今日の臨床サポート

ウェルニッケ(Wernicke)脳症

著者: 星野晴彦 東京都済生会中央病院 脳神経内科 脳卒中センター

監修: 永山正雄 国際医療福祉大学大学院医学研究科 脳神経内科学

著者校正済:2021/12/08
現在監修レビュー中
参考ガイドライン:
  1. EFNS guidelines for diagnosis, therapy and prevention of Wernicke encephalopathy.Eur J Neurol 2010, 17: 1408–1418
患者向け説明資料

概要・推奨   

  1. ウェルニッケ脳症を疑った場合十分量のビタミンB1を投与すること(推奨度1
薬剤監修について:
オーダー内の薬剤用量は日本医科大学付属病院 薬剤部 部長 伊勢雄也 以下、林太祐、渡邉裕次、井ノ口岳洋、梅田将光による疑義照会のプロセスを実施、疑義照会の対象については著者の方による再確認を実施しております。
※薬剤中分類、用法、同効薬、診療報酬は、エルゼビアが独自に作成した薬剤情報であり、 著者により作成された情報ではありません。
尚、用法は添付文書より、同効薬は、薬剤師監修のもとで作成しております。
※同効薬・小児・妊娠および授乳中の注意事項等は、海外の情報も掲載しており、日本の医療事情に適応しない場合があります。
※薬剤情報の(適外/適内/⽤量内/⽤量外/㊜)等の表記は、エルゼビアジャパン編集部によって記載日時にレセプトチェックソフトなどで確認し作成しております。ただし、これらの記載は、実際の保険適応の査定において保険適応及び保険適応外と判断されることを保証するものではありません。また、検査薬、輸液、血液製剤、全身麻酔薬、抗癌剤等の薬剤は保険適応の記載の一部を割愛させていただいています。
(詳細はこちらを参照)
著者のCOI(Conflicts of Interest)開示:
星野晴彦 : 講演料(ブリストル・マイヤーズスクイブ,大塚製薬,第一三共)[2022年]
監修:永山正雄 : 特に申告事項無し[2022年]

改訂のポイント:
  1. 病態と臨床症状、治療について追記した。

病態・疫学・診察

疾患(疫学・病態)のまとめ  
  1. ウェルニッケ脳症はビタミンB1(チアミン)欠乏による脳症であり、特徴的な臨床症状と画像所見が診断の契機となるが、診断のためには本疾患を疑うことが最も重要であり、見逃されている症例も多いと考えられている。
  1. 治療が遅れるとコルサコフ症候群に移行してしまうことから、ビタミンB1を速やかに大量に補給することが必要である。
  1. 剖検の検討では0.4~2.8%にウェルニッケ脳症が認められたと報告され、アルコール依存症患者ではさらに高率である[1]
  1. 男女比は1.7:1と男性で多い。
  1. ビタミンB1は体内には30-50 mg蓄えられており、1000kcalにつき0.5 mg消費され、1日消費量は2 mg程度とされている。
  1. ビタミンB1であるチアミンはthiamine pyrophosphateとなって、TCAサイクルのα-keto glutamate dehydrogenaseとpyruvate dehydrogenase、pentose phosphate pathwayのtransketolase、分子アミノ酸代謝のbranched chain alpha ketoacid dehydrogenaseの補酵素として働く。このうち、transketolaseがビタミンB1欠乏の指標としては最も鋭敏な指標である。
  1. ビタミンB1欠乏によって、脚気も生じるが、アジア人は脚気に、ヨーロッパ人はウェルニッケ脳症になりやすいとされている。環境要因と遺伝的な要因によると考えられている。
問診・診察のポイント  
  1. アルコール摂取歴、嗜好を確認すること。ただし、アルコール多飲者での発症例が有名であるが、アルコール摂取とは関連なく発症することもある。

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文献 

R Galvin, G Bråthen, A Ivashynka, M Hillbom, R Tanasescu, M A Leone, EFNS
EFNS guidelines for diagnosis, therapy and prevention of Wernicke encephalopathy.
Eur J Neurol. 2010 Dec;17(12):1408-18. doi: 10.1111/j.1468-1331.2010.03153.x.
Abstract/Text BACKGROUND: Although Wernicke encephalopathy (WE) is a preventable and treatable disease it still often remains undiagnosed during life.
OBJECTIVES: To create practical guidelines for diagnosis, management and prevention of the disease.
METHODS: We searched MEDLINE, EMBASE, LILACS, Cochrane Library.
CONCLUSIONS AND RECOMMENDATIONS: 1 The clinical diagnosis of WE should take into account the different presentations of clinical signs between alcoholics and non alcoholics (Recommendation Level C); although prevalence is higher in alcoholics, WE should be suspected in all clinical conditions which could lead to thiamine deficiency (good practice point - GPP). 2 The clinical diagnosis of WE in alcoholics requires two of the following four signs; (i) dietary deficiencies (ii) eye signs, (iii) cerebellar dysfunction, and (iv) either an altered mental state or mild memory impairment (Level B). 3 Total thiamine in blood sample should be measured immediately before its administration (GPP). 4 MRI should be used to support the diagnosis of acute WE both in alcoholics and non alcoholics (Level B). 5 Thiamine is indicated for the treatment of suspected or manifest WE. It should be given, before any carbohydrate, 200 mg thrice daily, preferably intravenously (Level C). 6 The overall safety of thiamine is very good (Level B). 7 After bariatric surgery we recommend follow-up of thiamine status for at least 6 months (Level B) and parenteral thiamine supplementation (GPP). 8 Parenteral thiamine should be given to all at-risk subjects admitted to the Emergency Room (GPP). 9 Patients dying from symptoms suggesting WE should have an autopsy (GPP).

© 2010 The Author(s). European Journal of Neurology © 2010 EFNS.
PMID 20642790
C G Harper, M Giles, R Finlay-Jones
Clinical signs in the Wernicke-Korsakoff complex: a retrospective analysis of 131 cases diagnosed at necropsy.
J Neurol Neurosurg Psychiatry. 1986 Apr;49(4):341-5.
Abstract/Text A recent necropsy study has shown that 80% of patients with the Wernicke-Korsakoff syndrome were not diagnosed as such during life. Review of the clinical signs of these cases revealed that only 16% had the classical clinical triad and 19% had no documented clinical signs. The incidence of clinical signs in this and other retrospective pathological studies is very different from that of prospective clinical studies. This discrepancy may relate to "missed" clinical signs but the magnitude of the difference suggests that at least some cases of the Wernicke-Korsakoff syndrome may be the end result of repeated subclinical episodes of vitamin B1 deficiency. In order to make the diagnosis, clinicians must maintain a high index of suspicion in the "at risk" group of patients, particularly alcoholics. Investigations of thiamine status may be helpful and if the diagnosis is suspected, parenteral thiamine should be given.

PMID 3701343
D Caine, G M Halliday, J J Kril, C G Harper
Operational criteria for the classification of chronic alcoholics: identification of Wernicke's encephalopathy.
J Neurol Neurosurg Psychiatry. 1997 Jan;62(1):51-60.
Abstract/Text OBJECTIVES: To establish better operational criteria for the diagnosis of Wernicke's encephalopathy. Current criteria for diagnosing Wernicke's encephalopathy require the presence of three clinical signs (oculomotor abnormalities, cerebellar dysfunction, and an altered mental state), although it has often been reported that most patients do not fulfil all these criteria.
METHODS: The clinical histories of 28 alcoholics with neurological and neuropsychological assessments and definitive neuropathological diagnoses were examined to determine clinical signs for use in a screening schedule. Operational criteria were then proposed for differentiating patients with Wernicke's encephalopathy alone or in combination with Korsakoff's psychosis or hepatic encephalopathy. The new criteria for Wernicke's encephalopathy require two of the following four signs; (1) dietary deficiencies, (2) oculomotor abnormalities, (3) cerebellar dysfunction, and (4) either an altered mental state or mild memory impairment. Reproducibility and validity testing of these criteria were performed on 106 alcoholics screened from a large necropsy sample.
RESULTS: Despite rater variability with regard to specific symptoms, within and between rater reliability for diagnostic classification using the criteria retrospectively on patient records was 100% for three independent raters. Validity testing showed that Wernicke's encephalopathy was underrecognized only when occurring with hepatic encephalopathy (50% sensitivity).
CONCLUSIONS: By contrast with current criteria, the proposed operational criteria show that the antemortem identification of Wernicke's encephalopathy can be achieved with a high degree of specificity.

PMID 9010400
Giulio Zuccoli, Nicolò Pipitone
Neuroimaging findings in acute Wernicke's encephalopathy: review of the literature.
AJR Am J Roentgenol. 2009 Feb;192(2):501-8. doi: 10.2214/AJR.07.3959.
Abstract/Text OBJECTIVE: Wernicke's encephalopathy is an acute neurological syndrome resulting from thiamine (vitamin B1) deficiency. Early recognition is important because timely thiamine supplementation can reverse the clinical features of the disease. The aim of this article is to provide an update on the typical and atypical neuroimaging findings of the acute phase of the disease.
CONCLUSION: Wernicke's encephalopathy is characterized by a quite distinct pattern of MR alterations, which include symmetrical alterations in the thalami, mamillary bodies, tectal plate, and periaqueductal area, but atypical alterations may also been seen. A thorough knowledge of the neuroimaging findings of Wernicke's encephalopathy will assist in arriving at an early diagnosis, thus reducing the morbidity and mortality associated with this disease.

PMID 19155417
N Latt, G Dore
Thiamine in the treatment of Wernicke encephalopathy in patients with alcohol use disorders.
Intern Med J. 2014 Sep;44(9):911-5. doi: 10.1111/imj.12522.
Abstract/Text Wernicke encephalopathy is an acute, reversible neuropsychiatric emergency due to thiamine deficiency. Urgent and adequate thiamine replacement is necessary to avoid death or progression to Korsakoff syndrome with largely irreversible brain damage. Wernicke Korsakoff syndrome refers to a condition where features of Wernicke encephalopathy are mixed with those of Korsakoff syndrome. Although thiamine is the cornerstone of treatment of Wernicke encephalopathy, there are no universally accepted guidelines with regard to its optimal dose, mode of administration, frequency of administration or duration of treatment. Currently, different dose recommendations are being made. We present recommendations for the assessment and treatment of Wernicke encephalopathy based on literature review and our clinical experience.

© 2014 The Authors; Internal Medicine Journal © 2014 Royal Australasian College of Physicians.
PMID 25201422
Simon J Scalzo, Stephen C Bowden, Margaret L Ambrose, Greg Whelan, Mark J Cook
Wernicke-Korsakoff syndrome not related to alcohol use: a systematic review.
J Neurol Neurosurg Psychiatry. 2015 Dec;86(12):1362-8. doi: 10.1136/jnnp-2014-309598. Epub 2015 Jan 14.
Abstract/Text OBJECTIVE: Although Wernicke-Korsakoff syndrome (WKS) is a common condition, diagnosis remains difficult. WKS not associated with alcohol is rare and thought to present differently to alcohol-related WKS. We conducted a systematic review of WKS not related to alcohol to enhance understanding of WKS not related to alcohol and WKS in general.
METHODS: A systematic review was conducted of case reports, published in English, of Wernicke's encephalopathy and WKS in patients without a history of alcohol-use disorder. Main data sources: MEDLINE, Index Medicus. Eligible cases totaled 623. Publication dates ranged from 1867 to 2014. Comparisons of clinical presentation were made with published data on samples comprising, almost exclusively, alcohol-related WKS.
RESULTS: A wide array of illnesses precipitated WKS. When diagnosis of WKS was performed postmortem, non-alcohol-related cases presented a similar number of signs of the classic triad as alcohol-related cases (p=0.662, Cohen's w=0.12) but more signs when diagnosed antemortem (p<0.001, Cohen's w=0.46). The most common sign was altered mental state. Korsakoff syndrome or ongoing memory impairment was reported in 25% of non-alcohol-related WKS, although cognitive status was not explicitly reported in many cases. When duration of memory impairment was reported, 56% had clinically obvious memory impairment lasting beyond the period of acute presentation. Non-alcohol-related WKS was more often associated with female gender, younger age, shorter duration of precipitating illness and better survival rate compared to alcohol-related WKS.
CONCLUSIONS: Thiamine deficiency in the absence of an alcohol-use disorder can cause the full clinical spectrum of WKS, including chronic cognitive impairment and Korsakoff syndrome.

Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/
PMID 25589780
Allan D Thomson, Christopher C H Cook, Robin Touquet, John A Henry, Royal College of Physicians, London
The Royal College of Physicians report on alcohol: guidelines for managing Wernicke's encephalopathy in the accident and Emergency Department.
Alcohol Alcohol. 2002 Nov-Dec;37(6):513-21.
Abstract/Text The Royal College of Physicians (London) recently published its latest report on alcohol misuse entitled 'Alcohol - Can the NHS Afford It?'. Part of this document, encompassing our views, has made specific recommendations for the management of patients in the Accident and Emergency (A&E) Department who may possibly have, or are at risk of developing, Wernicke's encephalopathy. Patients showing evidence of chronic alcohol misuse and suspected of having a poor diet should be treated at the outset with B vitamins intravenously or intramuscularly, especially when the clinical signs are initially masked by drunkenness at presentation to the A&E Department. This commentary offers a review of the scientific foundations on which these recommendations have been made.

PMID 12414541
Nathalie Pruckner, Josef Baumgartner, Barbara Hinterbuchinger, Alexander Glahn, Sandra Vyssoki, Benjamin Vyssoki
Thiamine Substitution in Alcohol Use Disorder: A Narrative Review of Medical Guidelines.
Eur Addict Res. 2019;25(3):103-110. doi: 10.1159/000499039. Epub 2019 Mar 21.
Abstract/Text AIMS: Patients with alcohol use disorder (AUD) frequently suffer from cognitive deficits ranging from mild symptoms to most severe forms. Wernicke encephalopathy (WE), caused by thiamine deficiency, is a potentially fatal syndrome characterized by the clinical triad of ophthalmoplegia, ataxia, and confusion. WE frequently presents in patients with AUD and, if left untreated, can progress to Wernicke-Korsakoff syndrome, which constitutes severe anterograde amnesia, confabulation, and behavioral abnormalities. Due to oftentimes indistinct clinical presentation, WE remains undiagnosed in up to 80% of cases. We conducted a review of current treatment guidelines for AUD in order to identify recommendations for the use of thiamine.
METHODS: Three different keyword combinations ("alcohol treatment guideline," "alcohol withdrawal guideline," and "alcohol treatment recommendation") were entered in PubMed and Scopus, additional guidelines were searched screening the online sites of the respective agencies or societies. In total, 14 guidelines were included.
RESULTS: Thiamine was mentioned in all but one of the reviewed publications. Specifications on application modalities and indications varied considerably. While the majority of reviewed guidelines recommended parenteral thiamine only for patients at high risk for WE, some gave no information regarding the application form or dosage.
CONCLUSION: Substitution of parenteral thiamine in individuals with suspected WE is a well-established treatment regimen. However, suggestions according to guidelines vary widely. Furthermore, hardly any evidence-based recommendations exist on a more general use of thiamine as a preventative intervention in individuals with AUD. Further research is of utmost importance to raise awareness for this potentially undervalued problem.

© 2019 S. Karger AG, Basel.
PMID 30897571
Erik Oudman, Jan W Wijnia, Misha J Oey, Mirjam van Dam, Albert Postma
Wernicke-Korsakoff syndrome despite no alcohol abuse: A summary of systematic reports.
J Neurol Sci. 2021 Jul 15;426:117482. doi: 10.1016/j.jns.2021.117482. Epub 2021 May 7.
Abstract/Text BACKGROUND: Wernicke-Korsakoff syndrome (WKS) is a neurological disorder typically found in alcohol use disorder. The fact that it also occurs in nonalcoholic patients is less well known and often ignored. For the first time, this review offers a systematic investigation of the frequency and associated features of nonalcoholic WKS in the published literature.
METHOD: We included 11 recent systematic reports, with a total of 586 nonalcoholic WKS cases following hyperemesis gravidarum (n = 177), cancer (n = 129), bariatric surgery (n = 118), hunger strike (n = 41), soft drink diet in children (n = 33), depression (n = 21), Crohn's disease (n = 21), schizophrenia (n = 15), anorexia nervosa (n = 12), ulcerative colitis (n = 10), and incidental thiamine-deficient infant formula (n = 9).
FINDINGS: Vomiting and extreme weight loss were strong predictors of nonalcoholic WKS in adults. Blurred vision was a common presenting sign in about one-fourth of the patients. The classic triad of WKS is characterized by confusion, ataxia, and eye-movement disorders. All reviewed studies reported high percentages of patients presenting with an altered mental status, while both motor symptoms were variably present.
INTERPRETATION: The foregoing observations led to several important conclusions. First, we can see that nutritional impoverishment leads to profound brain damage in the form of WKS. Second, it seems that physicians are either unaware of or underestimate the risks for nonalcoholic WKS. Physicians must be specifically vigilant in detecting and treating WKS in patients with sudden and severe weight loss and vomiting. Third, lower doses of thiamine frequently lead to chronic Wernicke-Korsakoff syndrome. We noticed that when thiamine treatment for WKS was administered, in many cases doses were too low. In line with proven interventions we therefore recommend a parenteral thiamine treatment of 500 mg 3 times per day in adults.

Copyright © 2021 The Author(s). Published by Elsevier B.V. All rights reserved.
PMID 34000679
Erlend Tuseth Aasheim
Wernicke encephalopathy after bariatric surgery: a systematic review.
Ann Surg. 2008 Nov;248(5):714-20. doi: 10.1097/SLA.0b013e3181884308.
Abstract/Text OBJECTIVE: To review the clinical essentials of Wernicke encephalopathy (WE) after bariatric surgery.
SUMMARY BACKGROUND DATA: An estimated 205,000 bariatric surgical procedures were performed in the United States in 2007. Such procedures may potentially lead to severe nutritional complications.
METHODS: Literature searches were performed in Medline, Embase, and abstract collections. Inclusion criteria were WE after bariatric surgery, diagnosed by the presence of two or more of the following signs: mental status changes, eye movement abnormalities, cerebellar dysfunction, and dietary deficiency.
RESULTS: Of 104 reported cases of WE after bariatric surgery, 84 cases were included. Gastric bypass or a restrictive procedure had been performed in 80 cases (95%). Admission to hospital for WE occurred within 6 months of surgery in 79 cases (94%). Frequent vomiting was a risk factor in 76 cases (90%) and had lasted for a median of 21 days at admission. Intravenous glucose administration without thiamine was a risk factor in 15 cases (18%). Brain magnetic resonance imaging identified lesions characteristic of WE in 14 of 30 cases (47%). Incomplete recovery was observed in 41 cases (49%); memory deficits and gait difficulties were frequent sequela. The recent increase in the use of bariatric surgery in the United States was associated with an increase in reported WE cases.
CONCLUSIONS: The number of WE cases after bariatric surgery is substantially higher than previously reported. Surgeons, allied health providers, and patients need to be aware of the predisposing factors and symptoms to prevent and optimize the management of this condition.

PMID 18948797
Gianpietro Sechi, Alessandro Serra
Wernicke's encephalopathy: new clinical settings and recent advances in diagnosis and management.
Lancet Neurol. 2007 May;6(5):442-55. doi: 10.1016/S1474-4422(07)70104-7.
Abstract/Text Wernicke's encephalopathy is an acute neuropsychiatric syndrome resulting from thiamine deficiency, which is associated with significant morbidity and mortality. According to autopsy-based studies, the disorder is still greatly underdiagnosed in both adults and children. In this review, we provide an update on the factors and clinical settings that predispose to Wernicke's encephalopathy, and discuss the most recent insights into epidemiology, pathophysiology, genetics, diagnosis, and treatment. To facilitate the diagnosis, we classify the common and rare symptoms at presentation and the late-stage symptoms. We emphasise the optimum dose of parenteral thiamine required for prophylaxis and treatment of Wernicke's encephalopathy and prevention of Korsakoff's syndrome associated with alcohol misuse. A systematic approach helps to ensure that patients receive a prompt diagnosis and adequate treatment.

PMID 17434099
Jeffrey I Mechanick, Caroline Apovian, Stacy Brethauer, W Timothy Garvey, Aaron M Joffe, Julie Kim, Robert F Kushner, Richard Lindquist, Rachel Pessah-Pollack, Jennifer Seger, Richard D Urman, Stephanie Adams, John B Cleek, Riccardo Correa, M Kathleen Figaro, Karen Flanders, Jayleen Grams, Daniel L Hurley, Shanu Kothari, Michael V Seger, Christopher D Still
CLINICAL PRACTICE GUIDELINES FOR THE PERIOPERATIVE NUTRITION, METABOLIC, AND NONSURGICAL SUPPORT OF PATIENTS UNDERGOING BARIATRIC PROCEDURES - 2019 UPDATE: COSPONSORED BY AMERICAN ASSOCIATION OF CLINICAL ENDOCRINOLOGISTS/AMERICAN COLLEGE OF ENDOCRINOLOGY, THE OBESITY SOCIETY, AMERICAN SOCIETY FOR METABOLIC & BARIATRIC SURGERY, OBESITY MEDICINE ASSOCIATION, AND AMERICAN SOCIETY OF ANESTHESIOLOGISTS - EXECUTIVE SUMMARY.
Endocr Pract. 2019 Dec;25(12):1346-1359. doi: 10.4158/GL-2019-0406. Epub 2019 Nov 4.
Abstract/Text Objective: The development of these updated clinical practice guidelines (CPGs) was commissioned by the American Association of Clinical Endocrinologists (AACE), The Obesity Society, American Society of Metabolic and Bariatric Surgery, Obesity Medicine Association, and American Society of Anesthesiologists Boards of Directors in adherence with the AACE 2017 protocol for standardized production of CPGs, algorithms, and checklists. Methods: Each recommendation was evaluated and updated based on new evidence from 2013 to the present and subjective factors provided by experts. Results: New or updated topics in this CPG include: contextualization in an adiposity-based chronic disease complications-centric model, nuance-based and algorithm/checklist-assisted clinical decision-making about procedure selection, novel bariatric procedures, enhanced recovery after bariatric surgery protocols, and logistical concerns (including cost factors) in the current health-care arena. There are 85 numbered recommendations that have updated supporting evidence, of which 61 are revised and 12 are new. Noting that there can be multiple recommendation statements within a single numbered recommendation, there are 31 (13%) Grade A, 42 (17%) Grade B, 72 (29%) Grade C, and 101 (41%) Grade D recommendations. There are 858 citations, of which 81 (9.4%) are evidence level (EL) 1 (highest), 562 (65.5%) are EL 2, 72 (8.4%) are EL 3, and 143 (16.7%) are EL 4 (lowest). Conclusion: Bariatric procedures remain a safe and effective intervention for higher-risk patients with obesity. Clinical decision-making should be evidence based within the context of a chronic disease. A team approach to perioperative care is mandatory, with special attention to nutritional and metabolic issues. A1C = hemoglobin A1c; AACE = American Association of Clinical Endocrinologists; ABCD = adiposity-based chronic disease; ACE = American College of Endocrinology; ADA = American Diabetes Association; AHI = Apnea-Hypopnea Index; ASA = American Society of Anesthesiologists; ASMBS = American Society of Metabolic and Bariatric Surgery; BMI = body mass index; BPD = biliopancreatic diversion; BPD/DS = biliopancreatic diversion with duodenal switch; CI = confidence interval; CPAP = continuous positive airway pressure; CPG = clinical practice guideline; CRP = C-reactive protein; CT = computed tomography; CVD = cardiovascular disease; DBCD = dysglycemia-based chronic disease; DS = duodenal switch; DVT = deep venous thrombosis; DXA = dual-energy X-ray absorptiometry; EFA = essential fatty acid; EL = evidence level; EN = enteral nutrition; ERABS = enhanced recovery after bariatric surgery; FDA = U.S. Food and Drug Administration; G4G = Guidelines for Guidelines; GERD = gastroesophageal reflux disease; GI = gastrointestinal; HCP = health-care professional(s); HTN = hypertension; ICU = intensive care unit; IGB = intragastric balloon(s); IV = intravenous; LAGB = laparoscopic adjustable gastric band; LAGBP = laparoscopic adjustable gastric banded plication; LGP = laparoscopic greater curvature (gastric) plication; LRYGB = laparoscopic Roux-en-Y gastric bypass; LSG = laparoscopic sleeve gastrectomy; MetS = metabolic syndrome; NAFLD = nonalcoholic fatty liver disease; NASH = nonalcoholic steatohepatitis; NSAID = nonsteroidal anti-inflammatory drug; OA = osteoarthritis; OAGB = one-anastomosis gastric bypass; OMA = Obesity Medicine Association; OR = odds ratio; ORC = obesity-related complication(s); OSA = obstructive sleep apnea; PE = pulmonary embolism; PN = parenteral nutrition; PRM = pulmonary recruitment maneuver; RCT = randomized controlled trial; RD = registered dietician; RDA = recommended daily allowance; RYGB = Roux-en-Y gastric bypass; SG = sleeve gastrectomy; SIBO = small intestinal bacterial overgrowth; TOS = The Obesity Society; TSH = thyroid-stimulating hormone; T1D = type 1 diabetes; T2D = type 2 diabetes; VTE = venous thromboembolism; WE = Wernicke encephalopathy; WHO = World Health Organization.

PMID 31682518

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