Evidence Of Thiamine Deficiency Research Articles

Prevalence of Low Plasma Vitamin B1 in the Stroke Population Admitted to Acute Inpatient Rehabilitation.

Objective: To determine the prevalence of vitamin B1 (VitB1) deficiency in the stroke population admitted to acute inpatient rehabilitation. Design: Retrospective cohort study. Setting: Acute inpatient rehabilitation facility at an academic medical center. Participants: 119 consecutive stroke patients admitted to stroke service from 1 January 2018 to 31 December 2018. Interventions: Not applicable. Main Outcome Measures: Plasma VitB1 level. Results: There were 17 patients (14%; 95% CI 9–22%) with low VitB1 with a range of 2–3 nmol/L, an additional 58 (49%; CI 40–58%) patients had normal low VitB1 with a range of 4–9 nmol/L, twenty-five patients (21%; CI 15–29%) had normal high VitB1 with a range of 10–15 nmol/L, and nineteen patients (16%; CI 10–24%) had high VitB1 with a range of 16–43 nmol/L. Conclusions: In this cohort of patients admitted to the stroke service at an acute rehabilitation facility, there is evidence of thiamine deficiency. Moreover, the data suggest that there is inadequate acute intake of VitB1. Given the role of thiamine deficiency in neurologic function, further study of the role of thiamine optimization in the acute stroke rehabilitation population is warranted.

Thiamine Levels in Muscle and Eggs of Adult Pacific Salmon from the Fraser River, British Columbia.

Multiple species and stocks of Pacific salmon Oncorhynchus spp. have experienced large declines in the number of returning adults over a wide region of the Pacific Northwest due to poor marine survival (low smolt-to-adult survival rates). One possible explanation for reduced survival is thiamine deficiency. Thiamine (vitamin B1 ) is an essential vitamin with an integral role in many metabolic processes, and thiamine deficiency is an important cause of salmonid mortality in the Baltic Sea and in the Laurentian Great Lakes. To assess this possibility, we (1) compared muscle thiamine content over time in a holding experiment using Fraser River (British Columbia) Sockeye Salmon O. nerka to establish whether adults that died during the holding period had lower thiamine levels than survivors, (2) measured infectious loads of multiple pathogens in held fish, and (3) measured egg thiamine content from four species of Pacific salmon collected on Fraser River spawning grounds. Chinook Salmon O. tshawytscha had the lowest egg thiamine, followed by Sockeye Salmon; however, egg thiamine concentrations were above levels known to cause overt fry mortality. Thiamine vitamers in the muscle of Fraser River adult Sockeye Salmon shifted over a 13-d holding period, with a precipitous decline in thiamine pyrophosphate (the active form of thiamine used in enzyme reactions) in surviving fish. Survivors also carried lower loads of Flavobacterium psychrophilum than fish that died during in the holding period. Although there is no evidence of thiamine deficiency in the adults studied, questions remain about possible thiamine metabolism-fish pathogen relationships that influence survival.

Tryptophan and nutritional status of patients with senile dementia.

The nutritional status of 23 severely demented patients was compared with that of 23 similarly aged controls in the community. A 3-day weighed intake on all subjects showed lower mean intakes of energy, protein, ascorbic acid and nicotinic acid in the mean intakes of energy, protein, ascorbic acid and nicotinic acid in the patient group. This group had lower levels of plasma ascorbic acid and red cell folate and of urinary N-methylnicotinamide excretion relative to creatinine. Over a third of both controls and patients had evidence of thiamin deficiency, as judged by a raised percentage erythrocyte transketolase activity. An earlier finding in patients with senile dementia of reduced fasting plasma concentrations of tryptophan was confirmed for total and protein bound fractions. With the possible exception of ascorbic acid, the data could not be explained satisfactorily in terms of intake. It is suggested that the association between the phenomena of aging, senile dementia and nutritional status merits further investigation.

Erythrocyte transketolase activity in alcoholic liver disease.

Erythrocyte transketolase activity and its stimulation in vitro by the addition of thiamine pyrophosphate (TPP effect) was measured in 64 normally nourished alcoholics with well-compensated liver disease and in 20 control subjects. Biochemical evidence of thiamine deficiency as judged by low transketolase activity was found in 19 alcoholics (29.7%). In 5 of these 19 patients the TPP effect was abnormally high, indicating depleted thiamine stores. IN the other 13 patients the TPP effect was either normal or low, suggesting a deficiency or an inability to use the transketolase apoenzyme, probably as a result o long-standing thiamine deficiency or the presence of liver disease. a further eight patients (12.5%) had normal transketolase activity but a low TPP effect, perhaps reflecting failure of hte coenzyme TPP to recombine with the transketolase apoenzyme in the presence of normal thiamine stores. There was no relationship between transketolase activity and the daily alcohol consumption, the duration of alcoholism, or the histological severity of the liver disease. Thiamine should be given routinely to alcoholics even if their diet appears adequate and their liver disease is minimal or well compensated.

Thiamine Status in Alcoholism

Summary :Thiamine status in alcoholism. Beverley Wood, Kerry J. Breen and D. G. Penington, Aust. N.Z. J. Med., 1977, 7, pp. 475–484. The erythrocyte transketolase assay was used to seek biochemical evidence of thiamine deficiency in 265 alcoholic persons attending an inner city Australian hospital. Fifty patients were found to have recent vitamin therapy and were excluded from further study. Wernicke's encephalopathy was diagnosed in 24 subjects (11.3%). The thiamine pyrophosphate (TPP) effect was elevated in only 13 of the 24 patients with Wernicke's encephalopathy; a much closer correlation was observed with erythrocyte transketolase activity which was depressed in 21 persons with this diagnosis. Low erythrocyte transketolase activity (32.6%) was more frequently seen than an elevated TPP effect (24-7%) in the overall group of 215 subjects. Of 47 patients with a low erythrocyte transketolase activity which failed to return to normal after the addition of TPP in vitro, only ten patients had liver disease. Twelve patients with Wernicke's encephalopathy studied following thiamine hydrochloride in vivo showed complete biochemical response despite the presence of biopsy proven severe liver disease in two patients and the lack of response of low erythrocyte transketolase activity to TPP in vitro in eleven of the twelve patients. Fiftyfive patients were studied before and after thiamine in vivo. Seventeen of these subjects had severe liver disease but only two of the 17 had low ETKA which failed to respond to TPP in vitro; both responded biochemically to thiamine hydrochloride in vivo. In the remaining 38 patients without evidence of severe liver disease, 14 had low ETKA which failed to return to normal with TPP in vitro; three of these failed to respond biochemically to thiamine hydrochloride in vivo. These data indicated that apparent deficiency of erythroc yte apotransketolase was infrequently linked with the presence of liver disease and that liver disease did not appear to interfere with the biochemical response to thiamine in vivo. Urinary thiamine excretion measured in 79 subjects did. not correlate with any means of expression of the transketolase assay or with clinical thiamine deficiency. It was concluded that the TPP effect was frequently misleading in subjects with gross thiamine deficiency (Wernicke'S encephalopathy) and it was suggested that erythrocyte transketolase activity may be the best parameter to use in assessing thiamine status with the erythrocyte transketolase assay. Finally, it is postulated that severe thiamine deficiency per se may lead to deficiency of erythrocyte apotransketolase which has been previously ascribed to liver damage.

Evidence of thiamine deficiency in calves affected with cerebrocortical necrosis.

Evidence of thiamine deficiency in calves affected with cerebrocortical necrosis.

The uptake of thiamine by a strain of Staphylococcus aureus from the duodenum of a case of polyneuritis.

SUMMARY: A strain of Staphylococcus aureus was isolated from the duodenum of a case of idiopathic steatorrhoea with polyneuritis and evidence of thiamine deficiency. This organism in washed cell suspension in glucose and thiamine at 37° was found to remove 75 % of the thiamine present within 1 ½ hr. This process was much retarded by reduction of the temperature to 4° and in the absence of glucose. The thiamine which was removed was not destroyed, and death of the organisms resulted in liberation of the thiamine from the organisms into the suspending fluid. The process may be due to an active transference across cell membranes and concentration of thiamine inside the organism. It is suggested that in the presence of an abnormal intestinal flora such a mechanism may play a part in producing clinical thiamine deficiency states.