SEARCH · PubMed Health

Results for “THIAMINE DEFICIENCY”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources

PubMed2006

Thiamine deficiency and parasitic infection in rural Thai children.

A study was carried out to determine whether thiamine deficiency in northeast Thailand is linked with parasitic infection. We assessed the thiamine status and tested for parasitic infections in 231 children between 6 and 12 years of age in Nam Phong District of Khon Kaen Province, Thailand. Thiamine deficiency [thiamine pyrophosphate effect (TPPE) > 20%] and parasitic infections (mostly Strongyloides stercoralis) were identified in 16 and 45% of the children, respectively. No association between thiamine deficiency and parasitic infection was found. The general health of the children, according to Thai standard anthropometric curves, was within the normal range. The suboptimal thiamine status and the high prevalence of parasitic infection require attention.

Child↗

PubMed1980

Furosemide-induced thiamine deficiency.

Male Wistar rats were separated into 4 groups: group 1, thiamine sufficient diet (control); group 2, thiamine sufficient diet with intraperitoneal administration of furosemide (20 mg . kg-1 of body weight); group 3, thiamine deficient diet; group 4, thiamine deficient diet within tra-peritoneal administration of furosemide. After 4 weeks, the rats were killed and the thiamine levels and activity of transketolase were assayed. Thiamine concentration and transketolase activity were significantly decreased and thiamine pyrophosphate effect was significantly increased in the blood, and various tissues in group 2 and 4 compared with group 1 and 3, respectively. The intraperitoneal administration of various concentrations of furosemide (20 mg, 10 mg, and 2 mg . kg-1 of body weight) resulted in a significant increase in urinary thiamine excretion. Thus, it is assumed that long-term administration of furosemide could induce a thiamine deficiency.

Animals↗

PubMed2005

Preoperative thiamine deficiency in obese population undergoing laparoscopic bariatric surgery.

BACKGROUND: Nutritional deficiencies are a recognized complication of bariatric surgery. Thiamine deficiency has been reported as a possible consequence of both restrictive and malabsorptive bariatric procedures. Most of the reported cases occurred after Roux-en-Y gastric bypass (RYGB) surgery; fewer were described after biliopancreatic diversion, vertical banded gastroplasty, or duodenal switch. Adults who have a high carbohydrate intake derived mainly from refined sugars and milled rice are at greater risk of developing thiamine deficiency, because thiamine is absent from fats, oils, and refined sugars. Currently, no reports have evaluated the preoperative thiamine status of bariatric patients. The aim of this study was to evaluate the degree of thiamine deficiency in obese patients before bariatric surgery at our institution. METHODS: The medical records of consecutive patients who underwent laparoscopic RYGB or laparoscopic adjustable gastric banding at our institution between March 2003 and February 2004 were retrospectively reviewed. Patients were selected for this study on the basis of predetermined criteria. Preoperative thiamine levels were retrospectively recorded. Excluded from this study were patients who had been taking multivitamins or other nutritional supplements before surgical intervention, had a history of frequent alcohol consumption, any malabsorptive diseases, or previous restrictive-malabsorptive surgical interventions, such as RYGB, biliopancreatic diversion, or adjustable gastric banding, according to the initial evaluation and questionnaire. RESULTS: Of 437 consecutive patients who underwent laparoscopic RYGB or laparoscopic adjustable gastric banding, 303 were included in the study. Forty-seven patients (15.5%) presented with low preoperative thiamine levels. The mean age and body mass index of these patients was 46 years and 60 kg/m(2), respectively. Male patients presented with greater mean preoperative thiamine levels (3.2 microg /dL) than female patients (2.4 microg/dL). CONCLUSION: Obese patients undergoing bariatric surgery may have significant thiamine deficiency before surgery.

Adolescent↗

PubMedDate not supplied

Effect of age on behavioral and enzymatic changes during thiamin deficiency.

Open field behavior and whole brain enzymatic activities were determined during thiamin deficiency in two strains of young, as well as in aged mice. In young CD-1 mice, thiamin deficiency reduced total distance traveled and vertical movements after 7 days and the decline was more than 50% by day 9. The behavioral deficit was highly correlated to decreases in 2-oxoglutarate dehydrogenase activity (KGDH). The open field behavior of Balb/c mice was about 40% less than in CD-1 mice and responded in a qualitatively different manner to thiamin deficiency. The activity of the Balb/c mice increased and then decreased with thiamin deficiency. The activity of 3 month old mice peaked on day 6 (126% of initial score), whereas 10 and 30 month mice showed a much greater increase (about 175% of initial scores), but on day 7. Although the activity of the thiamin dependent enzyme transketolase (TK) was affected similarly at all ages, the activity of KGDH in the aged brain was more sensitive to thiamin deficiency than in the young; KGDH activity declined 41%, 57% or 74% at 3, 10, or 30 months, respectively. Thus, the current mouse model is an attractive one to study the interaction of thiamin deficiency with aging.

Aging↗

PubMed1984

Effect of dietary thiamin deficiency on intestinal functions in rats.

The effect of dietary thiamin deficiency has been studied on intestinal functions and chemical composition of brush border membranes in rats. Intestinal uptake of glucose, glycine, alanine, and leucine was significantly stimulated in thiamin deficiency compared to pair-fed control group. Studies with glucose and glycine revealed that stimulation of the absorption process occurs only in the presence of Na+ but not in its absence. Km measured in the presence of 140 mM Na+ for glucose and glycine uptakes was reduced by 56 and 41%, respectively, but Vmax remained unaltered in vitamin deficiency. There was no change in these parameters in Na+-free medium (Km = 31.3 and 23.3 mM; Vmax = 17.2 to 19.7 and 13.5 to 16.4 mumol/10 min/g wet tissue, respectively) under these conditions. The activities of brush border sucrase, lactase, maltase, alkaline phosphatase, and leucine aminopeptidase were reduced by 42 to 66% in thiamin deficiency, compared to pair-fed controls. Kinetic studies with sucrase and alkaline phosphatase evinced that a decrease in Vmax (61 and 64%, respectively) with no change in Km (33.8 and 4.3 mM, respectively) was responsible for observed impairment in the enzyme activities in thiamin deficiency. Microvillus membrane proteins expressed on dry membrane basis were reduced by 20% in thiamin-deficient intestine. There was no difference in membrane sialic acid, cholesterol, phospholipids, and triglycerides fractions under these conditions. It is suggested that thinning of the microvillus membrane may be implicated in observed aberrations of intestinal functions in thiamin-deprived animals.

Alanine↗

PubMed1976

Lactate dehydrogenase and isoenzyme changes in rats with experimental thiamine deficiency.

Heat and liver lactate dehydrogenase (LDH) and isoenzyme distributions were studied in rats with experimental thiamine deficiency. No change in total heart LDH activity was observed on days 24 and 40 of a thiamine deficient diet. At the time of symptoms (average 53 days on diet), total heart muscle LDH was slightly decreased in thiamine deficient rats (248 +/- 12 U/g tissue, Mn +/- SE) compared to ad lib fed controls (293 +/- 12, p less than 0.05), but did not differ from pair fed controls (273 +/- 15). Heart muscle LDH isoenzyme distribution showed a relative increase in the H4 band and a decrease in the H2M2 and HM3 bands in thiamine deficiency on day 24. This pattern became more promient by day 40. Calculated total M-LDH activity of heart muscle in thiamine deficient rats was significantly decreased at day 40 (44 +/- 3) compared to pair fed controls (57 +/- 5, p less than 0.05) and ad lib fed controls (85 +/- 7 p less than 0.001). Further changes were not observed in the symptomatic stage. Total H-LDH in heart muscle did not change during the period of study, while total liver LDH activity was reduced in thiamine deficient rats at the symptomatic stage (137 +/- 15) compared with pair fed controls (193 +/- 12, p less than 0.05) and ad lib fed controls (407 +/- 50, p less than 0.01). Liver isoenzyme electrophoresis showed an almost 100% distribution to the M4 band. The present investigation demonstrates a decrease in cardiac muscle M-LDH in experimental thiamine deficiency. Differences in LDH isoenzyme distribution in chronic hypoxia and thiamine deficiency are discussed.

Animals↗

PubMed1981

Erythrocytosis in thiamine deficient rats.

A thiamine (T) deficient state in rats was produced by feeding the rats a T deficient diet (TDD). At the stage of 13 days (TDD13 group), the number of red blood cells (RBC) and white blood cells (WBC), hematocrit (Ht) and hemoglobin (Hb) values decreased. On the other hand, after 30 days on the TDD (TDD30 group), the number of RBC was 819 x 10(4)/mm3 as against 631 x 10(4)/mm3 in the normal control group (NC group). Ht and Hb values also increased in the TDD30 group. These changes observed in the TDD30 group were significantly different from findings in the equal weight control group (EWC group) or in the pair fed control group (PFC group). The number of reticulocytes increased, the levels of 2,3-diphosphoglycerate (2,3-DPG) of RBC decreased and plasma erythropoietin levels increased in the TDD30 group. T levels of blood in the TDD13 group were 62 (39-79) ng/ml as against 275 (196-412) ng/ml in the NC group. T levels of blood in the TDD30 group were 102 (17-365) ng/ml, and widely varied. Decrease in 2,3-DPG produces an increase in O2 affinity to Hb, and hypoxia is induced in the peripheral tissues. Furthermore these conditions stimulate erythropoietin production and finally the number of RBC increases. T deficiency produces anemia at an early stage and absolute erythrocytosis occurs at the late stage of T deficiency. The increased osmotic resistance of RBC in hypotonic solution was also observed in the TDD30 group. This increase in osmotic resistance correlated with the decrease in cholesterol and phospholipid levels in the membrane of RBC.

2,3-Diphosphoglycerate↗

PubMed1988

The influence of thiamine deficiency and ethanol on rat brain catecholamines.

In rats treated with a thiamine deficient diet for 30 days the brain content of total thiamine decreased by 27-50%. Thiamine deficiency decreased the dopamine (DA) concentration of the striatum indicating a reduced synthesis of DA. In the hypothalamus the levels of the catecholamine metabolites homovanillic acid (HVA) and 4-hydroxy-3-methoxyphenyl glycol (HMPG) were reduced indicating a reduced DA and noradrenaline (NA) turnover. Animals on a diet containing 5% ethanol had increased concentrations of HVA and HMPG in rest brain indicating an increased DA and NA turnover. The concentration of 1-carboxysalsolinol (1-CSAL) and salsolinol (SAL) in the brain stem was increased in animals receiving ethanol. Thus, both thiamine deficiency and ethanol treatment influenced the catecholamine system in a complex region-dependent way. In the brain regions most susceptible to brain damage in thiamine deficiency, i.e., hypothalamus and brain stem, 1-CSAL and SAL increased most following thiamine deficiency combined with ethanol intake.

Alcohol Drinking↗

PubMed1997

Aversion-preference patterns in amino acid- or protein-deficient rats: a comparison with previously reported responses to thiamin-deficient diets.

The purpose of the present experiments was to extend previous data on the strategy used by adult rats to select feed appropriately when faced with diets devoid of protein or an essential amino acid (EAA), and to compare this strategy with that used when facing vitamin (thiamin) deficiency. Rats fed on either balanced or deficient (EAA or protein) diets were offered a choice between a novel deficient and a familiar (deficient or corrected) diet and their choice was monitored. It was shown that protein- and EAA-deficient rats acquired an aversion for their corresponding familiar devoid diet, which by itself promoted a neophilia for the novel diet. This neophilia was not non-specific because protein-deficient rats facing a choice between a protein-devoid and an EAA-devoid diet did exhibit neophilia but only in the short term (less than 5 h), and then switched to a preference for the familiar protein-devoid diet. These results show that, in contrast to the case of vitamin deficiency, the protein- or EAA-devoid diet-induced neophilia can be rapidly reversed if the novel feed happens to be more deleterious than the familiar, inappropriate one. This behaviour suggests the existence of sensitive mechanisms able to reveal within a short time the EAA inadequacy of the ingested feed and to adapt the choice for the most appropriate feeds more promptly than in the face of thiamin deficiency. Thus it appears that balancing EAA is more urgent than balancing thiamin.

Animal Feed↗

PubMed1996

Thiamine pyrophosphate-requiring enzymes are altered during pyrithiamine-induced thiamine deficiency in cultured human lymphoblasts.

The most common of the severe complications of thiamine deficiency are beriberi and Wernicke-Korsakoff syndrome. To help clarify the biochemical basis for these disorders, a cell culture system has been established in which pyrithiamine, a potent thiamine transport inhibitor, was used to mimic different degrees of thiamine deficiency within human lymphoblasts. Activities of both transketolase and alpha-ketoglutarate dehydrogenase (alpha-KGDH) decreased at the same rate and to roughly the same levels in response to thiamine deficiency within a given cell line. However, variation in sensitivity to thiamine deficiency, as judged by the relative percentage of loss of enzymatic activities, was found when different cell lines were compared. When exogenous thiamine pyrophosphate was added to the activity assays, differences between transketolase and alpha-KGDH became readily apparent. Only 25% of the lost transketolase activity was present as apo-enzyme, whereas 70% of the lost alpha-KGDH activity was present in the apo-enzyme form. For transketolase, the non-recoverable activity was due mainly to a decrease in the synthesis rate of the protein during thiamine deficiency, suggesting that thiamine has a direct effect on the expression of the transketolase gene and/or protein.

Cell Culture Techniques↗

PubMed1999

Thiamin deficiency in HIV-positive patients: evaluation by erythrocyte transketolase activity and thiamin pyrophosphate effect.

BACKGROUND AND AIMS: The aim of the study was to determine the thiamin status in HIV-positive patients. METHODS: Measurement of erythrocyte transketolase activity (ETK) and thiaminpyrophosphate (TPP) effect in 55 consecutive HIV-positive patients of a specialized outpatient clinic were grouped into five groups according to their CD4 counts. Comparison of results of HIV-positive patients with age-matched control group of 22 healthy subjects. RESULTS: Of the patients, 27% had a pathologically-increased TPP effect, 18% of the patients had pathologically-low ETK. The percentage of pathological values of TPP effect in the patients was significantly higher compared with the control group. There was no statistically significant correlation between pathological thiamin status and stage of the disease, zidovudine therapy or nutritional status of the patients. CONCLUSIONS: Thiamin deficiency in HIV-positive patients was found in a higher percentage than previously reported. Thiamine deficiency is not only present in advanced stages of HIV-infection, but also in clinically asymptomatic patients.

Adult↗

PubMed2005

Polyneuropathy from thiamin deficiency associated with thyrotoxicosis.

Polyneuropathy from thiamin deficiency can occur in persons who consume a diet consisting mainly of polished rice with low protein and thiamin content in the setting of excessive physical activity or hypermetabolic states. The authors report here a 17-year-old fisherman who presented with a 3-month history of symptoms and signs consistent with polyneuropathy. There were also clinical features of thyrotoxicosis which was confirmed by thyroid function test. His dietary intake consisted mainly of polished rice and fish both of which contain a small amount of thiamin. This could not cope with his hypermetabolic condition from thyrotoxicosis resulting in thiamin deficiency with polyneuropathy.

Adolescent↗

PubMed1983

A biochemical and immunohistochemical study of central serotonin nerves in rats with chronic thiamine deficiency.

An immunohistochemical and neurochemical investigation of central serotonin (5-HT) nerves was made in rats deprived of dietary thiamine at various stages of development. The classical symptoms of severe thiamine deficiency were produced in adult rats which had been maintained on a synthetic thiamine-free diet for 5-8 weeks and in young rats reared from birth to weaning by thiamine-deficient mothers. Offspring of rats which had been thiamine-deficient throughout pregnancy were also studied; there were no visible symptoms of thiamine deficiency in these rats after weaning. The number and distribution of 5-HT nerve cell bodies in the brainstem were compared in control and thiamine-deficient rats after visualizing the cells by immunofluorescence of endogenous 5-HT. 5-HT nerve terminals and axons were also compared in normal and deficient rats by immunofluorescence after loading with 5,7-dihydroxytryptamine. The immunohistochemical examination showed that central 5-HT nerves were not affected in any of the groups of thiamine-deficient rats studied. This was confirmed by measurements of tryptophan hydroxylase activity and 5-HT concentration in several brain regions. These results do not support earlier reports of a selective impairment of central 5-HT nerves in chronic diet-induced thiamine deficiency.

Aging↗

PubMed2003

The role of thiamine deficiency in alcoholic brain disease.

A deficiency in the essential nutrient thiamine resulting from chronic alcohol consumption is one factor underlying alcohol-induced brain damage. Thiamine is a helper molecule (i.e., a cofactor) required by three enzymes involved in two pathways of carbohydrate metabolism. Because intermediate products of these pathways are needed for the generation of other essential molecules in the cells (e.g., building blocks of proteins and DNA as well as brain chemicals), a reduction in thiamine can interfere with numerous cellular functions, leading to serious brain disorders, including Wernicke-Korsakoff syndrome, which is found predominantly in alcoholics. Chronic alcohol consumption can result in thiamine deficiency by causing inadequate nutritional thiamine intake, decreased absorption of thiamine from the gastrointestinal tract, and impaired thiamine utilization in the cells. People differ in their susceptibility to thiamine deficiency, however, and different brain regions also may be more or less sensitive to this condition.

Alcohol Amnestic Disorder↗

PubMed1992

[Thiamin deficiency is common in Israel].

Diseases due to vitamin B1 (thiamin) deficiency are considered to be uncommon in Israel. We present 13 patients admitted during the course of a year who were found to have thiamin deficiency. 5 had classic syndromes such as beri-beri, Wernicke's encephalopathy and cerebellar degeneration. In another 8 the thiamin deficiency was found during workup for less specific neurological abnormalities. Only a minority were alcoholics. Mainly at risk for developing nutritional deficiency were the solitary elderly of low socio-economic status with poor nutrition. Other reasons for thiamin deficiency were drug abuse and hyperemesis gravidarum. Thiamin levels should be determined not only in alcoholics and those with classic B1 deficiency syndromes, but in the routine workup of patients with sensory-motor neuropathy, dementia, gait disorders, cerebellar syndromes and confusional states. It is advised to give vitamins prophylactically to asymptomatic high risk patients.

Adult↗

PubMed1988

The effect of thiamine deficiency on the structure and physiology of the rat forebrain.

Dietary thiamine deficiency, enhanced by pyrithiamine administration in adult rats, produces overt lesions in the brain that are especially prominent in the thalamus. The present study was undertaken to determine whether the thalamic lesions could be correlated with alterations in the physiological properties of neurons in the thalamus and somatosensory cortex. The regimen for experimentally inducing thiamine deficiency produced large lesions in the thalamus of every case; the lesions included most, if not all, of the neurons in the intralaminar thalamic nuclei. The extent of the lesion in the intralaminar thalamus was highly correlated with the loss of bilaterally synchronous spontaneous activity in the cerebral cortex. This correlation was seen in animals analyzed as early as 1-18 hr after the appearance of opisthotonus, the crisis state of thiamine deficiency, and as late as 2-9 weeks of recovery following thiamine replacement therapy. The loss of bilateral synchronous bursting neuronal activity following intralaminar thalamic lesions is consistent with the proposed role of the intralaminar thalamus as a pacemaker for rhythmic cortical activity (Armstrong-James et al., Exp. Brain Res., 1985; Fox and Armstrong-James, Exp. Brain Res. 63: 505-518, 1986). The location and size of the central lesions within the thalamus suggest that the observed neuronal loss could result from a nonhemorrhagic infarction in the ventromedial branches of the superior cerebellar arteries. Experimental thiamine deficiency also produced alterations in the receptive field properties of the somatosensory cortex neurons in all animals examined. Changes in cortical receptive field properties were correlated with the destruction of sensory relay neurons in the thalamic ventrobasal complex. The loss of the central lateral thalamic input to the cortex and the loss of somatosensory relay neurons in the ventrobasal thalamus in experimental thiamine deficiency produce alterations in cortical function which may contribute to deficits in memory and cognition analogous to those which characterize Korsakoff's psychosis in humans.

Animals↗

PubMed1997

Cortical and subcortical white matter damage without Wernicke's encephalopathy after recovery from thiamine deficiency in the rat.

The relative etiologic roles of ethanol and thiamine deficiency in the cortical atrophy and loss of cerebral white matter in chronic alcoholics are uncertain. The present study examined the distribution of degenerating axons within cortical and subcortical tracts 1 week after recovery from early to late symptomatic stages of thiamine deficiency in the absence of ethanol in Sprague-Dawley rats. The brains of rats exposed to an early symptomatic stage of pyrithiamine-induced thiamine deficiency, 12-13 days of treatment, contained degenerating axons in corpus callosum, anterior commissure, external and internal capsules, optic and olfactory tracts, and fornix and mammillothalamic tracts. A dense pattern of degenerating axons was evident in layers III-IV of frontal and parietal cortex. Less intense and more evenly distributed degenerating axons were present in layers IV-VI of frontal, parietal, cingulate, temporal, retrosplenial, occipital, and granular insular cortex. Neuronal counts in mammillary body nuclei and areal measurements of the mammillary body were unchanged from controls and the thalamus was relatively undamaged. In animals reversed at later and more advanced symptomatic stages of thiamine deficiency, 14-15 days of treatment, degenerating axons were found in other cortical regions and hippocampus and there was extensive neuronal loss and gliosis within mammillary body and medial thalamus. These results demonstrate that a single episode of thiamine deficiency can selectively damage cortical white matter tracts while sparing the thalamus and mammillary body and may be a critical factor responsible for the pathological and behavioral changes observed in alcoholics without Wernicke's encephalopathy.

Alcoholism↗

PubMed1992

Shoshin beriberi in an infant of a thiamine-deficient mother.

The classical form of thiamine deficiency in children is comprised of peripheral neuropathy, encephalopathy and high-output cardiac failure, predominantly right-sided. "Shoshin beriberi" cardiac failure has a different presentation, with vasoconstriction, hypotension and severe metabolic acidosis. A three-month breast-fed infant developed these features (biochemical tests confirmed the diagnosis). His mother, although non-symptomatic, had biochemical evidence of thiamine deficiency.

Adult↗