Development Of Thiamine Deficiency 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.

Thiamine and Thiaminase Status in Forage Fish of Salmonines from Lake Michigan

AbstractDietary sources of thiamine (vitamin B1) and thiamine‐degrading enzymes (thiaminases) are thought to be primary factors in the development of thiamine deficiency among Great Lakes salmonines. We surveyed major forage fish species in Lake Michigan for their content of thiamine, thiamine vitamers, and thiaminase activity. Concentrations of total thiamine were similar (P ≤ 0.05) among most forage fishes (alewife Alosa pseudoharengus, bloater Coregonus hoyi, spottail shiner Notropis hudsonius, deepwater sculpin Myoxocephalus thompsonii, yellow perch Perca flavescens, ninespine stickleback Pungitius pungitius, and round goby Neogobius melanostomus) and slightly lower in rainbow smelt Osmerus mordax. Concentrations of total thiamine were all above the dietary requirements of coldwater fishes, suggesting the thiamine content of forage fish is not the critical factor in the development of thiamine deficiency in Lake Michigan salmonines. Thiamine pyrophosphate was the predominant form of thiamine in most species of forage fish, followed by free thiamine and thiamine monophosphate. Total thiamine was slightly greater in summer collections of alewife and rainbow smelt than in spring and fall collections, but the same was not true for bloater. Thiaminase activity varied among species and was greatest in gizzard shad Dorosoma cepedianum, spottail shiner, alewife, and rainbow smelt. Thiaminase activity in alewife varied among collection locations, season (greatest in spring), and size of the fish. Size and condition factors were positively correlated with both total thiamine and thiaminase activity in alewife. Thus, thiamine and thiaminase activity in forage fishes collected in Lake Michigan varied among species, seasons, year caught, and size (or condition). Therefore, multiple factors must be considered in the development of predictive models for the onset of thiamine deficiency in Great Lakes salmonines. Most importantly, thiaminase activity was great in alewives and rainbow smelt, suggesting that these prey fish are key causative factors of the thiamine deficiency in Great Lakes salmonines.

Immunohistochemical determination of rat spinal cord substance P, and antinociceptive effect during development of thiamine deficiency

During 30 days of thiamine deficiency (TD) feeding, the rat antinociceptive effect (pain threshold) to noxious heat stimulation was significantly increased in proportion to the decrease substance P (SP) fluorescent intensity in the spinal cord. Only a single injection of thiamine HCl (0.5 mg/kg, s.c.) on the early treatment day during TD feeding effectively reversed the analgesic effect to the pair-fed control level. Whereas this reversal effect by thiamine treatment was not found if this treatment was done on the relatively late day. However, either treatment day, except muricide, complete disappearance of various animal behaviours induced by TD was found. These results indicate that, after certain degree of TD development, TD-induced behavioral effects might be reversible, but the afferent nerve fibers might be irreversibly damaged, probably by the similar mechanism as found for an excitotoxin(s) mediated injury in the certain brain region(s). The results also suggest a possibly that SP and an excitotoxin, glutamate, in the dorsal part of the spinal cord greatly contribute to the pain transmission induced by noxious heat stimulation.

The influence of hepatic insufficiency due to alcoholic cirrhosis on the erythrocyte transketolase activity (ETKA).

The erythrocyte transketolase activity (ETKA), the stimulated erythrocyte transketolase activity (ETKAS), and the thiaminepyrophosphate effect (TPPE) were measured in 21 alcoholic patients with cirrhosis and hepatic insufficiency, 13 alcoholic patients without cirrhosis and 21 non-alcoholic persons before and after oral treatment with 100 mg of thiamine daily for 2 weeks in order to investigate the influence of hepatic insufficiency on these variables. A statistically significant rise in ETKA and fall in TPPE were found in all three groups. ETKA, ETKAS and TPPE did not differ from each other in alcoholic patients with and without cirrhosis, but TPPE was significantly higher in these patients than in the non-alcoholic persons. The conclusions are that severe cirrhosis does not affect the erythrocyte transketolase apoenzyme, the ability of the tissues to convert thiamine to thiaminepyrophosphate for use in the erythrocytes or the absorption of thiamine from the gastrointestinal tract. Besides alcoholism seems to dispose to thiamine deficiency to a higher degree than cirrhosis, and the role of the liver as a thiamine store appears to be of minor importance in the development of thiamine deficiency. Finally, ETKA, ETKAS, and TPPE are considered to be usable as thiamine deficiency indicators in patients with cirrhosis as well as in patients without cirrhosis.

Effect of Thiamine Deficiency and Thiamine Repletion on Neutral Glyceride, Total and Free Cholsterol, Phospholipids, and Plasmalogens in Rat Liver

Intraperitoneal injection of 1 mg of thiamine in severely thiamine-deficient rats is followed by a 3- and 20-fold elevation of liver total cholesterol and neutral glycerides, respectively. These elevations continue up to 8 and 20 times normal after a second thiamine injection.Phospholipid levels per gram of liver or per 100 g of body weight fall to below normal during development of thiamine deficiency. Little change in plasmalogens occurred, however, when expressed in either manner although there was a tendency for them to fall slightly below the ad libitum-fed control level. After a single thiamine injection, phospholipids tend to return to normal, whereas plasmalogens increase to far above normal levels. A second injection of thiamine decreases phospholipids to below normal, which then return nearly to normal. Plasmalogens return nearly to normal without fluctuating after a second thiamine injection.During thiamine deficiency the ratio of free to total cholesterol is significantly higher than normal, suggesting either a breakdown in the cholesterol esterification system or a severe deficiency of fatty acids available for esterification. After thiamine repletion the ratio rapidly falls to well below normal.After thiamine repletion fine droplet lipidosis and a striking increase in glycogen in the portal areas precedes the massive paracentral fatty change which is reflected biochemically. When massive fatty deposition occurs, stainable glycogen decreases. Cellular regenerative activity after thiamine repletion is slight, indicating that the changes observed with thiamine repletion are unassociated with cell destruction and subsequent cell proliferation.Although oral or parenteral administration of thiamine generally produced similar effects on liver lipids, the magnitude of the effects on total cholesterol and plasmalogens was much greater with parentral administration.

Pyruvate accumulation and development of thiamine deficiency in cultures of Proteus vulgaris.

SUMMARY: The accumulation of pyruvate in cultures of Proteus vulgaris grown with limiting concentrations of nicotinic acid has been investigated. Nicotinic acid-deficient organisms remaining in contact with a lactate medium under conditions where pyruvate accumulation is occurring gradually become deficient in thiamine. The thiamine content of organisms at various stages of growth was estimated, and a relationship between thiamine content and length of lag phase found. Maximum rates of pyruvate oxidation were obtained in organisms which were not deficient in either nicotinic acid or thiamine. The possible metabolic significance of these findings is discussed.

Development of Thiamine Deficiency in the Cat on a Diet of Raw Fish

SummaryCats fed an exclusive diet of raw carp or raw herring develop all the signs of thiamine deficiency characteristic for this species.