Vitamin Deficiency

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Allan D. Thomson - One of the best experts on this subject based on the ideXlab platform.

  • mechanisms of Vitamin Deficiency in chronic alcohol misusers and the development of the wernicke korsakoff syndrome
    Alcohol and Alcoholism, 2000
    Co-Authors: Allan D. Thomson
    Abstract:

    The classic signs of Vitamin Deficiency only occur in states of extreme depletion and are unreliable indicators for early treatment or prophylaxis of alcoholic patients at risk. Post-mortem findings demonstrate that thiamine (Vitamin Bj) Deficiency sufficient to cause irreversible brain damage is not diagnosed ante mortem in 80-90% of these patients. The causes of Vitamin Deficiency are reviewed with special attention to the inhibition of oral thiamine hydrochloride absorption in man caused by malnutrition present in alcoholic patients or by the direct effects of ethanol on intestinal transport. As the condition of the patient misusing alcohol progresses, damage to brain, liver, gastrointestinal tract, and pancreas continue (with other factors discussed) to further compromise the patient. Decreased intake, malabsorption, reduced storage, and impaired utilization further reduce the chances of unaided recovery. Failure of large oral doses of thiamine hydrochloride to provide an effective treatment for Wernicke's encephalopathy emphasizes the need for adequate and rapid replacement of depleted brain thiamine levels by repeated parenteral therapy in adequate doses.

  • B Vitamin Deficiency and neuropsychiatric syndromes in alcohol misuse
    Alcohol and Alcoholism, 1998
    Co-Authors: Christopher C.h. Cook, Phillip M. Hallwood, Allan D. Thomson
    Abstract:

    Alcohol misuse and alcohol withdrawal are associated with a variety of neuropsychiatric syndromes, some of which are associated with significant morbidity and mortality. B Vitamin Deficiency is known to contribute to the aetiology of a number of these syndromes, and B Vitamin supplementation thus plays a significant part in prophylaxis and treatment. In particular, the Wernicke Korsakoff syndrome (WKS). due to thiamine Deficiency, is a common condition in association with alcohol misuse, and is associated with high morbidity and mortality. Nicotinamide Deficiency may result in a rarer condition, alcoholic pellagra encephalopathy, which often has a similar clinical presentation to WKS. This review considers the role of B Vitamins in the aetiology and treatment of neuropsychiatric syndromes associated with alcohol misuse, with particular emphasis on WKS.

Christopher C.h. Cook - One of the best experts on this subject based on the ideXlab platform.

  • B Vitamin Deficiency and neuropsychiatric syndromes in alcohol misuse
    Alcohol and Alcoholism, 1998
    Co-Authors: Christopher C.h. Cook, Phillip M. Hallwood, Allan D. Thomson
    Abstract:

    Alcohol misuse and alcohol withdrawal are associated with a variety of neuropsychiatric syndromes, some of which are associated with significant morbidity and mortality. B Vitamin Deficiency is known to contribute to the aetiology of a number of these syndromes, and B Vitamin supplementation thus plays a significant part in prophylaxis and treatment. In particular, the Wernicke Korsakoff syndrome (WKS). due to thiamine Deficiency, is a common condition in association with alcohol misuse, and is associated with high morbidity and mortality. Nicotinamide Deficiency may result in a rarer condition, alcoholic pellagra encephalopathy, which often has a similar clinical presentation to WKS. This review considers the role of B Vitamins in the aetiology and treatment of neuropsychiatric syndromes associated with alcohol misuse, with particular emphasis on WKS.

Sigfrido Scarpa - One of the best experts on this subject based on the ideXlab platform.

  • S-adenosylmethionine reduces the progress of the Alzheimer-like features induced by B-Vitamin Deficiency in mice
    Neurobiology of aging, 2012
    Co-Authors: Andrea Fuso, Vincenzina Nicolia, Rosaria A. Cavallaro, Maria Teresa Fiorenza, Laura Ricceri, Elisa Isopi, Franco Mangia, Sigfrido Scarpa
    Abstract:

    Methylation reactions linked to homocysteine in the one-carbon metabolism are increasingly elicited in Alzheimer's disease, although the association of hyperhomocysteinemia and of low B Vitamin levels with the disease is still debated. We previously demonstrated that hyperhomocysteinemia and DNA hypomethylation induced by B Vitamin Deficiency are associated with PSEN1 and BACE1 overexpression and amyloid production. The present study is aimed at assessing S-adenosylmethionine effects in mice kept under a condition of B Vitamin Deficiency. To this end, TgCRND8 mice and wild-type littermates were assigned to control or B Vitamin deficient diet, with or without S-adenosylmethionine supplementation. We found that S-adenosylmethionine reduced amyloid production, increased spatial memory in TgCRND8 mice and inhibited the upregulation of B Vitamin Deficiency-induced PSEN1 and BACE1 expression and Tau phosphorylation in TgCRND8 and wild-type mice. Furthermore, S-adenosylmethionine treatment reduced plaque spreading independently on B Vitamin Deficiency. These results strengthen our previous observations on the possible role of one-carbon metabolism in Alzheimer's disease, highlighting hyperhomocysteinemia-related mechanisms in dementia onset/progression and encourage further studies aimed at evaluating the use of S-adenosylmethionine as a potential candidate drug for the treatment of the disease.

  • changes in presenilin 1 gene methylation pattern in diet induced b Vitamin Deficiency
    Neurobiology of Aging, 2011
    Co-Authors: Andrea Fuso, Vincenzina Nicolia, Rosaria A. Cavallaro, Alessia Pasqualato, Maria Teresa Fiorenza, Sigfrido Scarpa
    Abstract:

    Abstract We have previously shown that a nutritional model of B Vitamin Deficiency and homocysteine cycle alteration could lead to increased amyloid β deposition, due to PSEN1 and BACE over-expression and consequent increase in secretase activity. We hypothesize that nutritional factors causing homocysteine cycle alterations (i.e. hyperhomocysteinemia) could induce sequence-specific DNA hypomethylation and “aberrant” gene activation. Aim of present study was to analyze the methylation pattern of PSEN1 promoter in SK-N-BE neuroblastoma cells and TgCRND8 mice, in a B Vitamin (folate, B12 and B6) Deficiency paradigm. PSEN1 methylation status has been evaluated through bisulphite modification and genomic sequencing. We demonstrate that B Vitamin Deficiency induces hypomethylation of specific CpG moieties in the 5′-flanking region; S-adenosylmethionine has been supplemented as methyl donor to reverse this effect. PSEN1 promoter methylation status is correlated with gene expression. These findings pinpoint a direct relationship between B Vitamin-dependent alteration of homocysteine cycle and DNA methylation and also indicate that PSEN1 promoter is regulated by methylation of specific CpG moieties.

Kris V. Kowdley - One of the best experts on this subject based on the ideXlab platform.

  • acg clinical guideline primary sclerosing cholangitis
    The American Journal of Gastroenterology, 2015
    Co-Authors: Keith D Lindor, Kris V. Kowdley, Edwyn M Harrison
    Abstract:

    Primary sclerosing cholangitis is a chronic cholestatic liver disease that can shorten life and may require liver transplantation. The cause is unknown, although it is commonly associated with colitis. There is no approved or proven therapy, although ursodeoxycholic acid is used by many on an empiric basis. Complications including portal hypertension, fat-soluble Vitamin Deficiency, metabolic bone diseases, and development of cancers of the bile duct or colon can occur.

  • Vitamin E Deficiency and impaired cellular immunity related to intestinal fat malabsorption
    Gastroenterology, 1992
    Co-Authors: Kris V. Kowdley, Joel B. Mason, Simin Nikbin Meydani, Steve Cornwall, Richard J. Grand
    Abstract:

    Abstract This report describes a patient in whom a severe Vitamin E Deficiency developed secondary to an intestinal malabsorptive disorder. In vivo and in vitro impairment of T-cell function, as well as a polyneuropathy, were observed in conjunction with this Vitamin Deficiency. Repletion of the Vitamin Deficiency was associated with marked improvement in the T-cell functions and modest improvement in the neuropathy. Observations in this patient suggest that severe Vitamin E Deficiency in humans may impair T-cell activity and that correction of the deficient state may reverse these T-cell abnormalities. Further studies will need to be performed to confirm these findings.

Michael M. Rothkopf - One of the best experts on this subject based on the ideXlab platform.

  • Reversible neurologic dysfunction caused by severe Vitamin Deficiency after malabsorptive bariatric surgery
    Surgery for Obesity and Related Diseases, 2006
    Co-Authors: Michael M. Rothkopf
    Abstract:

    Abstract Significant deficiencies of both fat- and water-soluble Vitamins have been reported to occur after malabsorptive bariatric surgery. However, despite the potential for neurologic manifestations of such deficiencies, few cases of central neurologic dysfunction have been reported. Our group previously reported reversible neurologic dysfunction as an unusual manifestation of Vitamin Deficiency in a postjejunoileostomy patient. We report on a second case of reversible neurologic dysfunction associated with severe, prolonged Vitamin Deficiency many years after jejunoileostomy. Neurologic function returned to normal with Vitamin repletion. Patients who have undergone malabsorptive surgery are at risk of late metabolic complications and should be closely monitored.