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      Thiamine Deficiency as a Cause for Acute Circulatory Failure: An Overlooked Association in Western Countries

      case-report
      , MD a , b , , a , b , , MD, PhD b , c , , MD, PhD a , b , , MD, PhD a , b
      CJC Open
      Elsevier

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          Abstract

          A 42 year-old patient presented with circulatory failure and lactic acidosis. Clinical features, later coupled with biological tests, led to the diagnosis of wet beriberi syndrome and scurvy. Echocardiography showed a pattern of thiamine deficiency with high cardiac output and low vascular resistance. The patient's condition and biological parameters immediately improved after treatment injections of thiamine. Wet BeriBeri is often overlooked in western countries and is a diagnosis that must be considered based on history, and clinical and echocardiographical findings.

          Résumé

          Un patient âgé de 42 ans a présenté une insuffisance circulatoire et une acidose lactique. Ses caractéristiques cliniques et les résultats de laboratoire obtenus ultérieurement ont mené au diagnostic de béribéri humide et de scorbut. Une échocardiographie a révélé un profil indiquant une carence en thiamine accompagnée d’un débit cardiaque élevé et d’une faible résistance vasculaire. L’état et les paramètres biologiques du patient se sont améliorés immédiatement après l’administration de thiamine par injection. Le diagnostic de béribéri humide est souvent négligé dans les pays occidentaux, mais il faut en tenir compte en présence des signes appropriés : antécédents du patient, observations cliniques et résultats à l’échocardiographie.

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          Most cited references8

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          Vitamin C improves endothelium-dependent vasodilation by restoring nitric oxide activity in essential hypertension.

          Essential hypertension is associated with impaired endothelium-dependent vasodilation. Inactivation of endothelium-derived nitric oxide by oxygen free radicals participates in endothelial dysfunction in experimental hypertension. To test this hypothesis in humans, we evaluated the effect of antioxidant vitamin C on endothelium-dependent responses in essential hypertensive patients. In 14 healthy subjects (47.1+/-4.8 years; blood pressure, 120.6+/-4.5/80.9+/-3.5 mm Hg) and 14 essential hypertensive patients (47.3+/-5.1 years; blood pressure, 153.9+/-7.1/102.3+/-4.1 mm Hg), we studied forearm blood flow (strain-gauge plethysmography) modifications induced by intrabrachial acetylcholine (0.15, 0.45, 1.5, 4.5, and 15 microg x 100 mL(-1) x min(-1)) or sodium nitroprusside (1, 2, and 4 microg/100 mL forearm tissue per minute), an endothelium-dependent and -independent vasodilator, respectively, in basal conditions and during infusion of intrabrachial vitamin C (2.4 mg/100 mL forearm tissue per minute). In hypertensive patients but not in control subjects, vitamin C increased (P<0.01) the impaired vasodilation to acetylcholine, whereas the response to sodium nitroprusside was unaffected. Moreover, in another 14 hypertensive patients (47.1+/-5.2 years; blood pressure, 155.2+/-6.9/103.7+/-4.5 mm Hg), the facilitating effect of vitamin C on vasodilation to acetylcholine was reversed by N(G)-monomethyl-L-arginine (100 microg/100 mL forearm tissue per minute), a nitric oxide synthase inhibitor, suggesting that in essential hypertension superoxide anions impair endothelium-dependent vasodilation by nitric oxide breakdown. Finally, because in adjunctive 7 hypertensive patients (47.8+/-6.1 years; blood pressure, 155.3+/-6.8/103.5+/-4.3 mm Hg), indomethacin (50 microg/100 mL forearm tissue per minute), a cyclooxygenase inhibitor, prevented the potentiating effect of vitamin C on vasodilation to acetylcholine, it is possible that in essential hypertension a main source of superoxide anions could be the cyclooxygenase pathway. In essential hypertensive patients, impaired endothelial vasodilation can be improved by the antioxidant vitamin C, an effect that can be reversed by the nitric oxide synthase inhibitor N(G)-monomethyl-L-arginine. These findings support the hypothesis that nitric oxide inactivation by oxygen free radicals contributes to endothelial dysfunction in essential hypertension.
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            Thiamine deficiency disorders: diagnosis, prevalence, and a roadmap for global control programs

            Abstract Thiamine is an essential micronutrient that plays a key role in energy metabolism. Many populations worldwide may be at risk of clinical or subclinical thiamine deficiencies, due to famine, reliance on staple crops with low thiamine content, or food preparation practices, such as milling grains and washing milled rice. Clinical manifestations of thiamine deficiency are variable; this, along with the lack of a readily accessible and widely agreed upon biomarker of thiamine status, complicates efforts to diagnose thiamine deficiency and assess its global prevalence. Strategies to identify regions at risk of thiamine deficiency through proxy measures, such as analysis of food balance sheet data and month‐specific infant mortality rates, may be valuable for understanding the scope of thiamine deficiency. Urgent public health responses are warranted in high‐risk regions, considering the contribution of thiamine deficiency to infant mortality and research suggesting that even subclinical thiamine deficiency in childhood may have lifelong neurodevelopmental consequences. Food fortification and maternal and/or infant thiamine supplementation have proven effective in raising thiamine status and reducing the incidence of infantile beriberi in regions where thiamine deficiency is prevalent, but trial data are limited. Efforts to determine culturally and environmentally appropriate food vehicles for thiamine fortification are ongoing.
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              The Role of Thiamine Deficiency in Alcoholic Brain Disease

              A deficiency in the essential nutrient thiamine resulting from chronic alcohol consumption is one factor underlying alcohol-induced brain damage. Thiamine is a helper molecule (i.e., a cofactor) required by three enzymes involved in two pathways of carbohydrate metabolism. Because intermediate products of these pathways are needed for the generation of other essential molecules in the cells (e.g., building blocks of proteins and DNA as well as brain chemicals), a reduction in thiamine can interfere with numerous cellular functions, leading to serious brain disorders, including Wernicke-Korsakoff syndrome, which is found predominantly in alcoholics. Chronic alcohol consumption can result in thiamine deficiency by causing inadequate nutritional thiamine intake, decreased absorption of thiamine from the gastrointestinal tract, and impaired thiamine utilization in the cells. People differ in their susceptibility to thiamine deficiency, however, and different brain regions also may be more or less sensitive to this condition.
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                Author and article information

                Contributors
                Journal
                CJC Open
                CJC Open
                CJC Open
                Elsevier
                2589-790X
                19 July 2020
                November 2020
                19 July 2020
                : 2
                : 6
                : 716-718
                Affiliations
                [a ]Cardiac Intensive Care Unit, Louis Pradel Hospital, Bron, France
                [b ]Claude Bernard University Lyon 1, Lyon, France
                [c ]Investigation Clinical Center, Louis Pradel Hospital, Bron, France
                Author notes
                []Corresponding author: Dr Ahmad Hayek, Hôpital cardiologique Louis Pradel, Unité d'urgence et soins intensifs cardiologiques, 28 avenue Doyen Lépine, 69677 Bron, France. Tel.: 0472357549. ahmad.hayek0@ 123456gmail.com
                Article
                S2589-790X(20)30106-2
                10.1016/j.cjco.2020.07.011
                7710995
                5630206c-917a-402f-986a-08d0fca672da
                © 2020 Canadian Cardiovascular Society. Published by Elsevier Inc.

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 22 June 2020
                : 16 July 2020
                Categories
                Case Report

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