Thiamine Levels Research Articles

Shoshin beriberi induced by long-term administration of diuretics: a case report.

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.

Pulmonary Hypertension Associated With Scurvy and Vitamin Deficiencies in an Autistic Child

Restricted dietary intake is common among children with behavioral issues. Here we report a case of a severely autistic child who presented initially with limp but who soon developed cough, tachypnea, hypoxia, and tachycardia. An echocardiogram revealed evidence of pulmonary hypertension (PH) with severely dilated right ventricle and elevated right-sided pressures. The etiology of his PH was unclear but further laboratory evaluation demonstrated severe nutritional deficiencies, in particular an undetectable ascorbic acid (vitamin C) level as well as deficient levels of thiamine (vitamin B1), pyridoxine (vitamin B6), cobalamin (vitamin B12), and vitamin D. Repletion of these vitamins was associated with resolution of his PH and his musculoskeletal complaints. We report this case and a review of the relevant literature as a clinical lesson to expand the differential diagnosis of limp in children who may be difficult to assess as well as to report on an unusual association between severe vitamin deficiencies and PH.

The effects of dietary thiamin on oxidative damage and antioxidant defence of juvenile fish

The present study explored the effects of thiamin on antioxidant capacity of juvenile Jian carp (Cyprinus carpio var. Jian). In a 60-day feeding trial, a total of 1,050 juvenile Jian carp (8.20±0.02g) were fed graded levels of thiamin at 0.25, 0.48, 0.79, 1.06, 1.37, 1.63 and 2.65mg thiamin kg(-1) diets. The results showed that malondialdehyde and protein carbonyl contents in serum, hepatopancreas, intestine and muscle were significantly decreased with increasing dietary thiamin levels (P<0.05). Conversely, the anti-superoxide anion capacity and anti-hydroxyl radical capacity in serum, hepatopancreas, intestine and muscle were the lowest in fish fed the thiamin-unsupplemented diet. Meanwhile, the activities of catalase (CAT), glutathione peroxidase, glutathione S-transferase and glutathione reductase, and the contents of glutathione in serum, hepatopancreas, intestine and muscle were enhanced with increasing dietary thiamin levels (P<0.05). Superoxide dismutase (SOD) activity in serum, hepatopancreas and intestine followed a similar trend as CAT (P<0.05). However, SOD activity in muscle was not affected by dietary thiamin level (P>0.05). The results indicated that thiamin could improve antioxidant defence and inhibit lipid peroxidation and protein oxidation of juvenile Jian carp.

Slowly progressive folate-deficiency myelopathy: Report of a case

BackgroundFolate deficiency is known to be associated with subacute combined degeneration of the spinal cord; however, reports of long-standing cases are rare. Although neurological deficits due to folate deficiency have been reported to respond to folic acid supplementation, the functional outcomes have not been fully elucidated. ObjectiveThe aim of the study was to evaluate the clinical features and response to folate supplementation in a patient with folate deficiency manifested over 10years as a slowly progressive myelopathy. MethodsWe performed comprehensive clinical screening, electrophysiological testing, and posturography before and after folate supplementation. ResultsA 49-year-old man had a slowly progressive gait disturbance for 10years. He had not eaten fresh green vegetables for more than 10years. Neurological examination revealed spastic paraplegia and absence of any vibration sense in the lower limbs accompanied by a positive Romberg's sign. Serum folate level was low, and plasma homocysteine level was elevated. Levels of blood thiamine and serum cobalamin were normal. We diagnosed the patient with myelopathy due to folate deficiency. Folic acid supplementation led to improvement of his symptoms; posturography and walking speed tests showed partial improvement, while the somatosensory-evoked potentials and central motor conduction time remained unchanged. ConclusionsFolate deficiency should be considered as a differential diagnosis of chronic slowly progressive myelopathy. The present case suggests the importance of early diagnosis and treatment before the adverse neurological manifestations of folate deficiency become irreversible.

Thiamine and its phosphate esters in relation to cardiometabolic risk factors in Saudi Arabs

BackgroundThiamine deficiency has suggested to be linked to several insulin-resistance complications. In this study, we aim to associate circulating thiamine levels among cardiometabolic parameters in an Arab cohort using a simple, sensitive, rapid and selective high-performance liquid chromatography (HPLC) method that has recently been developed.MethodsA total of 236 randomly selected, consenting Saudi adult participants (166 males and 70 females) were recruited and screened for the presence of the metabolic syndrome (MetS) using the modified National Cholesterol Education Program–Adult Treatment Panel III definition. Blood thiamine and its derivatives were quantified using HPLC.ResultsA total of 140 participants (53.9%) had MetS. The levels of thiamine and its derivatives of those with MetS were not significantly different from those without. However, hypertensive subjects had significantly higher urinary thiamine (P = 0.03) as well as significantly lower levels of thiamine diphosphate (TDP) (P = 0.01) and total thiamine (P = 0.02) than the normotensive subjects, even after adjusting for age and body mass index (BMI). Furthermore, age- and BMI-matched participants with elevated blood glucose levels had significantly lower levels of thiamine monophosphate (P = 0.020), TDP (P < 0.001) and total thiamine (P < 0.001) and significantly elevated levels of urinary thiamine (P = 0.005) compared to normoglycemic participants.ConclusionsLow thiamine levels are associated with elevated blood glucose and hypertension in Saudi adults. Determination of thiamine status may be considered and corrected among patients with, or at high risk for, MetS, but the question whether thiamine deficiency correction translates to improved cardiometabolic status needs further longitudinal investigation.

Assessment of thiamine content in some dairy products and rice milk

The levels of thiamine were compared between different types of milk, fermented milk products and rice milk. The analysed products were mainly from the markets, so vitamin analysis may be a good parameter for the quality of commercial food. Thiamine concentrations were determined by high performance liquid chromatography (HPLC) using a reversed-phase C-18 column with fluorescence detector. The average thiamine contents were 0.46 µg/mL for ultra high temperature (UHT), 0.39 µg/mL for pasteurized and 0.38 µg/mL for chocolate milk. Unprocessed cow milk had average thiamine concentration of 0.47 µg/mL. The highest thiamine content (11.95 µg/mL) was found in rice milk. Sour cream samples had higher concentration of thiamine (0.54 µg/mL) than yogurt (0.45 µg/mL) and sour milk (0.47 µg/mL). In the opened UHT milk packages, which were stored in refrigerator for 10 days, significant thiamine loss was not observed. Investigated products contained appropriate amounts of thiamine and had satisfactory nutritional value with respect to vitamin B1.

Impacts of Diet on Thiamine Status of Lake Ontario American Eels

AbstractThe Lake Ontario–upper St. Lawrence River (LOUSL) population of American Eels Anguilla rostrata (hereafter, “eels”) was once one of the most important groups of the species but is now in a state of serious decline. Given that thiamine deficiency has been observed in almost all of the top predators in Lake Ontario, we assessed the potential that a diet‐induced thiamine deficiency associated with consumption of Alewives Alosa pseudoharengus could be involved. Muscle thiamine was measured in eels from throughout the LOUSL corridor and was compared with putative threshold effect levels established from the literature. Mirex concentrations were used to separate Lake Ontario‐resident eels from non‐Lake Ontario‐resident eels. Stable isotope analyses of eel muscle samples and potential prey, including Alewives, were combined with mixing model software to infer the diets consumed by Lake Ontario eels. Although residence in Lake Ontario was associated with a significant decline in muscle thiamine concentration, estimated Alewife consumption by eels was unexpectedly low. Instead, mixing model results indicated that crayfish and Round Goby Neogobius melanostomus were the major prey. Both taxa are known to contain thiaminase and have the potential to cause thiamine deficiency, but there are no reports of thiamine deficiency associated with Round Goby consumption, thus implicating crayfish. There was no recovery in thiamine levels prior to the initiation of oceanic migration. As a result, thiamine levels of Lake Ontario‐resident eels prior to migration were only slightly above putative threshold effect levels for pathological and behavioral effects in Japanese Eels Anguilla japonica, but this would require confirmation with American Eels. Since thiamine levels are expected to decline further during migration, additional effects on eel behavior, reproduction, and survival seem probable. Because of panmixia, such effects—when combined with the relatively high reproductive potential of Lake Ontario‐resident eels—may have consequences for the entire species.

Adaptive regulation of human intestinal thiamine uptake by extracellular substrate level: a role for THTR-2 transcriptional regulation

The intestinal thiamine uptake process is adaptively regulated by the level of vitamin in the diet, but the molecular mechanism involved is not fully understood. Here we used the human intestinal epithelial Caco-2 cells exposed to different levels of extracellular thiamine to delineate the molecular mechanism involved. Our results showed that maintaining Caco-2 cells in a thiamine-deficient medium resulted in a specific and significant increase of [3H]thiamine uptake compared with cell exposure to a high level of thiamine (1 mM). This adaptive regulation was also associated with a higher level of mRNA expression of thiamine transporter-2 (THTR-2), but not thiamine transporter-1 (THTR-1), in the deficient condition and a higher level of promoter activity of gene encoding THTR-2 (SLC19A3). Using 5'-truncated promoter-luciferase constructs, we identified the thiamine level-responsive region in the SLC19A3 promoter to be between -77 and -29 (using transcriptional start site as +1). By means of mutational analysis, a key role for a stimulating protein-1 (SP1)/guanosine cytidine box in mediating the effect of extracellular thiamine level on SLC19A3 promoter was established. Furthermore, extracellular level of thiamine was found to affect SP1 protein expression and binding pattern to the thiamine level-responsive region of SLC19A3 promoter in Caco-2 cells as shown by Western blotting and electrophoretic mobility shift assay analysis, respectively. These studies demonstrate that the human intestinal thiamine uptake is adaptively regulated by the extracellular substrate level via transcriptional regulation of the THTR-2 system, and report that SP1 transcriptional factor is involved in this regulation.

The relationship between lactate and thiamine levels in patients with diabetic ketoacidosis

PurposeThiamine functions as an important cofactor in aerobic metabolism and thiamine deficiency can contribute to lactic acidosis. Although increased rates of thiamine deficiency have been described in diabetic outpatients, this phenomenon has not been studied in relation to diabetic ketoacidosis (DKA). In the present study, we hypothesize that thiamine deficiency is associated with elevated lactate in patients with DKA. Materials and MethodsThis was a prospective observational study of patients presenting to a tertiary care center with DKA. Patient demographics, laboratory results, and outcomes were recorded. A one-time blood draw was performed and analyzed for plasma thiamine levels. ResultsThirty-two patients were enrolled. Eight patients (25%) were thiamine deficient, with levels lower than 9 nmol/L. A negative correlation between lactic acid and plasma thiamine levels was found (r = −0.56, P = .002). This relationship remained significant after adjustment for APACHE II scores (P = .009). Thiamine levels were directly related to admission serum bicarbonate (r = 0.44, P = .019), and patients with thiamine deficiency maintained lower bicarbonate levels over the first 24 hours (slopes parallel with a difference of 4.083, P = .002). ConclusionsPatients with DKA had a high prevalence of thiamine deficiency. Thiamine levels were inversely related to lactate levels among patients with DKA. A study of thiamine supplementation in DKA is warranted.

Constipation in Patients with Thiamine Deficiency after Roux-en-Y Gastric Bypass Surgery

Background/Aims: Roux-en-Y gastric bypass surgery is the most common bariatric surgery worldwide. We have described thiamine deficiency in patients with small intestinal bacterial overgrowth after gastric bypass. We hypothesized that symptoms of thiamine deficiency are common after gastric bypass. The aims of this study were to examine the prevalence of and treatment of symptoms of thiamine deficiency after gastric bypass. Methods: This is a prospective study performed in a large urban, community hospital. Consecutive gastric bypass patients seen from February 1, 2008 to May 1, 2009 are included. Thiamine deficiency in this study included both: consistent clinical symptoms and either (1) low blood thiamine level or (2) resolution of clinical symptoms after receiving thiamine. Results: Of 151 patients, 25 females and 2 males met the criteria for thiamine deficiency (prevalence of 18%). In these 27 patients, 12 had one symptom of thiamine deficiency, while 15 had symptoms consistent with multiple subtypes. Eleven patients reported constipation at 0.33-12 years (mean 4.8) after gastric bypass. Elevated serum folate levels were seen in 6 of 10 tested patients and there was an abnormal glucose-hydrogen breath test in 9 of 10 tested patients, supporting the presence of small intestinal bacterial overgrowth. Frequency of defecation improved after thiamine treatment. Conclusion: Thiamine deficiency resulting from small intestinal bacterial overgrowth should be considered in patients being seen for constipation after gastric bypass surgery.

Understanding the role of sulfur–thiamine interaction in the pathogenesis of sulfur-induced polioencephalomalacia in beef cattle

This study examined the role of sulfur (S) in the pathogenesis of S-induced polioencephalomalacia (PEM) in beef cattle in the context of thiamine status and metabolism. Thiamine, thiamine monophosphate (TMP) and thiamine pyrophosphate (TPP) status in rumen fluid, blood and brain tissue were determined in beef heifers fed 2 levels of S [low S (LS) vs. high S (HS)] at 2 forage-to-concentrate ratios (F:C). High S diet did not affect ruminal and blood thiamine status. Interestingly, however, HS diet showed increased brain thiamine levels. No gross or histopathological changes indicative of PEM were detected in the brains of the heifers. Of note, during the course of the present study, we documented an outbreak of S-induced PEM in commercial feedlot steers. Brain thiamine variables in experimental animals fed HS diet were then contrasted with brain thiamine status in PEM affected feedlot steers. Interestingly, in clinically normal animals, exposure to HS diet resulted in increased levels of both TMP and TPP in the brain tissue, in comparison to animals fed LS diet. In contrast, the PEM affected brains showed overall lower levels of thiamine phosphates. It is noteworthy that TPP levels were 36.5% lower, despite 4.9-fold higher free thiamine in PEM brains compared to normal brains. Our results indicate that high dietary S may increase the metabolic demand for TPP, and that animals incapable of maintaining requisite levels of brain TPP are at high risk to develop fulminant cerebrocortical necrosis.

Use of Stable Isotopes to Identify Redds of Putative Hatchery and Wild Atlantic Salmon and Evaluate Their Spawning Habitat and Egg Thiamine Status in a Lake Ontario Tributary

AbstractBoth wild and hatchery Atlantic Salmon Salmo salar can contribute to restoration but can exhibit differences in spawning habitat selection (e.g., water depth, current speed) and egg nutritional quality (e.g., thiamine), which affect reproductive success. Hence, there is a need to be able to differentiate the spawning contribution of the two groups in the wild. As diets of wild and hatchery‐reared spawners are markedly dissimilar and diet is known to influence stable isotope signature, egg stable isotope signatures offer the potential to discriminate redds of each. Using stable isotope analysis of carbon and nitrogen (δ13C and δ 15N) of naturally spawned Atlantic Salmon eggs, we were able to discriminate the redds of putative wild (i.e., previously stocked life stage feeding in Lake Ontario; EWSR) from putative hatchery‐reared Atlantic Salmon (EHSR). Eggs of EWSR were significantly more enriched in nitrogen (δ15N: 15.0 ± 0.5‰ [mean ± SE]) but more depleted in carbon (δ13C: −26.6 ± 0.3‰) than eggs of EHSR (δ15N = 9.8 ± 0.6‰; δ13C = −17.5 ± 0.0‰). Eggs of EHSR were indistinguishable from eggs of known hatchery Atlantic Salmon for both δ13C and δ 15N. Using stable isotopes to discriminate redd type, few differences were found between the spawning habitat of putative wild and hatchery spawners. Similarly using the same criteria, thiamine levels in eggs of EWSR (8,474 ± 840 pmol/g) were not significantly different from eggs of known wild Atlantic Salmon (3,691 ± 782 pmol/g) or of eggs of EHSR (14,865 ± 1,050 pmol/g), whose thiamine levels were indistinguishable from eggs of known hatchery Atlantic Salmon (14,200 ± 1,167 pmol/g). Egg thiamine levels for all groups were above established mortality thresholds. Our results indicate that both hatchery and wild Atlantic Salmon can make reproductive contributions, which can be differentiated and quantified using stable isotope signatures.Received August 24, 2012; accepted May 15, 2013

Serum thiamin concentration is negatively correlated with lactate levels in survivors of septic shock

Thiamine deficiency can be present in 20% of patients in the ICU. This deficiency is considered to be an uncommon source of lactic acidosis in septic patients. An elevated serum lactate level is associated with morbidity and mortality [1]. Increased levels of thiamine increase the activity of glutathione peroxidase (GPx), a major component of the cellular antioxidant system [2]. The objective of this study was to determine the influence of serum thiamine concentrations on lactate levels, GPx activity, length of hospital stay, length of ICU stay and ICU mortality in patients with septic shock.

Up-regulation of vitamin B1 homeostasis genes in breast cancer

An increased carbon flux and exploitation of metabolic pathways for the rapid generation of biosynthetic precursors is a common phenotype observed in breast cancer. To support this metabolic phenotype, cancer cells adaptively regulate the expression of glycolytic enzymes and nutrient transporters. However, activity of several enzymes involved in glucose metabolism requires an adequate supply of cofactors. In particular, vitamin B1 (thiamine) is utilized as an essential cofactor for metabolic enzymes that intersect at critical junctions within the glycolytic network. Intracellular availability of thiamine is facilitated by the activity of thiamine transporters and thiamine pyrophosphokinase-1 (TPK-1). Therefore, the objective of this study was to establish if the cellular determinants regulating thiamine homeostasis differ between breast cancer and normal breast epithelia. Employing cDNA arrays of breast cancer and normal breast epithelial tissues, SLC19A2, SLC25A19 and TPK-1 were found to be significantly up-regulated. Similarly, up-regulation was also observed in breast cancer cell lines compared to human mammary epithelial cells. Thiamine transport assays and quantitation of intracellular thiamine and thiamine pyrophosphate established a significantly greater extent of thiamine transport and free thiamine levels in breast cancer cell lines compared to human mammary epithelial cells. Overall, these findings demonstrate an adaptive response by breast cancer cells to increase cellular availability of thiamine.

Abstract 1903: Up-regulation of vitamin B1 homeostasis genes in breast cancer.

Abstract Malignant cells exhibit alterations in metabolic enzymes requiring an adequate supply of cofactors to support enzymatic activity. In particular, Vitamin B1 (thiamine) is an important component of cellular growth and metabolism within all cells, functioning as an essential enzyme cofactor in key metabolic pathways within in the glycolytic network. Intracellular availability of thiamine is facilitated by the activity of thiamine transporters and the conversion of thiamine to the active coenzyme, thiamine pyrophosphate (TPP) by thiamine pyrophosphokinase (TPK1). Therefore, the objective was to establish if the cellular determinants regulating thiamine homeostasis differ between breast cancer and normal breast epithelia. This work will aid in linking the metabolic phenotype of cancer cells with the adaptive regulation of thiamine homeostasis. This may provide a molecular basis for dietary interventions and new therapeutic targets directed towards cancer cell metabolism. Methods: cDNA arrays of breast cancer and normal breast tissues were employed to determine expression of SLC19A2, SLC19A3, SLC25A19 and TPK-1. Western blotting was used to determine whole cell protein expression. To test the extent of cell surface localization of the transporters, cell surface proteins were biotinylated and run on Western Blot. Transport assays were used to quantify thiamine transport and free thiamine levels in breast cancer cell lines compared to human mammary epithelial cells (HMEC). Results: SLC19A2, SLC25A19 and TPK-1were found to be significantly up-regulated in clinical tissues and breast cancer cell lines 6.48 (P=0.0013), 5.97 (P=0.0003), and 2.33 (P=0.0063) folds, respectively. Additionally, thiamine transporters THTR1 and THTR2 exhibited different cellular localization and expression depending on the ER status of the cancer cell. The increase in thiamine homeostasis genes correlated with an increase in intracellular free thiamine levels but not with the coenzyme TPP. Conclusions: Overall, these findings demonstrate an adaptive response by breast cancer cells to bolster an increase in the cellular availability of thiamine. Citation Format: Jason Zastre, Brad Hanberry, Rebecca Sweet, Cary McGinnis, Kristen Venuti, Michael Bartlett, Raj Govindarajan. Up-regulation of vitamin B1 homeostasis genes in breast cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1903. doi:10.1158/1538-7445.AM2013-1903

Tobacco–alcohol amblyopia: A diagnostic dilemma

IntroductionTobacco alcohol amblyopia is an outdated term for a rare condition characterized by visual impairment due to tobacco and alcohol abuse usually associated with nutritional deficiencies. The more accurate term used now is Nutritional Optic Neuropathy. The visual impairment generally presents as a centrocecal scotoma. Its pathophysiology is poorly understood but it is generally attributed to toxic effects of cyanide and B12 deficiency. Design/subjects61year old male presented with one month history of altered mental status and progressive, painless, bilateral vision loss in the setting of severe alcohol and tobacco abuse and poor nutrition. Patient developed loss of central vision in the left-eye and blurring of vision in the right-eye after 1week, which was reduced to only perception of hand movements by the time of presentation. His BMI was 19.3 with an emaciated appearance. On ophthalmological exam, visual-acuity was 20/200 (right) and 20/300 (left), with a left central scotoma and normal fundoscopic exam. Neurological examination was significant for confabulation and gait instability consistent with Wernickes Korsakoff. Workup included negative imaging and normal B12, folate and thiamine levels, undetectable cyanide levels, and negative Leber's Hereditary Optic Neuropathy mutation. He was discharged after 30days, after a steady reversal of his symptoms in the setting of abstinence and nutritional supplementation. A diagnosis of tobacco alcohol amblyopia was made by exclusion and by history. ResultsThis case of tobacco alcohol amblyopia has an atypical presentation because of normal fundoscopic exam, undetectable cyanide levels and normal B12 levels. It reinforces the need for biomarkers for this disease. Nutritional fortification has made these cases rare, but a neurological perspective may be essential for accurate diagnosis, treatment and positive outcome for these patients. ConclusionTobacco alcohol amblyopia can be a difficult diagnosis due to lack of biomarkers and rare occurrence. A neurologist can facilitate diagnosis in atypical cases.

The beneficial role of thiamine in Parkinson disease.

Parkinson disease (PD) is the second most common form of neurodegeneration among elderly individuals. PD is clinically characterized by tremors, rigidity, slowness of movement, and postural imbalance. In this paper, we review the evidence for an association between PD and thiamine. Interestingly, a significant association has been demonstrated between PD and low levels of serum thiamine, and thiamine supplements appear to have beneficial clinical effects against PD. Multiple studies have evaluated the connection between thiamine and PD pathology, and candidate pathways involve the transcription factor Sp1, p53, Bcl-2, caspase-3, tyrosine hydroxylase, glycogen synthase kinase-3β, vascular endothelial growth factor, advanced glycation end products, nuclear factor kappa B, mitogen-activated protein kinase, and the reduced form of nicotinamide adenine dinucleotide phosphate. Thus, a review of the literature suggests that thiamine plays a role in PD, although further investigation into the effects of thiamine in PD is needed.

MR spectroscopy in pediatric Wernicke encephalopathy

The patient is a 7-year-old girl with a history of repaired gastroschisis and short gut syndrome. She presented with a 4-day history of progressive encephalopathy, truncal ataxia, and omnidirectional gaze-evoked nystagmus. Peripheral lactate was 7.1 mmol/L. Serum thiamine level was decreased (<5 nmol/L). Brain magnetic resonance with spectroscopy is shown in the figure. A clinical diagnosis of Wernicke encephalopathy was made. The patient was started on thiamine and demonstrated a rapid clinical recovery. Peripheral lactate normalized within 1 day. Increased lactate has been reported in thiamine deficiency, presumed secondary to the role of thiamine as a cofactor for the pyruvate dehydrogenase complex and α-ketoglutarate dehydrogenase.1

Isolation and Purification of Thiamine Binding Protein from Mung Bean

Thiamine has fundamental role in energy metabolism. The organs mostly sensitive to the lack of thiamine levels in the body are the nervous system and the heart. Thiamine deficiency causes symptoms of polyneuritis and cardiovascular diseases. Because of its importance in the metabolism of carbohydrates, we need to measure the levels of thiamine in the body fluids by using an easy and inexpensive way without compromising the sensitivity and selectivity. An option to it is thiamine measurement based on the principle of which is analogous to ELISA, in which a thiamine binding protein (TBP) act by replacing antibodies. The presence of TBP in several seeds have been reported by previous researchers, but the presence of TBP in mung beans has not been studied. This study was aimed to isolate and purify TBP from mung bean. The protein was isolated from mung bean through salting out by ammonium sulphate of 40, 70, and 90% (w/v). TBP has a negative charge as shown by cellulose acetate electrophoresis. The result obtained after salting out by ammonium sulphate was further purified bymeans of DEAE-cellulose chromatography and affinity chromatography. In precipitation of 90% of salting out method, one peak protein was obtained by using affinity chromatography. The protein was analyzed by SDS PAGE electrophoresis. The result of SDS PAGE electrophoresis showed that TBP has a molecular weight of 72.63 kDa.

Thiamine and Fatigue in Inflammatory Bowel Diseases: An Open-label Pilot Study

To demonstrate that fatigue and other disorders related to ulcerative colitis and Crohn's disease are the manifestation of an intracellular mild thiamine deficiency and not due to malabsorbtion, augmented requirements, or nutritional factors, and that this dysfunction is curable with high doses of thiamine administered orally or parenterally. In this pilot study, we treated fatigue in eight patients with ulcerative colitis and four patients affected by Crohn's disease from January to April 2011. The patients were recruited through general practitioners' surveys and among personnel and affiliated personnel of the clinic Villa Immacolata. Fatigue was measured using the chronic fatigue syndrome scale, and the determination of thiamine and thiamine pyrophosphate levels in the blood was carried out through blood tests. The levels of thiamine and thiamine pyrophosphate in the blood were normal. All patients were assigned to receive high doses of thiamine orally. Depending upon the body weight of each patient, dosage ranged from 600 mg/day (60 kg) to 1,500 mg/day (90 kg). The chronic fatigue syndrome scale as well as thiamine and thiamine pyrophosphate levels in the blood were measured 20 days after the beginning of the therapy. Ten patients out of twelve showed complete regression of fatigue, while the remaining two patients showed nearly complete regression of fatigue compared to the chronic fatigue syndrome scale scores before therapy. The absence of blood thiamine deficiency and the efficacy of high-dose thiamine in our patients suggest that fatigue is the manifestation of a thiamine deficiency, likely due to a dysfunction of the active transport of thiamine inside the cells, or due to structural enzymatic abnormalities. The administration of large quantities of thiamine increases the concentration in the blood to levels in which the passive transport restores the normal glucose metabolism in all cells and leads to a complete regression of fatigue.