Showing papers on "Thiamine published in 1991"
TL;DR: Preliminary findings suggest that long-term furosemide therapy may be associated with clinically significant thiamine deficiency due to urinary loss and contribute to impaired cardiac performance in patients with CHF.
197 citations
TL;DR: It is recommended that dietary thiamine supplementation be initiated in all newly diagnosed cases of AIDS or AIDS-related complex and the difficulties of clinical diagnosis of Wernicke's Encephalopathy.
Abstract: Several neuropathological reports in the last 5 years have described brain lesions characteristic of Wernicke's Encephalopathy in patients with AIDS. Using the erythrocyte transketolase activation assay, we now report biochemical evidence of thiamine deficiency in 9/39 (23%) of patients with AIDS or AIDS-related complex. In no cases was there history of alcohol abuse nor were there clinical signs of Wernicke's Encephalopathy. Thiamine deficiency in these patients most likely results from the cachexia and catabolic state characteristic of AIDS. In view of (i) the confirmed neuropathological evidence of Wernicke's Encephalopathy in AIDS patients, (ii) the significant thiamine deficiency in these patients and (iii) the difficulties of clinical diagnosis of Wernicke's Encephalopathy, it is recommended that dietary thiamine supplementation be initiated in all newly diagnosed cases of AIDS or AIDS-related complex.
89 citations
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TL;DR: Sulfide concentrations progressively increased in all 9 calves after the feeding of the PEM-inducing diet commenced and were significantly higher in the calves that developed PEM than in those that did not, suggesting that PEM can result from sulfide toxicosis following excess production of sulfide in the rumen.
Abstract: Nine 115- to 180-kg, hay-adapted, Holstein steers were fed an experimental diet with added sodium sulfate that induces polioencephalomalacia (PEM). Five calves developed the disease. Thiamine concentrations in blood, CSF, brain, and liver were not indicative of thiamine deficiency. The odor of hydrogen sulfide in eructated rumen gas was associated with the onset of PEM. Sulfide concentrations in rumen fluid were measured 1 or 2 times a week by 2 techniques. Sulfide concentrations progressively increased in all 9 calves after the feeding of the PEM-inducing diet commenced. The highest concentrations coincided with the onset of clinical signs of PEM and were significantly higher in the calves that developed PEM than in those that did not. This suggests that PEM can result from sulfide toxicosis following excess production of sulfide in the rumen.
86 citations
TL;DR: The hypothesis that long-term administration of thiamine at 3 g/d might slow the progression of dementia of the Alzheimer's type is not supported and overall means for the Mini-Mental State Examination, verbal learning, and naming scores decreased significantly over the 12-month study period.
Abstract: Because a previous short-term study demonstrated a statistically significant, but not clinically important, improvement in cognitive test scores during thiamine treatment in patients with dementia of the Alzheimer's type, a 12-month, double-blind, parallel-group study was conducted to examine whether long-term administration of thiamine at 3 g/d might slow the progression of dementia of the Alzheimer's type Fifteen subjects were enrolled and 10 completed the 1-year study Data are available for two additional subjects through the first 9 months of study No significant differences were found between the placebo and thiamine groups at any point during the study In both groups, overall means for the Mini-Mental State Examination, verbal learning, and naming scores decreased significantly over the 12-month study period These results do not support the hypothesis that long-term administration of thiamine at 3 g/d might slow the progression of dementia of the Alzheimer's type
62 citations
TL;DR: The authors report a case of severe lactic acidosis in a 3-year-old boy, after 20 days of total parenteral nutrition without vitamin supplementation, which led to a complete recovery within 5 days and no sequelae were noted after 12 months.
Abstract: The authors report a case of severe lactic acidosis in a 3-year-old boy, after 20 days of total parenteral nutrition without vitamin supplementation. This child with acute lymphoblastic leukemia underwent a period of severe refractory lactic acidosis (pH between 6.81 and 7.00 and a serum lactate level up to 38 mmol/liter) leading to cardiac arrest. After the initial resuscitation and the subsequent treatment of shock and vitamin K deficiency, acute peritoneal dialysis was instituted to correct the severe lactic acidosis. Initial low plasma thiamine levels confirmed the diagnosis of thiamine deficiency. An associated transient pancreatic dysfunction was also noted. The patient's overall course with thiamine replacement therapy led to a complete recovery within 5 days and no sequelae were noted after 12 months.
59 citations
TL;DR: No effect on BMS of vitamin replacement therapy or placebo therapy could be demonstrated and patients with therapy-resistant burning mouth syndrome were given replacement therapy.
Abstract: The aim of the study was to determine, in a group of patients with therapy-resistant burning mouth syndrome (BMS), the possible deficiency of vitamins B1, B2, and B6 and the effect of proper vitamin replacement therapy. Sixteen individuals, aged 47 to 81 years, participated in the study. All underwent a base-line examination comprising anamnestic information, subjective assessment of symptoms, dietary registration, salivary analysis, and serum analysis of thiamine (B1), riboflavine (B2), and pyridoxine (B6). Fifteen individuals had low thiamine and/or riboflavine levels in accordance with suggested levels in the literature and were given replacement therapy. No effect on BMS of vitamin replacement therapy or placebo therapy could be demonstrated.
58 citations
TL;DR: The thiamine metabolism in Schizosaccharomyces pombe is investigated and it is shown thatThiamine-repressible acid phosphate, coded for by the gene pho4, dephosphorylates thiamines phosphates indicating that the enzyme acts as a Thiamine phosphate phosphatase.
Abstract: We have investigated the thiamine metabolism in Schizosaccharomyces pombe and shown that: (1) Thiamine-repressible acid phosphate, coded for by the gene pho4, dephosphorylates thiamine phosphates indicating that the enzyme acts as a thiamine phosphate phosphatase. (2) In vivo synthesized thiamine is present intracellulary mainly as thiamine diphosphate. Starving cells for glucose decreases the intracellular thiamine pool. (3) The genes thi2, thi3 and thi4 control thiamine biosynthesis and probably code for thiamine biosynthetic enzymes. Thi3, which is involved in the synthesis of the pyrimidine moiety of the thiamine molecule, is allelic to the thiamine repressible gene nmt1. (4) Thiamine uptake is a thiamine regulated process, probably occurs by active transport and is controlled by the gene ptr1.
54 citations
TL;DR: In this article, the pyridine moiety of thiamine pyrophosphate (TPP) has been investigated in the context of resynthesizing and incubation with the apoenzymes of pyruvate decarboxylase, pyruve dehydrogenase complex and transketolase.
46 citations
Journal Article•
TL;DR: The results suggest that in thiamine deficiency the insulin secretion is impaired due to the decreased glucose oxidation.
Abstract: Isolated pancreatic islets from thiamine deficient rats secrete less insulin. The secretion of insulin in response to glucose and tolbutamide is also decreased in these islets. Glucose and pyruvate oxidations to CO2, were decreased in the islets isolated from thiamine deficient rats. In the islets from control but not from thiamine deficient rats the oxidations of glucose and pyruvate to CO2 were increased by tolbutamide. The results suggest that in thiamine deficiency the insulin secretion is impaired due to the decreased glucose oxidation.
45 citations
TL;DR: The transcriptional activity of the thiamine-sensitive gene nmt1 as a function of intracellularThiamine concentration is studied and it is shown that transcription of this gene is rapidly repressed as the internal thienine concentration rises and is only reactivated as the concentration falls to below about 50 pmoles/107 cells.
Abstract: Wild-type fission yeast, growing in minimal medium, actively synthesizes thiamine and maintains an internal concentration which we have measured to be around 10 pmoles/107 cells. If thiamine is added to such cultures it is rapidly sequestered by the cell, and if added in excess (20μM) the internal concentration of thiamine rises almost 1000-fold to a maximum of around 9000 pmoles/107 cells before the transport mechanism is shut down. The kinetics of decay of intracellular thiamine to the basal level are consistent with simple dilution as the cell mass doubles. In parallel with this analysis, we have studied the transcriptional activity of the thiamine-sensitive gene nmt1 as a function of intracellular thiamine concentration. Transcription of this gene is rapidly repressed as the internal thiamine concentration rises and is only reactivated as the concentration falls to below about 50 pmoles/107 cells.
43 citations
TL;DR: The results suggest that the utilization and synthesis of thiamine in Saccharomyces cerevisiae is controlled negatively by the intracellularThiamine pyrophosphate level.
Abstract: We identified a strain carrying a recessive constitutive mutation (thi80-1) with an altered thiamine transport system, thiamine-repressible acid phosphatase, and several enzymes of thiamine synthesis from 2-methyl-4-amino-5-hydroxymethylpyrimidine and 4-methyl-5-beta-hydroxyethylthiazole. The mutant shows markedly reduced activity of thiamine pyrophosphokinase (EC 2.7.6.2) and high resistance to oxythiamine, a thiamine antagonist whose potency depends on thiamine pyrophosphokinase activity. The intracellular thiamine pyrophosphate content of the mutant cells grown with exogenous thiamine (2 x 10(-7) M) was found to be about half that of the wild-type strain under the same conditions. These results suggest that the utilization and synthesis of thiamine in Saccharomyces cerevisiae is controlled negatively by the intracellular thiamine pyrophosphate level.
TL;DR: It was concluded that inorganic sulphur was associated with polioencephalomalacia, and that dietary thiamine may decrease the severity of lesions in some affected areas of the central nervous system.
Abstract: Fifty-six female crossbred two-month-old lambs were housed in individual cages, and fed a basic ration of barley (59%), soybean meal (5%), and alfalfa (32%) prepared to meet NRC nutrient requirements. Four percent of the diet contained a standard salt mix to which the factors inorganic sulphur (S) and thiamine (B1) were added. Four treatment groups were used: low sulphur and normal thiamine (0.19% S, 13.7 mg/kg B1) low sulphur and high thiamine (0.19% S, 243 mg/kg B1), high sulphur and normal thiamine (0.63% S, 13.7 mg/kg B1), high sulphur and high thiamine (0.63% S, 243 mg/kg B1). All animals had free access to water and were offered 1 kg/animal/day of diet for 14 weeks, when necropsy was undertaken. Seven lambs fed unsupplemented (normal B1) diets containing added sulphur developed clinical symptoms of polioencephalomalacia (PEM) between the 3rd and 7th week of the trial. Morbidity (P less than 0.013) and mortality (P = 0.08) differences were attributed to S administration. None of the B1 supplemented lambs developed clinical signs of PEM. Body weight and relative organ weights did not differ among treatment groups. Serial sections of all brains were examined grossly and microscopically. Nonparametric statistical analysis revealed sulphur related effects in the cerebrum, midbrain and hindbrain (P less than 0.0001), no thiamine-related effects or interaction between the factors were seen, except in the amygdaloid body. It was concluded that inorganic sulphur was associated with polioencephalomalacia, and that dietary thiamine may decrease the severity of lesions in some affected areas of the central nervous system.
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TL;DR: The possibility of thiamine deficiency must be considered in patients on chronic dialysis who present with central nervous system disturbances, even if all of the classical features of Wernicke's encephalopathy are not present.
Abstract: We report the case of a patient with terminal renal disease on chronic hemodialysis who developed acute thiamine deficiency as confirmed by erythrocyte transketolase determinations. The patient presented with a confusional state and severe memory disturbances, but other classical features of Wernicke's encephalopathy were absent. Almost all central nervous system symptoms rapidly disappeared after thiamine therapy. Therefore the possibility of thiamine deficiency must be considered in patients on chronic dialysis who present with central nervous system disturbances, even if all of the classical features of Wernicke's encephalopathy are not present.
TL;DR: In this paper, a total of 157 epileptic patients were studied with respect to (1) biogenic amine precursors and metabolites in the CSF, (2) levels of folate and thiamine in the blood, (3) length of treatment with phenytoin (PHT), (4) PHT intoxication, and (5) CNS atrophy.
Abstract: A total of 157 epileptic patients were studied with respect to (1) biogenic amine precursors and metabolites in the CSF, (2) levels of folate and thiamine in the blood and CSF, (3) length of treatment with phenytoin (PHT), (4) PHT intoxication, (5) CNS atrophy. Alterations in CSF amine metabolite levels were related primarily to PHT intoxication, and low CSF folate and thiamine levels, but not to length of treatment or CNS atrophy. PHT intoxication increased CSF 5-hydroxyindoleacetic acid (5HIAA). Low folate levels were associated with decreased CSF 5HIAA and homovanillic acid, while low thiamine levels were associated with decreased CSF 5HIAA and 3-methyoxy-4-hydroxyphenylethylene glycol. It remains to be seen to what extent these alterations in biogenic amine metabolism, mediated by low CNS vitamin levels, also lead to deficits in cerebral function.
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TL;DR: The results suggest that the biosynthesis of insulin is impaired in thiamine deficiency, and even tolbutamide could not increase the biosynthesisation of insulin in this condition.
Abstract: The effect of thiamine deficiency on insulin biosynthesis was studied. In thiamine deficient rats the total pancreatic protein content was not altered when compared to control rats whereas the pancreatic insulin content was decreased. Though the in vivo incorporation of 3H-leucine and the in vivo conversion of U-14C-glucose into proinsulin and insulin were not affected in thiamine deficient rats, the tolbutamide induced increased in vivo incorporation of 3H-leucine and in vivo conversion of U-14C-glucose into proinsulin and insulin was not seen in thiamine deficient rats. These results suggest that the biosynthesis of insulin is impaired in thiamine deficiency. Even tolbutamide could not increase the biosynthesis of insulin in this condition.
TL;DR: An adult with Crohn's disease on home total parenteral nutrition (TPN) for 8 months presented with peripheral neuropathy and ataxia and a prompt symptomatic response to intravenous thiamine suggests that the patient had the chronic form of dry beriberi.
Abstract: An adult with Crohn's disease on home total parenteral nutrition (TPN) for 8 months presented with peripheral neuropathy and ataxia. The patient was found to be deficient of thiamine. A prompt symptomatic response to intravenous thiamine suggests that the patient had the chronic form of dry beriberi. To our knowledge, this variety of beriberi in a patient on TPN has not previously been reported. (Journal of Parenteral and Enteral Nutrition15: 200-201, 1991)
TL;DR: It appears that thiamine deficiency may provoke epileptic phenomena in those patients who have subclinical predisposition for seizures, and the presence of irritative activity on electroencephalographic recordings in the patients may be a consequence of a vitamin B1 deficiency state.
Abstract: Sixteen of 50 consecutive neurological patients with a diagnosis of thiamine deficiency showed epileptic (10) or epileptiform (6) manifestations. A survey of the literature revealed only few reports o
TL;DR: Electrically-stimulated, Ca2+-dependent release of glutamate from hippocampal slices obtained from symptomatic pyrithiamine-treated rats was significantly decreased compared to pair-fed controls and there is evidence to suggest that the latter mechanism with ensuing excitotoxic neuronal damage could be involved in the pathogenesis of selective neuronal death in thiamine deficiency.
Abstract: Alterations of excitatory amino acids in brain may be of pathophysiological significance in thiamine-deficiency encephalopathy. The present study was undertaken to evaluate the effects of thiamine deficiency induced by the central thiamine antagonist, pyrithiamine, on the glutamate content of glutamatergic nerve terminals. Electrically-stimulated, Ca2+-dependent release of glutamate from hippocampal slices obtained from symptomatic pyrithiamine-treated rats was significantly decreased compared to pair-fed controls. Possible explanations for the decreased “neurotransmitter pool” of glutamate in thiamine-deficient rat brain include decreased synthesis of glutamate as a result of decreased activities of the thiamine-dependent enzyme α-ketoglutarate dehydrogenase or increased release of glutamateper se. There is evidence to suggest that the latter mechanism with ensuing excitotoxic neuronal damage could be involved in the pathogenesis of selective neuronal death in thiamine deficiency. Similar mechanisms could be implicated in Wemicke's encephalopathy in humans.
TL;DR: It has been concluded that thiamine enhances elimination of Pb from the body and this feature may be beneficial in chelation therapy.
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TL;DR: Significant relationship existed between number of days from Pb exposure to slaughter and concentration of Pb in blood, liver, and skeletal muscles and treatment with thiamine was more effective than treatment with Na2,Ca-EDTA orThiamine plus Na1,Ca,EDTA in inducing remission of clinical signs of plumbism.
Abstract: Twenty mature Holstein cows were randomized into 5 treatment groups. Cows of groups 2 to 5 were given 2 mg of elemental Pb/kg of body weight for 28 days. Clinical signs of plumbism were scored, and blood for Pb, progesterone, and hematologic analyses was collected weekly. Cows also were examined weekly for anomalous ovarian cycles. Starting on study day 28, cows in group 3 were treated once daily with 2 mg of thiamine HCl/kg (IM) for 13 days, cows in group 4 were treated twice daily with 62 mg of Na2,Ca-EDTA/kg (IV) for 4 days, and cows in group 5 were given thiamine (dosage regimen the same as for group 3) plus Na2,Ca-EDTA (dosage regimen the same as for group 4). On study days 96 through 139, cows were slaughtered in a commercial abattoir and samples of blood, skeletal muscles, bones, liver, and kidneys were collected and assayed for Pb concentration. Thiamine was not effective in reducing blood Pb concentration, and treatment with Na2,Ca-EDTA and thiamine plus Na2,Ca-EDTA was effective in reducing the concentration of Pb in blood. However, treatment with thiamine was more effective than treatment with Na2,Ca-EDTA or thiamine plus Na2,Ca-EDTA in inducing remission of clinical signs of plumbism. The concentration of Pb in blood was significantly (P less than 0.05) correlated to the concentration of Pb in liver, kidneys, skeletal muscles, and bones. Significant (P less than 0.05) relationship existed between number of days from Pb exposure to slaughter and concentration of Pb in blood, liver, and skeletal muscles. Exposure to Pb did not significantly alter CBC values.(ABSTRACT TRUNCATED AT 250 WORDS)
TL;DR: A population study was undertaken to survey the distribution of sulfate levels in water and thiamine status of beef cattle on Saskatchewan farms and the relationship between high sulfate in the drinking water and bloodThiamine concentration in feedlot cattle was examined.
Abstract: A population study was undertaken to survey the distribution of sulfate levels in water and thiamine status of beef cattle on Saskatchewan farms. Fifty farms took part in this study. The sampled animals represented all major breeds raised in Saskatchewan. The sulfate content in drinking water varied greatly across the province ranging from 70 to 3200 ppm. Approximately 43% of the farms from southern and central parts of the province had water with sulfate concentration exceeding 1000 ppm. The concentration of blood thiamine was (mean ± SD) 24.9 ± 10.1 μg L−1. Subsequently, a comparative study was undertaken to examine the relationship between high sulfate in the drinking water and blood thiamine concentration in feedlot cattle. The farms with high (> 1000 ppm) and low (< 200) levels of sulfate in the water were used for the comparative study. Blood thiamine concentrations differed (P < 0.0001) between beef cattle drinking low sulfate-water and those drinking high sulfate-water and were 47.3 ± 9.8 and 37.9...
TL;DR: Nicotinic acid, pyridoxine, and picloram were stable in a liquid MS culture medium during autoclaving and during cell-free incubation in the dark at 5°C or 25°C for up to 6 weeks, and thiamine loss under the same conditions was 16% at 5 °C and 18% at 25 °C.
Abstract: Nicotinic acid, pyridoxine, and picloram were stable in a liquid MS culture medium (pH 5.5–5.6) during autoclaving and during cell-free incubation in the dark at 5°C or 25°C for up to 6 weeks. Thiamine loss under the same conditions was 16% at 5°C and 18% at 25°C. Five percent of the sucrose in the liquid medium was hydrolyzed during autoclaving. During cell-free incubation in the light (100 μE m−2 s−1) at 25°C, pyridoxine was not detected after 6 days, while 78% of the picloram and 56% of the thiamine were degraded after 6 weeks. All of the niacin and pyridoxine, 13% of the picloram and 42% of the thiamine in a liquid MS culture medium were utilized in 4 days by potato (cv. Lemhi Russet) tuber suspension cultures growing in the dark at 25°C.
TL;DR: Electromyographic evaluation revealed significant reductions of motor and sensory conduction velocities in the alcoholic group, consistent with a contributory (but not exclusive) role of thiamine deficiency in the pathogenesis of alcoholic peripheral neuropathy.
Abstract: Thiamine status was evaluated using the erythrocyte transketolase activation assay in 20 alcoholic patients admitted on a voluntary basis to a Detoxification Unit. Electromyographic evaluation revealed significant reductions of motor and sensory conduction velocities in the alcoholic group. 38% of alcoholic patients showed significant erythrocyte transketolase activation deficits indicative of severe thiamine deficiency. In the case of peroneal nerve, reduced conduction velocities were negatively correlated with abnormal transketolase parameters. These findings are consistent with a contributory (but not exclusive) role of thiamine deficiency in the pathogenesis of alcoholic peripheral neuropathy. Deficiencies of other vitamins as well as direct neurotoxic effects of alcohol could also be involved in this phenomenon.
TL;DR: The gradient system avoids the use of a modifier and an ion-pairing reagent and can be used for screening of thiamine deficiency and for clinical study of various diseases related to vitamin B1 deficiency.
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TL;DR: Thiamine responsive anemia in a three years old boy with the characteristic association of anemia, diabetes mellitus and deafness is reported, and etiology of the syndrome is not only a thiamine pyrophosphokinase deficiency as previously suggested.
Abstract: We report a new case of thiamine responsive anemia in a three years old boy with the characteristic association of anemia, diabetes mellitus and deafness. Thiamine therapy corrected anemia as described. A thiamine pyrophosphokinase deficiency (TPK) was found which was not influenced by treatment. However normal levels of thiamine pyrophosphate (TPP) were obtained without correction of all symptoms particularly dyserythropoiesis. Thus, etiology of the syndrome is not only a thiamine pyrophosphokinase deficiency as previously suggested.
TL;DR: The crystal structures of Zn(thiamine) and Cd(cadmium) have been determined by X-ray diffraction methods as discussed by the authors, where the zinc complex 1 forms a discrete structure in which the tetrahedral ZnII ion is bonded by the pyrimidine ring nitrogen N(I′) and three thiocyanato ligands through nitrogen atoms.
TL;DR: Results showed that alcohol-treated mice exhibited a behavioral impairment in a sequential alternation task characterized by a progressive decay of alternation rates as a function of the number of trials; such a deficit was not observed in controls and thiamine-deficient subjects.
TL;DR: A general trend toward a slower T pyroph phosphorylation and a faster T phosphate dephosphorylation was observed in the small intestine, kidney, heart and liver, and Skeletal muscle was unaffected.
Abstract: The effects of chronic ethanol administration on different steps in the metabolism of thiamine (T), thiamine mono- (TMP) and pyrophosphate (TPP) were determined in vivo in the liver, kidney, heart, skeletal muscle and small intestinal mucosa. The radioactivity of T and its phosphoesters was measured in plasma and in the selected organs under steady-state conditions and at fixed time intervals (0.25–240 hr) after an i.p. injection of Thiazole-[2-14C]-thiamine (30 (μg: 1.25 μCi) in rats chronically (35 days) ethanol-treated (daily dose of 4.7 g kg− body wt by gastric gavage). Two types of controls were used: pair-fed rats treated with a sucrose solution isoenergetic with ethanol, and water-treated rats. A nutritionally adequate diet, which supplied an excess of thiamine, was given to the rats, producing a virtually steady content of thiamine compounds in the tissues. The analytical data obtained were elaborated using appropriate compartmental mathematical models, which allowed the fractional rate constants, turnover rates and turnover times to be calculated.
Alterations in thiamine metabolism were modest and differed according to the organs. The most widespread modification was to facilitate the entry of T (small intestine, kidney and heart) or TMP (small intestine and kidney), while no significant change of T and TMP release was seen. Sucrose had minimal effect in both steps. Enzymatic transformations of thiamine were likewise marginally affected. A general trend toward a slower T pyrophosphorylation and a faster T phosphate dephosphorylation was observed in the small intestine, kidney, heart and liver. Skeletal muscle was unaffected. These results seem to indicate an imbalance in the dynamics of thiamine, which may eventually lead to a decreased concentration of the phosphorylated forms. On the contrary, sucrose administration did not alter thiamine metabolism.
TL;DR: The crystal structure of [Mn(thiamine)Cl2(H2O)]2[thiamines]2Cl4·2H 2O has been determined by X-ray diffraction methods as mentioned in this paper.