans. The present study has thus been conducted to understand the role of thiamine deficiency with respect to alteration in the peripheral blood of Swiss albino mice. For this purpose, adult Swiss albino mice (6–8 week old) were divided into three groups. The first group was control; the second (group II) and the third group (group III) were made thiamine deficient for 08 and 10 days respectively. Thiamine deficiency was induced in mice by injecting pyrithiamine (5 µg/10 g bwt) and feeding a thiamine deficient diet. The erythrocytes, leukocytes count, hemoglobin, hematocrit value, mass cell volume, mean corpuscular hemoglobin in blood of mice were determined by hematoanalyzer. Malondialdehyde (MDA) and reduced glutathione (GSH) level was also determined in serum of treated and non-treated groups. A significant reduction in leukocyte and erythrocyte count was observed in both the thiamine deficient groups as compared to control. Levels of hemoglobin and hematocrit value were also declined in the thiamine deficient groups. Enhancement in mass cell volume (MCV) level and decline in mean corpuscular hemoglobin (MCH) levels were observed in both thiamine deficient groups with respect to control. Inter-group comparison of all parameters also showed a significant value at p<0.01. In comparison with the control group, elevation in MDA and decline in GSH level was observed in both thiamine deficient groups which were statistically significant. These data indicate that thiamine deficiency leads to significant alterations in the hematological parameters as well as in MDA and GSH level.

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Romanski, Susan A., and M. Molly McMahon. "Metabolic Acidosis and Thiamine Deficiency." Mayo Clinic Proceedings 74, no. 3 (March 1999): 259–63. http://dx.doi.org/10.4065/74.3.259.

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Bateman, Kathleen. "Encephalopathy caused by thiamine deficiency." South African Medical Journal 105, no. 7 (September 21, 2015): 513. http://dx.doi.org/10.7196/samjnew.8022.

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NARISAWA, K., H. ENDO, S. MIYABAYASHI, and K. TADA. "Thiamine Responsive Pyruvate Dehydrogenase Deficiency." Journal of Nutritional Science and Vitaminology 38, Special (1992): 585–88. http://dx.doi.org/10.3177/jnsv.38.special_585.

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Kauffman, Greta, Debra Coats, Somonn Seab, Mark D. Topazian, and Philip R. Fischer. "Thiamine deficiency in ill children." American Journal of Clinical Nutrition 94, no. 2 (August 1, 2011): 616–17. http://dx.doi.org/10.3945/ajcn.111.018457.

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Gans, Dian A. "Biochemical measures of thiamine deficiency." American Journal of Clinical Nutrition 65, no. 4 (April 1, 1997): 1090. http://dx.doi.org/10.1093/ajcn/65.4.1090a.

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Vaamonde, Carlos A. "Thiamine Deficiency and Hepatorenal Syndrome." Nephron 49, no. 3 (1988): 261–63. http://dx.doi.org/10.1159/000185070.

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Wilcox, Christopher S. "Do diuretics cause thiamine deficiency?" Journal of Laboratory and Clinical Medicine 134, no. 3 (September 1999): 192–93. http://dx.doi.org/10.1016/s0022-2143(99)90198-1.

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Eshak, E. S., and A. E. Arafa. "Thiamine deficiency and cardiovascular disorders." Nutrition, Metabolism and Cardiovascular Diseases 28, no. 10 (October 2018): 965–72. http://dx.doi.org/10.1016/j.numecd.2018.06.013.

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Koike, H. "Postgastrectomy polyneuropathy with thiamine deficiency." Journal of Neurology, Neurosurgery & Psychiatry 71, no. 3 (September 1, 2001): 357–62. http://dx.doi.org/10.1136/jnnp.71.3.357.

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Ricci, Zaccaria, and Stefano Romagnoli. "The 11th pitfall: thiamine deficiency." Intensive Care Medicine 44, no. 9 (June 22, 2018): 1597. http://dx.doi.org/10.1007/s00134-018-5271-0.

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Madl, C., A. Kranz, B. Liebisch, O. Traindl, K. Lenz, and W. Druml. "Lactic acidosis in thiamine deficiency." Clinical Nutrition 12, no. 2 (April 1993): 108–11. http://dx.doi.org/10.1016/0261-5614(93)90060-h.

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Kril, Jillian J. "Neuropathology of thiamine deficiency disorders." Metabolic Brain Disease 11, no. 1 (March 1996): 9–17. http://dx.doi.org/10.1007/bf02080928.

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SUZUKI, Shigeaki, Takashi KUMANOMIDO, Eiichiro NAGATA, Jun INOUE, and Osamu NIIKAWA. "Optic Neuropathy from Thiamine Deficiency." Internal Medicine 36, no. 7 (1997): 532. http://dx.doi.org/10.2169/internalmedicine.36.532.

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Lonsdale, D. "Thiamine deficiency and sudden deaths." Lancet 336, no. 8711 (August 1990): 376. http://dx.doi.org/10.1016/0140-6736(90)91918-z.

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46

Gadoth, Natan. "Extarapontine myelinolysis versus thiamine deficiency." Brain and Development 33, no. 8 (September 2011): 700. http://dx.doi.org/10.1016/j.braindev.2010.10.018.

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Misumida, Naoki, Hisashi Umeda, and Mitsunori Iwase. "Shoshin Beriberi Induced by Long-Term Administration of Diuretics: A Case Report." Case Reports in Cardiology 2014 (2014): 1–5. http://dx.doi.org/10.1155/2014/878915.

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Previous studies have suggested that diuretic therapy for heart failure may lead to thiamine deficiency due to the increased urinary thiamine excretion. Herein, we present the case of a 61-year-old man with shoshin beriberi, a fulminant form of wet beriberi, induced by long-term diuretic therapy. The patient had a history of heart failure with preserved ejection fraction and was receiving furosemide and trichlormethiazide therapy. He presented with worsening exertional dyspnea and was admitted for heart failure exacerbation. His condition failed to improve even after intensive treatment. A hemodynamic evaluation with the Swan-Ganz catheter revealed high-output heart failure with low peripheral vascular resistance. Thiamine was administered for suspected shoshin beriberi; his hemodynamic status improved dramatically within the next six hours. The serum thiamine level was below the normal range; the patient was therefore diagnosed with shoshin beriberi. The common causes of thiamine deficiency were not identified. Long-term diuretic therapy with furosemide and thiazide was thought to have played a major role in the development of thiamine deficiency. This case illustrates the importance of considering wet beriberi as a possible cause of heart failure exacerbation in patients taking diuretics, even when the common thiamine deficiency causes are not identified with history-taking.

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Gul-Hinc, Sylwia, Anna Michno, Marlena Zyśk, Andrzej Szutowicz, Agnieszka Jankowska-Kulawy, and Anna Ronowska. "Protection of Cholinergic Neurons against Zinc Toxicity by Glial Cells in Thiamine-Deficient Media." International Journal of Molecular Sciences 22, no. 24 (December 11, 2021): 13337. http://dx.doi.org/10.3390/ijms222413337.

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Brain pathologies evoked by thiamine deficiency can be aggravated by mild zinc excess. Cholinergic neurons are the most susceptible to such cytotoxic signals. Sub-toxic zinc excess aggravates the injury of neuronal SN56 cholinergic cells under mild thiamine deficiency. The excessive cell loss is caused by Zn interference with acetyl-CoA metabolism. The aim of this work was to investigate whether and how astroglial C6 cells alleviated the neurotoxicity of Zn to cultured SN56 cells in thiamine-deficient media. Low Zn concentrations did not affect astroglial C6 and primary glial cell viability in thiamine-deficient conditions. Additionally, parameters of energy metabolism were not significantly changed. Amprolium (a competitive inhibitor of thiamine uptake) augmented thiamine pyrophosphate deficits in cells, while co-treatment with Zn enhanced the toxic effect on acetyl-CoA metabolism. SN56 cholinergic neuronal cells were more susceptible to these combined insults than C6 and primary glial cells, which affected pyruvate dehydrogenase activity and the acetyl-CoA level. A co-culture of SN56 neurons with astroglial cells in thiamine-deficient medium eliminated Zn-evoked neuronal loss. These data indicate that astroglial cells protect neurons against Zn and thiamine deficiency neurotoxicity by preserving the acetyl-CoA level.

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Doyle, Andrew, Michael E. Barnes, Jeremy L. Kientz, and Micheal H. Zehfus. "Landlocked Fall Chinook Salmon Maternal Liver and Egg Thiamine Levels in Relation to Reproductive Characteristics." Open Fish Science Journal 10, no. 1 (June 30, 2017): 23–32. http://dx.doi.org/10.2174/1874401x01710010023.

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Object: Landlocked fall Chinook Salmon Oncorhynchus tshawytscha in Lake Oahe, South Dakota, typically experience poor reproductive success. Introduction: Salmon diets consist of rainbow smelt Osmerus mordax and other potentially thiaminase-containing fish that could impact reproduction. Methods: The thiamine levels of spawning female Salmon, eggs, and reproductive characteristics, were measured in 2000, 2001, 2002, 2003, and 2005. Results: Thiamine concentrations varied significantly from year-to-year, with the highest mean values recorded in 2001 at 8.70 nmol/g in maternal livers and 28.80 nmol/g in eggs. Most of the thiamine in the eggs was present as free thiamine, while most of the thiamine in maternal livers was present as thiamine pyrophosphate. The lowest recorded egg total thiamine level was 2.75 nmol/g in 2000. Egg survival to hatch ranged from 20.7% in 2005 to 35.4% in 2002, and was not correlated to egg thiamine levels. Twenty-two spawns experienced total mortality prior to hatch, and had significantly lower egg free thiamine and total thiamine concentrations than eggs from the 77 successful spawns. The eggs from spawns with total mortality were also significantly smaller than those eggs from spawns that did survive, and were produced by females that weighed significantly less. Several small, but significant, correlations were observed between egg size and egg thiamine levels, and female size and liver thiamine. There was also a significant negative correlation between the number of eggs per spawning female and egg thiamine pyrophosphate, liver thiamine monophosphate, and liver total thiamine levels. Conclusion: In general, Lake Oahe Chinook Salmon eggs show little indication of thiamine deficiency in the years sampled, indicating other factors are likely responsible for poor egg survival.

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Laroussi, S., K. S. Moalla, O. Hdiji, S. Sakka, S. Daoud, H. Hadjkacem, N. Farhat, and C. Mhiri. "Gayet wernicke encephalopathy: Don’t miss this neuropsychiatric emergency!" European Psychiatry 64, S1 (April 2021): S361. http://dx.doi.org/10.1192/j.eurpsy.2021.967.

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IntroductionGayet Wernicke Encephalopathy (GWE) is a diagnostic and therapeutic neuropsychiatric emergency due to thiamin deficiency (vitamin B1).ObjectivesThe purpose of our work is to recall some clinical situations suspecting GWE, along with radiological and evolutionary profile.MethodsWe conducted a retrospective study concerning patients who were hospitalized in the neurology department of Habib Bourguiba Hospital between 2013 and 2020 for management of GWE.ResultsThe median age of 7 patients was 39.57 years with sex ratio (H/F):1.33. The most common risk factor found is incoercible vomiting (5 patients), followed by chronic alcoholism (3 patients). Confusional state was the most frequent symptom found in 4 patients. The characteristic clinical triad of confusion, oculomotor disorders and ataxia was only found in 2 patients. Neuroimaging showed a typical aspect in 3 patients. The serum levels of thiamine were low in five patients and normal in two patients. After receiving parental than oral thiamin supplementation, three patients were independent after one month with a mRS score <3.ConclusionsGWE is an acute neuropsychiatric emergency. Chronic alcoholism is recognized as its most common cause. The clinical triad is not constantly present. MRI shows typically bilateral symmetrical hyperintensities in periaqueductal area, periventricular region, thalami and mammillary bodies. Thiamin level can be normal since it does not accurately represent body thiamine status or in case of mutations in a thiamine-transporter gene. Thiamine therapy is warranted if any component of the GWE triad is present in an appropriate clinical setting to prevent irreversible neurological sequelae.

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Journal articles on the topic 'Thiamine deficiency'

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