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PubMedDate not supplied

Postgastrectomy polyneuropathy with thiamine deficiency is identical to beriberi neuropathy.

OBJECTIVE: We assessed whether postgastrectomy polyneuropathy associated with thiamine deficiency is clinicopathologically identical to beriberi neuropathy, including a biochemical determination of thiamine status. METHODS: Clinicopathologic features of 17 patients who had postgastrectomy polyneuropathy with thiamine deficiency were compared with those of 11 patients who had thiamine-deficiency neuropathy caused by dietary imbalance. RESULTS: The typical presentation for the two etiologies was as a symmetric sensorimotor polyneuropathy predominantly involving the lower limbs. A variety of clinical features, including neuropathic symptoms, progression, and coexistence of heart failure or Wernicke's encephalopathy, was seen similarly in both conditions. In both groups, the main electrophysiologic findings were those of axonal neuropathy, most prominently in the lower limbs. Sural nerve biopsy specimens also indicated axonal degeneration in both groups. Subperineurial edema was commonly observed. CONCLUSION: This study showed that thiamine-deficiency neuropathies due to gastrectomy and dietary imbalance are identical despite variability in their clinicopathologic features and suggested that thiamine deficiency can be a major cause of postgastrectomy polyneuropathy.

Beriberi↗
PubMed1981

The effect of thiamine deficiency on local cerebral glucose utilization.

Rats maintained on a thiamine-free diet for two to seven weeks and control animals were studied by the [14C]deoxyglucose technique prior to the development of histological lesions. This technique permits measurement of local cerebral glucose utilization (LCGU) in discrete nuclei and tracts. Levels of thiamine in brain and blood were also determined. In the 41 central nervous system (CNS) structures in which it was measured, cerebral glucose utilization decreased with diminishing concentration of cerebral thiamine. Thus, the primary metabolic consequence of thiamine deficiency is a widespread reduction in cerebral glucose utilization. Furthermore, with decreasing cerebral thiamine concentrations, glucose utilization declined more rapidly in many of the structures which in humans develop histological lesions with prolonged thiamine deficiency than in structures less susceptible to the development of lesions. One determinant of the specific distribution of histological lesions occurring in human thiamine deficiency may be the variable rate at which the CNS structures lose their metabolic activity with continuing thiamine deficiency.

Animals↗
PubMed1977

[Thiamine deficiency in chronic alcoholics. Value of pre- and postoperative treatment].

Thiamine deficiency in the chronic alcoholic would appear to have a triple origin: inadequate intake, absorption and utilisation. Its consequences are well known: peripheral neuropathy, WERNICKE and KORSAKOFF type encephalopathies and cardiac problems (with asystole at the extreme). The active principle of thiamine, TPP or cocarboxylase, is involved as a coenzyme of pyruvate decarboxylase and of alphaketoglutarate decarboxylase in the ocidative decarboxylation reactions of the Krebs cycle. TPP is involved as a coenzyme of transketolase in the transketolisation reactions of the pentose pathway. The stimation of transketolase demonstrates a deficiency in thiamine. Fourteen patients suffering from surgical ENT malignancies were involved in the present study. Seven patients received vitamin B therapy before and after the operation. The results showed a significant decrease in thiamine deficiency. Seven were used as controls and did not receive vitamin B therapy. Transketolase estimations showed and increase in the deficiency. Thiamine deficiency exists in the chronic alcoholic and may be corrected by the administration of B vitamins.

Alcoholism↗
PubMed1982

Sleep and indolamine alterations induced by thiamine deficiency.

Behavioral, polygraphic, biochemical and histological aspects of thiamine deficiency in rats induced by thiamine-deficient food and pyrithiamine treatment (40 mg/kg daily for 4 days) are described. Behavioral alterations were essentially characterized by ataxia, pilo-erection and paresis. Polygraphic data indicated an increase in slow-wave sleep (SWS) of 33% and decreases in paradoxical sleep (PS) and wakefulness (W), respectively, of 69% and 27%. These effects were reversed by complete food and thiamine administration, the reversal including an overshoot in PS. Biochemical assays, performed when the polygraphic data indicated a large effect, demonstrated a significant increase in serotonin (5-HT) and 5-hydroxyindolacetic-acid (5-HIAA). These effects were particularly evident in the raphe system and the locus coeruleus. Histological data from the raphe dorsalis displayed a notable increase in yellow fluorescence in pyrithiamine-treated animals over controls. We conclude from these experiments that a deficiency in thiamine affects the serotonergic system and that the subsequent effects on sleep are a consequence of this serotonergic change.

Animals↗
PubMed1978

[Muricide induced by thiamine deficiency in the rats (author's transl)].

The emotional behavioral aspects and the interaction between the changes of the polyamine contents and muricide response in thiamine deficient rats were investigated. In the thiamine deficient group, there was evidence of muricide and such increased progressively with advanced thiamine deficient feeding. This muricide was characteristic in the following respects; 1) the killer-rats did not eat but only kill a mouse and it was quite difficult to remove a sacrificed animal from the cage. 2) they bit at random into any body region of the mouse. 3) the killer-rats did not bite inanimate objects such as nails nor chalk. 4) the muricide induced by thiamine deficiency could not be suppressed by a single injection of thiamine HCl. On the 30th day of the experimental feeding, both spermidine and spermine levels in the brain of the thiamine deficient group decreased significantly as compared to the control and the pair-fed groups. Both spermidine and spermine levels were reversed to the control levels with a intraperitoneal administration of thiamine. There were no significant differences in spermine and spermidine levels between the killer-rats and non-killer-rats in the thiamine deficient group.

Aggression↗
PubMed1981

Impairment of behavior and acetylcholine metabolism in thiamine deficiency.

After only 1 day of treatment with a thiamine-deficient diet and pyrithiamine, a centrally and peripherally acting thiamine antagonist, 37.5% of rats performed poorly on a standardized string test. By day 12, 89.6% of the pyrithiamine-treated rats, but only 8.1% of the pair-fed controls, had decreased string test scores. Scores for rats treated with a thiamine-deficient diet and oxythiamine, a peripherally acting thiamine antagonist, did not decrease even on the day before death. The acetylcholinesterase inhibitor physostigmine improved the low string test scores in 69.2% of trials with the pyrithiamine-treated rats, whereas neostigmine, which acts peripherally, had no effect. The effect of physostigmine was inhibited by the muscarinic blocker atropine, but not by methatropine, its peripherally acting analog. Arecoline, a direct muscarinic agonist, was as effective as physostigmine or thiamine in restoring string test performance. Nicotine had no effect and the nicotinic blocker mecamylamine did not alter the effect of physostigmine. Incorporation of [2H4]choline and [U-14C]glucose into acetylcholine was decreased by 32 and 48%, respectively, relative to pair-fed controls after 12 days of pyrithiamine treatment. Acetylcholine levels were unchanged. Thiamine deficiency induces an early functionally significant central muscarinic cholinergic lesion.

Acetylcholine↗
PubMedDate not supplied

Evaluation of a clinical screening instrument to identify states of thiamine deficiency in inpatients with severe alcohol dependence syndrome.

AIMS: To develop a Thiamine Deficiency Questionnaire (TDQ), and to assess its reliability in the identification of Thiamine deficiency, in patients with severe alcohol dependence. METHODS: 58 severely alcohol dependent patients underwent socio-demographic, medical, psychiatric, and alcohol use assessment, including administration of the Thiamine Deficiency Questionnaire (TDQ). The Red Blood Cell Thiamine Pyrophosphate concentration provided the 'gold standard' to test the validity of the instrument. Univariate 2 x 2 diagnostic test tables and multivariate analysis were performed. RESULTS: A set of eight questionnaire items had an overall predictive power of 73.7%. Two of these were highly specific: 'missed meals due to lack of funds', and the clinical co-occurrence of medical conditions potentially related to poor nutrition. The Michigan Alcohol Screening Test and serum gamma glutamyl transferase were moderately predictive. CONCLUSIONS: Screening that combines socio-demographic, clinical and biological factors, and/or standardized questionnaires, could improve early recognition of thiamine deficiency.

Adult↗
PubMed1989

Brain glutamate and gamma-aminobutyrate (GABA) metabolism in thiamin-deficient rats.

The brain metabolism of glutamate and gamma-aminobutyrate (GABA) was investigated in thiamin-deficient and pair-fed control rats, in order to determine whether the GABA shunt may provide an important alternative to 2-oxo-glutarate dehydrogenase (EC 1.2.4.2) in energy-yielding metabolism in thiamin deficiency. Brains from thiamin-deficient animals contained less glutamate, 2-oxo-glutarate and GABA than those from control animals. The brain content of ATP was unaffected by thiamin deficiency. After intracerebroventricular injection of [14C]glutamate, the specific radioactivity of GABA in the brains from deficient animals was 45-50% higher than that in controls, suggesting a considerable increase in the metabolic flux through the GABA shunt in thiamin deficiency. Brain GABA showed a marked circumannual variation, with a peak in mid-summer and a minimum value in mid-winter.

Animals↗
PubMed1987

Effects of decarboxylase inhibitors on muricidal suppression by L-dopa in thiamine deficient rats.

Male Wistar rats maintained on a thiamine deficient diet showed mouse-killing behavior (muricide). On the 30th day of experimental feeding, the incidence of the muricide was 70%. Intraperitoneal (i.p.) injection of 3-(3,4-dihydroxyphenyl)-l-alanine (l-dopa) suppressed the muricide in a dose-dependent manner. This suppressive effect was potentiated with carbidopa, but was quite reduced by pretreatment with alpha-monofluoromethyldopa or FLA-63. These results indicated that the effect of l-dopa was dependent on its decarboxylation, and its conversion to noradrenaline (NA) essential for muricidal suppression in the brain. The NA precursors, l-dopa, l-threo-dops or maprotiline and Y-8894, which can increase the availability of synaptic catecholamines (CA), also showed muricidal suppression. CA depletors (alpha-methyl-p-tyrosine, FLA-63 and alpha-monofluoromethyl-p-tyrosine) did not significantly increase the incidence of muricide induced by thiamine deficiency nor decrease the number of killer-rats. These findings suggest that brain CA may not participate in the mediation of muricide induced by thiamine deficiency in this experiment, but such muricide can be pharmacologically characterized by the effects which are brought about by catecholaminergic agents.

Aggression↗
PubMed1996

[Failure in self care and heart failure, thiamine deficiency in geriatric patients].

In two patients admitted to a geriatric ward cardiac failure was based on a thiamine deficiency (wet beri-beri). After supplementation with thiamine they recovered completely. The first patient had a insufficient diet of only canned food, whereas the second patient suffered from both alcoholism and insufficient nutrients. These geriatric patients suffered from a serious illness due to a combination of somatic, psychological, functional en social factors. Thiamine is a co-enzyme in many metabolic processes. A thiamine deficiency is defined as a serum concentration below 95 nmol/1. Other diseases associated with thiamine deficiency are the Wernicke-Korsakoff syndrome and peripheral polyneuropathy (dry beri-beri). Not only alcoholics but also elderly patients with malnutrition are at risk of thiamine deficiency and associated diseases. Do not hesitate to supplement thiamine in case of cardiac failure because of possible thiamine deficiency.

Aged↗
PubMed1990

Hypothesis and case reports: possible thiamin deficiency.

Three family members are reported with functional symptoms considered to be caused by intracellular deficiency of thiamin. Persistence of desaturation of erythrocyte transketolase in the face of megadose thiamin hydrochloride (THCl), accompanied by a balanced multivitamin and mineral formula, suggested a familial thiamin dependency state. Each of three individuals responded clinically to the administration of thiamin tetrahydrofurfuryl disulfide (TTFD), and erythrocyte transketolase (TKA) became fully saturated with thiamin pyrophosphate (TPP). Dysautonomic symptoms observed are compared with those seen in classical beriberi, the nutritional prototype for dysautonomia, and changes in blood pressure are described which support this premise. Although there is no proof from the laboratory, it is hypothesized that the biochemical lesion might be due either to malabsorption of thiamin or its inadequate phosphorylation.

Adult↗
PubMed1985

Ocular signs in thiamine-deficient monkeys and in Wernicke's disease in humans.

Thiamine deficiency in the monkey is the animal counterpart of Wernicke's disease in humans. In the present study, thiamine deficiency was induced in 11 monkeys while three monkeys were given paired feedings supplemented by thiamine hydrochloride and three monkeys were maintained on regular chow. The typical clinical symptoms were apathy, inattention to peripheral stimuli, ataxia, ptosis, mydriasis progressing to pupillary areflexia, nystagmus, and ophthalmoparesis progressing to total ophthalmoplegia. With thiamine treatment, recovery was prompt and complete in mild to moderate cases but delayed and incomplete in severe cases. The animals were killed six or more months after discontinuance of the experiments to determine the chronic effects of treated thiamine deficiency. The significant abnormalities in the brain stem were symmetric gliosis and neuronal loss in the inferior colliculi, the regions of the third and sixth nerve nuclei, and the medial vestibular nuclei. White matter was characteristically spared. With the exception of the inferior colliculi, the target sites for neuropathologic changes were the centers for ocular motor control.

Animals↗
PubMed1990

Effect of thiamin deficiency on energy metabolites in the turkey.

The effects of thiamin deficiency on selected energy-related metabolites was investigated. A basal diet (B) was formulated to be 11% of NRC recommended level of 2 mg/kg of thiamin. Thiamin was added to this basal diet to generate the control diet (C). Twenty one-week-old female turkeys were fed either the B or C diet. On days four and five of the experiment, food intake was decreased significantly in B fed turkeys (P < 0.05). Plasma and brain samples were collected at this time. Brains were dissected and analyzed for ATP, ADP, uric acid, free fatty acids, glucose, and GABA. Adenosine triphosphate and the ATP/ADP ratio were decreased in the hindbrain (medulla-pons area) of thiamin deficient birds (P < 0.01). Uric acid was increased (P < 0.001) and free fatty acids were decreased (P < 0.0005) in the plasma of thiamin deficient birds. Based on the data, changes in ATP and ATP/ADP levels may be related to the anorectic behavior exhibited by the thiamin deficient bird.

Journal Article↗
PubMed1984

Lactate and pyruvate production in isolated thiamine-deficient rat diaphragm strips.

Rats were maintained on a thiamine-deficient diet to deplete skeletal muscle of thiamine pyrophosphate, and thus decrease the oxidative metabolism of pyruvate. The blood lactate concentration was significantly elevated in thiamine-deficient (TD) animals when compared with pair-fed (TP) controls. Analysis of diaphragm strips from these animals revealed that tissue lactate and pyruvate concentrations were not affected by any of the treatments employed. The rate of lactate efflux from TD tissues was, however, twice that from TP and 4.5 times that from weight-control (WC) tissues. The H+ efflux rate was also much greater in the TD muscle preparation than either of the control groups. Following 3 min of stimulation (150-Hz, 200-ms pulse train every 0.5 s), the degree of fatigue of tissues from each of these three treatment groups was not different. The observation in this study that glycolysis becomes the predominant metabolic pathway in thiamine deficiency without increasing the intracellular level of products, indicates that this treatment also has other effects which increase the effective lactate permeability of the fibre membranes.

Animals↗