Inmates from a detention centre in Perak were evaluated for ankle oedema.
Physical examination and biochemical evaluation did not show any evidence of renal or hepatic dysfunction. Cardiac origin was suggested by the presence of other signs of heart failure and by radiological evidence of cardiomegaly in 40% of them. All the patients who returned for review demonstrated a prompt clinical response to thiamine replacement therapy.
Thiamine responsive ankle oedema in detention centre inmates. Jeyakumar-D. Med-J-Malaysia. 1995 Mar; 50(1): 17-20.
The work by Christiaan Eijkman in Batavia (now Djakarta, the capital of Indonesia) between 1890 and 1900, for which he received a Nobel Prize, is reviewed.
While searching for a microorganism responsible for beriberi, he found that a condition of polyneuritis, with similarities to beriberi, could be produced consistently in chickens by feeding them polished rice, and that addition of the silverskin removed during polishing prevented this.
His successor was able to show that silverskin supplied some unknown factor(s) that was required regardless of whether or not the diet contained starch. Fractionation eventually showed thiamin to be the active factor.
Eijkman's contribution to the discovery of vitamins. Carpenter-KJ; Sutherland-B. J-Nutr. 1995 Feb; 125(2): 155-63.
Circadian rhythm disturbance
Circadian rhythm disturbance
Thiamine deficiency may disturb circadian rhythms in animals, according to this study which measured the rhythm of locomotor activity in a murine model of dietary thiamine deficiency. About 1 month before the expected onset of overt neurological illness, locomotor rhythmicity in deficient animals exhibited a shortened free-running period without a change in amplitude. This effect was fully reversible by thiamine administration. Disordered circadian timekeeping may contribute to altered physiological responses in Wernicke's encephalopathy.
Bennett MR, Schwartz WJ: Altered circadian rhythmicity is an early sign of murine dietary thiamine deficiency, J Neurol Sci 1999 Feb 1;163(1):6-10
Congestive heart failure
Cardiovascular disease is the leading cause of death in the United States. Congestive heart failure (CHF) is often the result of many non-fatal heart problems. Many patients who suffer from heart failure die as a result of cardiac dysrhythmias. This article discusses the normal heart, the changes from normal seen in CHF and dysrhythmias, the medical management of these conditions, including medications used, and the implications for the dental management of these patients.
Weaver T & Eisold JF: Congestive heart failure and disorders of the heart beat. Dent Clin North Am, 40:543-61, 1996 Jul.
Genetic transport mechanism
Genetic transport mechanism
According to this study, the gene SLC19A2 (for solute carrier family 19 (thiamine transporter), member 2) encodes the first known mammalian thiamine transporter, designated as thiamine transporter-1 (THTR-1). Thiamine-responsive megaloblastic anaemia with diabetes and deafness (TRMA; MIM 249270) is an autosomal recessive disease thought to be due to a defect in thiamine (vitamin B1) transport. Pharmacological doses of thiamine correct the anaemia, and in some cases improve the diabetes, although progressive sensorineural deafness is irreversible. Previous studies localized the TRMA gene to a 4-cM region on chromosome 1q23.3 (ref. 5), and fine-mapping has recently narrowed that region further. Fibroblasts from people with TRMA lack high-affinity thiamine transport. Expression of a gene encoding a known yeast thiamine transporter, THI10 (refs 8-10), in TRMA mutant cells prevents apoptotic cell death in thiamine-depleted medium. The researchers used a candidate gene approach to identify putative thiamine transporters in the 1q23.3 critical region.
Fleming JC, Tartaglini E, Steinkamp MP, Schorderet DF, Cohen N, Neufeld EJ:
The gene mutated in thiamine-responsive anaemia with diabetes and deafness (TRMA) encodes a functional thiamine transporter, Nat Genet 1999 Jul;22(3):305-8
Pregnant, alcoholic women who exhibit a high anion gap should be examined for lactic acidosis caused by thiamine deficiency. According to this study, a large dose of thiamine should be administered immediately upon examination of the patient. The researchers studied a pregnant alcoholic patient who presented with hyperemesis and a high anion gap acidosis. Lactic acidosis and thiamine deficiencies were confirmed. The patient's symptoms and acidosis resolved with thiamine administration.
Mukunda BN: Lactic acidosis caused by thiamine deficiency in a pregnant alcoholic patient, Am J Med Sci 1999 Apr;317(4):261-2
In some parts of southeast Asia (notably Thailand), thiamine deficiency commonly complicates acute falciparum malaria, and could contribute to dysfunction of the central nervous system. The researchers studies patients admitted to a Thailand hospital with malaria or other febrile illness, during summer 1992. About 52% of patients with severe malaria and 19% of patients with uncomplicated malaria exhibited severe thiamine deficiency. Thiamine deficiency was more severe in patients with cerebral malaria than in those with uncomplicated malaria and the controls. These results suggest that thiamine deficiency aggravates malaria, particularly in severe infections.
Krishna S, Taylor AM, Supanaranond W, Pukrittayakamee S, ter Kuile F, Tawfiq KM, Holloway PA, White NJ: Thiamine deficiency and malaria in adults from southeast Asia, Lancet 1999 Feb 13;353(9152):546-9
The Cross-sectional Cooking, Eating, Nutrition, and Shopping (CENAS) Survey was used to obtain data on food consumption patterns of low-income Mexicans living in Chicago, Ill.
The proportion of respondents reporting intakes less than two thirds of Recommended Dietary Allowances for nine micronutrients ranged from 11% (thiamin and riboflavin) to 82% (folacin).
Ballew-C & Sugerman-SB: High-risk nutrient intakes among low-income Mexican women in Chicago, Illinois.. J-Am-Diet-Assoc. 1995 Dec; 95(12): 1409-13.
Thiamine deficiency due to various events may contribute to Wernicke's encephalopathy, a condition largely associated with alcoholism. During a three-year period, nine patients with no history of alcohol abuse developed Wernicke's encephalopathy in association with specific precipitating events, including vomiting, crash dieting, renal colic in postpartum woman, colonic surgery, and chronic hemodialysis. In all nine cases, treatment with intravenous thiamine completely reversed the neurological disorder.
Merkin-Zaborsky H, et al: Thiamine-responsive acute neurological disorders in nonalcoholic patients, Eur Neurol 2001;45(1):34-7
Wernicke's encephalopathy is caused by thiamin deficiency and can be recognized by severe neurological symptoms that are occasionally accompanied by systemic signs.
Present 3 intravenously fed patients who developed the syndrome, even though in 2 cases they were given thiamin. Only the third patient's history included chronic alcoholism, and this patient also suffered severe cardiac symptoms and amaurosis. The amount of thiamin provided through parenteral nutrition, as well as the medium in which it is delivered, must be reviewed.
[Wernicke encephalopathy in patients given parenteral nutrition] Tapiador-Sanjuan-MJ; Lopez-Gaston-JI; Gracia-Naya-M; Ayuso-Blanco-T. Neurologia. 1995 Feb; 10(2): 104-6.
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