Database : MEDLINE
Search on : Thiamine [Words]
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[PMID]: 29520660
[Au] Autor:Amrein K; Oudemans-van Straaten HM; Berger MM
[Ad] Address:Division of Endocrinology and Diabetology, Department of Internal Medicine, Medical University of Graz, Graz, Austria. karin.amrein@medunigraz.at.
[Ti] Title:Vitamin therapy in critically ill patients: focus on thiamine, vitamin C, and vitamin D.
[So] Source:Intensive Care Med;, 2018 Mar 08.
[Is] ISSN:1432-1238
[Cp] Country of publication:United States
[La] Language:eng
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.1007/s00134-018-5107-y

  2 / 13301 MEDLINE  
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[PMID]: 29188542
[Au] Autor:Tanabe N; Hiraoka E; Kataoka J; Naito T; Matsumoto K; Arai J; Norisue Y
[Ad] Address:Department of Internal Medicine, Tokyo Bay Urayasu Ichikawa Medical Center, 3-4-32, Todaijima, Urayasu-city, Chiba, 279-0001, Japan.
[Ti] Title:Wet Beriberi Associated with Hikikomori Syndrome.
[So] Source:J Gen Intern Med;33(3):384-387, 2018 Mar.
[Is] ISSN:1525-1497
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Wet beriberi, characterized by high cardiac output with predominantly right-sided heart failure and lactic acidosis, is a disease caused by thiamine deficiency, and is rarely seen in modern society. However, patients with social withdrawal syndrome, also known as hikikomori syndrome, may be a new population at risk of thiamine deficiency. Hikikomori syndrome, first recognized in Japan, is becoming a worldwide issue. A 39-year-old Japanese patient was brought to our hospital, with a 3-week history of progressive shortness of breath and generalized edema. The patient had right-sided high-output heart failure, lactic acidosis, and Wernicke-Korsakoff syndrome. Because of his history of social isolation, we diagnosed hikikomori syndrome according to the Japanese government's definition, which is as follows: lifestyle centered at home; no interest or willingness to attend school or work; persistence of symptoms beyond 6 months; and exclusion of other psychiatric and developmental disorders. Considering his diagnosis of hikikomori syndrome and social isolation, we suspected malnutrition, particularly thiamine deficiency, and successfully treated him. Clinicians should be aware of the potential risk of thiamine deficiency associated with hikikomori syndrome and initiate thiamine replacement in cases of high-output heart failure associated with lactic acidosis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1007/s11606-017-4208-6

  3 / 13301 MEDLINE  
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[PMID]: 29286589
[Au] Autor:Guirguis M; Manning S; Chavez M; Nelson J; Baronia R; Bobba S; Ahmed J; Ajufo I
[Ad] Address:Department of Psychiatry, Texas Tech University Health Sciences Center, 3601 4th St Stop 8103, Lubbock, TX 79430. medhat74@yahoo.com.
[Ti] Title:Are Psychiatric Inpatients at Risk of Developing Wernicke's Encephalopathy Being Identified and Adequately Treated?
[So] Source:Prim Care Companion CNS Disord;19(6), 2017 Dec 28.
[Is] ISSN:2155-7780
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Objective: Wernicke's encephalopathy is caused by thiamine deficiency and occurs predominantly in alcohol-dependent individuals but also develops in those who are malnourished due to other reasons including medical and psychiatric disorders. This study examined the frequency rate and management of Wernicke's encephalopathy in alcohol-dependent and non-alcohol-dependent patients admitted to a psychiatric hospital. Methods: Data were retrospectively collected from electronic medical records of psychiatric inpatients admitted to a teaching hospital located in Texas between September 2013 and March 2014. The diagnostic criteria of Caine and colleagues and thiamine dosing strategies were used to identify cases of suboptimal management. Results: A total of 486 charts were reviewed. Nine patients (1.85%) had clinical signs of Wernicke's encephalopathy, and 36 (7%, n = 486) were at a high risk for developing the disorder. None of these patients received adequate doses of parenteral thiamine, and of those who were prescribed thiamine, the majority, including high-risk patients, were prescribed oral thiamine at the traditional dose of 100 mg/d. Conclusions: The findings suggest that Wernicke's encephalopathy is underdiagnosed and undertreated. Our study also highlights the need for clarifying diagnostic criteria, identifying the risk factors for thiamine deficiency, and improving awareness among physicians about diagnosis, prevention, and adequate treatment of Wernicke's encephalopathy in alcohol-dependent and non-alcohol-dependent patients.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Process

  4 / 13301 MEDLINE  
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[PMID]: 29512374
[Au] Autor:Aurich S; Simon JC; Treudler R
[Ad] Address:Department of Dermatology, Venereology and Allergology, University Hospital, Leipzig, Germany AND LICA-Leipziger Interdisziplinäres Centrum für Allergologie, University Hospital, Leipzig, Germany.
[Ti] Title:A Case of Anaphylaxis to Intramuscular but Not to Oral Application of Thiamine (Vitamin B1).
[So] Source:Iran J Allergy Asthma Immunol;17(1):94-96, 2018 Feb.
[Is] ISSN:1735-1502
[Cp] Country of publication:Iran
[La] Language:eng
[Ab] Abstract:We report a 78 year-old non-atopic female with polyneuropathy who started to receive monthly intramuscular injections of thiamine hydrochloride. She had an anaphylaxis after the fourth injection. Skin prick test (SPT) with pure commercially available aqueous preparations was positive for thiamine hydrochloride. A titrated, single blinded, placebo-controlled oral provocation test with thiamine hydrochloride was well tolerated. The patient was then diagnosed as compartment allergy with hypersensitivity to parenteral but not to oral thiamine. Because in our patient, oral intake of thiamine has never been reported to lead to any adverse reaction. Oral tolerability might be due to the uptake mechanism of thiamine in the gastrointestinal system.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Data-Review

  5 / 13301 MEDLINE  
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[PMID]: 29511074
[Au] Autor:Sannino DR; Dobson AJ; Edwards K; Angert ER; Buchon N
[Ad] Address:Department of Microbiology, Cornell University, Ithaca, New York, USA.
[Ti] Title:The Gut Microbiota Provisions Thiamine to Its Host.
[So] Source:MBio;9(2), 2018 Mar 06.
[Is] ISSN:2150-7511
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The microbiota of has a substantial impact on host physiology and nutrition. Some effects may involve vitamin provisioning, but the relationships between microbe-derived vitamins, diet, and host health remain to be established systematically. We explored the contribution of microbiota in supplying sufficient dietary thiamine (vitamin B ) to support at different stages of its life cycle. Using chemically defined diets with different levels of available thiamine, we found that the interaction of thiamine concentration and microbiota did not affect the longevity of adult Likewise, this interplay did not have an impact on egg production. However, we determined that thiamine availability has a large impact on offspring development, as axenic offspring were unable to develop on a thiamine-free diet. Offspring survived on the diet only when the microbiota was present or added back, demonstrating that the microbiota was able to provide enough thiamine to support host development. Through gnotobiotic studies, we determined that , a common member of the microbiota, was able to rescue development of larvae raised on the no-thiamine diet. Further, it was the only microbiota member that produced measurable amounts of thiamine when grown on the thiamine-free fly medium. Its close relative also rescued larvae; however, a thiamine auxotrophic mutant strain was unable to support larval growth and development. The results demonstrate that the microbiota functions to provision thiamine to its host in a low-thiamine environment. There has been a long-standing assumption that the microbiota of animals provides their hosts with essential B vitamins; however, there is not a wealth of empirical evidence supporting this idea, especially for vitamin B (thiamine). To determine whether this assumption is true, we used and chemically defined diets with different thiamine concentrations as a model. We found that the microbiota does provide thiamine to its host, enough to allow the development of flies on a thiamine-free diet. The power of the -microbiota system allowed us to determine that one microbiota member in particular, , is responsible for the thiamine provisioning. Thereby, our study verifies this long-standing hypothesis. Finally, the methods used in this work are applicable for interrogating the underpinnings of other aspects of the tripartite interaction between diet, host, and microbiota.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Data-Review

  6 / 13301 MEDLINE  
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[PMID]: 29490669
[Au] Autor:Sang S; Pan X; Chen Z; Zeng F; Pan S; Liu H; Jin L; Fei G; Wang C; Ren S; Jiao F; Bao W; Zhou W; Guan Y; Zhang Y; Shi H; Wang Y; Yu X; Wang Y; Zhong C
[Ad] Address:Department of Neurology, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, China.
[Ti] Title:Thiamine diphosphate reduction strongly correlates with brain glucose hypometabolism in Alzheimer's disease, whereas amyloid deposition does not.
[So] Source:Alzheimers Res Ther;10(1):26, 2018 Mar 01.
[Is] ISSN:1758-9193
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: The underlying mechanism of brain glucose hypometabolism, an invariant neurodegenerative feature that tightly correlates with cognitive impairment and disease progression of Alzheimer's disease (AD), remains elusive. METHODS: Positron emission tomography with 2-[ F]fluoro-2-deoxy-D-glucose (FDG-PET) was used to evaluate brain glucose metabolism, presented as the rate of 2-[ F]fluoro-2-deoxy-D-glucose standardized uptake value ratio (FDG SUVR) in patients with AD or control subjects and in mice with or without thiamine deficiency induced by a thiamine-deprived diet. Brain amyloid-ß (Aß) deposition in patients with clinically diagnosed AD was quantified by performing assays using C-Pittsburgh compound B PET. The levels of thiamine metabolites in blood samples of patients with AD and control subjects, as well as in blood and brain samples of mice, were detected by high-performance liquid chromatography with fluorescence detection. RESULTS: FDG SUVRs in frontal, temporal, and parietal cortices of patients with AD were closely correlated with the levels of blood thiamine diphosphate (TDP) and cognitive abilities, but not with brain Aß deposition. Mice on a thiamine-deprived diet manifested a significant decline of FDG SUVRs in multiple brain regions as compared with those in control mice, with magnitudes highly correlating with both brain and blood TDP levels. There were no significant differences in the changes of FDG SUVRs in observed brain regions between amyloid precursor protein/presenilin-1 and wild-type mice following thiamine deficiency. CONCLUSIONS: We demonstrate, for the first time to our knowledge, in vivo that TDP reduction strongly correlates with brain glucose hypometabolism, whereas amyloid deposition does not. Our study provides new insight into the pathogenesis and therapeutic strategy for AD.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Data-Review
[do] DOI:10.1186/s13195-018-0354-2

  7 / 13301 MEDLINE  
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[PMID]: 29440497
[Au] Autor:Lonhienne T; Garcia MD; Pierens G; Mobli M; Nouwens A; Guddat LW
[Ad] Address:School of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, QLD 4072, Australia; t.lonhienne@uq.edu.au luke.guddat@uq.edu.au.
[Ti] Title:Structural insights into the mechanism of inhibition of AHAS by herbicides.
[So] Source:Proc Natl Acad Sci U S A;115(9):E1945-E1954, 2018 Feb 27.
[Is] ISSN:1091-6490
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Acetohydroxyacid synthase (AHAS), the first enzyme in the branched amino acid biosynthesis pathway, is present only in plants and microorganisms, and it is the target of >50 commercial herbicides. Penoxsulam (PS), which is a highly effective broad-spectrum AHAS-inhibiting herbicide, is used extensively to control weed growth in rice crops. However, the molecular basis for its inhibition of AHAS is poorly understood. This is despite the availability of structural data for all other classes of AHAS-inhibiting herbicides. Here, crystallographic data for AHAS (2.3 Å) and AHAS (2.5 Å) in complex with PS reveal the extraordinary molecular mechanisms that underpin its inhibitory activity. The structures show that inhibition of AHAS by PS triggers expulsion of two molecules of oxygen bound in the active site, releasing them as substrates for an oxygenase side reaction of the enzyme. The structures also show that PS either stabilizes the thiamin diphosphate (ThDP)-peracetate adduct, a product of this oxygenase reaction, or traps within the active site an intact molecule of peracetate in the presence of a degraded form of ThDP: thiamine aminoethenethiol diphosphate. Kinetic analysis shows that PS inhibits AHAS by a combination of events involving FAD oxidation and chemical alteration of ThDP. With the emergence of increasing levels of resistance toward front-line herbicides and the need to optimize the use of arable land, these data suggest strategies for next generation herbicide design.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Data-Review
[do] DOI:10.1073/pnas.1714392115

  8 / 13301 MEDLINE  
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[PMID]: 29489643
[Au] Autor:Lei Y; Zheng MH; Huang W; Zhang J; Lu Y
[Ad] Address:Department of Emergency Medicine.
[Ti] Title:Wet beriberi with multiple organ failure remarkably reversed by thiamine administration: A case report and literature review.
[So] Source:Medicine (Baltimore);97(9):e0010, 2018 Mar.
[Is] ISSN:1536-5964
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:RATIONALE: Circulatory failure, especially with low systemic vascular resistance (SVR), as observed in septic shock, thyrotoxicosis, and anemia, is a particular pattern that should suggest thiamine (vitamin B1) deficiency. The clinical picture of wet beriberi secondary to thiamine deficiency only demonstrates non-specific clinical manifestations. For a diagnosis of wet beriberi, medical history is very important. Interestingly, imprisonment was also found to be related to thiamine deficiency. This article presents a rare case of wet beriberi associated with multiple organ failure (MOF) in a prison patient with years of heavy alcohol consumption. PATIENT CONCERNS: The patient reported repetitive symptoms of nausea, vomiting, respiratory distress, and palpitations for a period of 1 month; dyspnea and edema for 5 days; and decreased blood pressure and urine volume for 2 days. DIAGNOSES: The heart failure patient had a history of dietary deficiency. Right heart catheterization showed high cardiac output (CO) and low SVR. Measurement of serum thiamine concentration was low. The most important factor was that the hemodynamic indices were remarkably reversed by thiamine administration. INTERVENTIONS: The patient started treatment with thiamine (100 mg) by intramuscular injection, together with basic supportive care. OUTCOMES: The hemodynamic indices improved within 12 hours after thiamine administration. Echocardiographic examinations revealed right ventricular function improvement within a few days, which were normal within a month. LESSONS: A diagnosis of wet beriberi should be considered for a prison patient who has unexplained heart failure, lactic acidosis, and/or MOF. Moreover, the patient should be empirically given thiamine administration without delay.
[Mh] MeSH terms primary: Beriberi/complications
Beriberi/drug therapy
Multiple Organ Failure/complications
Multiple Organ Failure/drug therapy
Thiamine/therapeutic use
[Mh] MeSH terms secundary: Adult
Alcoholism/complications
Beriberi/etiology
Beriberi/physiopathology
Cardiac Output
Humans
Male
Multiple Organ Failure/etiology
Multiple Organ Failure/physiopathology
Prisoners
Thiamine Deficiency/complications
Thiamine Deficiency/drug therapy
Vascular Resistance
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:X66NSO3N35 (Thiamine)
[Em] Entry month:1803
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:180301
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000010010

  9 / 13301 MEDLINE  
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[PMID]: 29427613
[Au] Autor:Bowyer JF; Tranter KM; Sarkar S; Hanig JP
[Ad] Address:Division of Neurotoxicology, National Center for Toxicological Research/FDA, Jefferson, AR, 72079, United States. Electronic address: john.bowyer@fda.hhs.gov.
[Ti] Title:Microglial activation and vascular responses that are associated with early thalamic neurodegeneration resulting from thiamine deficiency.
[So] Source:Neurotoxicology;65:98-110, 2018 Feb 07.
[Is] ISSN:1872-9711
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Thiamine/vitamin B1 deficiency can lead to behavioral changes and neurotoxicity in humans. This may due in part to vascular damage, neuroinflammation and neuronal degeneration in the diencephalon, which is seen in animal models of pyrithiamine-enhanced thiamine deficiency. However, the time course of the progression of these changes in the animal models has been poorly characterized. Therefore, in this study, the progression of: 1) activated microglial association with vasculature; 2) neurodegeneration; and 3) any vascular leakage in the forebrain during the progress of thiamine deficiency were determined. A thiamine deficient diet along with 0.25 mg/kg/d of pyrithiamine was used as the mouse model. Vasculature was identified with Cd31 and microglia with Cd11b and Iba1 immunoreactivity. Neurodegeneration was determined by FJc labeling. The first sign of activated microglia within the thalamic nuclei were detected after 8 d of thiamine deficiency, and by 9 d activated microglia associated primarily with vasculature were clearly present but only in thalamus. At the 8 d time point neurodegeneration was not present in thalamus. However at 9 d, the first signs of neurodegeneration (FJc + neurons) were seen in most animals. Over 80% of the microglia were activated at 10 d but almost exclusively in the thalamus and the number of degenerating neurons was less than 10% of the activated microglia. At 10 d, there were sporadic minor changes in IgG presence in thalamus indicating minor vascular leakage. Dizocilpine (0.2-0.4 mg/kg) or phenobarbital (10-20 mg/kg) was administered to groups of mice from day 8 through day 10 to block neurodegeneration but neither did. In summary, activated microglia start to surround vasculature 1-2 d prior to the start of neurodegeneration. This response may be a means of controlling or repairing vascular damage and leakage. Glutamate excitotoxicity and vascular leakage likely only play a minor role in the early neurodegeneration resulting from thiamine deficiency. However, failure of dysfunctional vasculature endothelium to supply sufficient nutrients to neurons could be contributing to the neurodegeneration.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180304
[Lr] Last revision date:180304
[St] Status:Publisher

  10 / 13301 MEDLINE  
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[PMID]: 29329694
[Au] Autor:Jentzer JC; Vallabhajosyula S; Khanna AK; Chawla LS; Busse LW; Kashani KB
[Ad] Address:Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN; Division of Pulmonary and Critical Care Medicine, Mayo Clinic, Rochester, MN. Electronic address: jentzer.jacob@mayo.edu.
[Ti] Title:Management of Refractory Vasodilatory Shock.
[So] Source:Chest;, 2018 Jan 09.
[Is] ISSN:1931-3543
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Refractory shock is a lethal manifestation of cardiovascular failure defined by an inadequate hemodynamic response to high doses of vasopressor medications. Approximately 7% of critically ill patients will develop refractory shock, with short-term mortality exceeding 50%. Refractory vasodilatory shock develops from uncontrolled vasodilation and vascular hyporesponsiveness to endogenous vasoconstrictors, causing failure of physiologic vasoregulatory mechanisms. Standard approaches to the initial management of shock include fluid resuscitation and initiation of norepinephrine. When these measures are inadequate to restore BP, vasopressin or epinephrine can be added. Few randomized studies exist to guide clinical management and hemodynamic stabilization in patients who do not respond to this standard approach. Adjunctive therapies, such as hydrocortisone, thiamine, and ascorbic acid, may increase BP in severe shock and should be considered when combination vasopressor therapy is needed. Novel vasopressor agents, such as synthetic human angiotensin II, can increase BP and reduce the need for high doses of catecholamine vasopressors in severe or refractory vasodilatory shock. Few effective rescue therapies exist for established refractory shock, which emphasizes the importance of aggressive intervention before refractory shock develops, including the earlier initiation of rational combination vasopressor therapy. The present review discusses the diagnosis and management of refractory shock to offer guidance for management of this important clinical problem and to provide a framework for future research.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1801
[Cu] Class update date: 180304
[Lr] Last revision date:180304
[St] Status:Publisher


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