Neurology -- Correspondence for Singh and Kumar, 68 (11) 807-811

Correspondence published:

Wernicke encephalopathy after obesity surgery: A systematic review: Alessandro Serra, GianPietro Sechi (23 May 2007)

Reply from the authors: Sonal Singh, Abhay Kumar (23 May 2007)

Wernicke encephalopathy after obesity surgery: A systematic review 23 May 2007

Alessandro Serra,
Institute of Clinical Neurology, University of Sassari
Viale S. Pietro 10, 07100 Sassari, Italy,
GianPietro Sechi
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Re: Wernicke encephalopathy after obesity surgery: A systematic review

alserra{at}uniss.it Alessandro Serra, et al.

We read the article by Singh and Kumar with interest.[1] The authors suggest that prospective studies to determine the prevalence of Wernicke encephalopathy after obesity surgery and protocols for preventive thiamine supplementation need evaluation. [1] In the past few years, the number of people with morbid obesity has increased. Because of this, the number of obesity surgical procedures has also been increasing, [2] as has the number of published cases of Wernicke encephalopathy related to these surgical procedures. [3]
However, the statement that the half- life of thiamine is 10 to 20 days is incorrect and, in our opinion, this item should be further clarified. Twenty days is the sufficient time to deplete the body’s reserves of thiamine. [3] Thus, in a healthy individual, any condition of unbalanced nutrition that lasts 2-3 weeks may lead to Wernicke encephalopathy. [3] The half-life of thiamine after IV administration is 96 minutes, while the elimination half-life after oral administration is 154 minutes. [4] This short half-life explains the need of administering thiamine three times per day for patients with Wernicke encephalopathy and those at risk of developing it. This is mandatory when thiamine supplementation is administered by mouth, because this vitamin is absorbed in the duodenum by a rate-limiting process. In healthy individuals, the calculated maximum amount of thiamine that can be absorbed from a single oral dose is about 4.5 mg, [5] whereas in an individual with chronic malnutrition this amount can be reduced by about 70%. [5]
References
1. Singh S,Kumar A. Wernicke encephalopathy after obesity surgery. A systematic review. Neurology 2007;68:807-811.
2. Steinbrook R. Surgery for severe obesity. N Engl J Med 2004;350:1075-1079.
3. Sechi GP, Serra A. Wernicke’s encephalopathy: new clinical settings and recent advances in diagnosis and management. Lancet Neurol 2007;6:442-455.
4. Tallaksen CM, Sande A, Bohmer T, Bell H, Karlsen J. Kinetics of thiamin and thiamin phosphate esters in human blood, plasma and urine after 50 mg intravenously or orally. Eur J Clin Pharmacol 1993;44:73-78.
5. Thomson AD, Cook CCH, Touquet R, Henry JA. The Royal College of Physicians report on alcohol: guidelines for managing Wernicke’s encephalopathy in the accident and emergency department. Alcohol Alcohol Suppl 2002;37:513-521.
Disclosure: the authors report no conflicts of interest.

Reply from the authors 23 May 2007

Sonal Singh,
Wake Forest University School of Medicine
Section on General Internal Medicine, One Medical Center Blvd, Winston-Salem, NC, 27157,
Abhay Kumar
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Re: Reply from the authors

sosingh{at}wfubmc.edu Sonal Singh, et al.

We thank Drs. Serra and Sechi for clarifying that the pharmacological half-life of orally or parenterally administered thiamine is in the order of minutes, rather than days, requiring frequent administration of thiamine for the treatment of Wernicke encephalopathy.
We correlated the time taken to deplete body stores of thiamine with the time required for the onset of symptoms of Wernicke encephalopathy.[1] The daily requirement of thiamine for healthy individuals is related to their daily carbohydrate intake and is between 1-2 mg per day. [6] Since the body stores about 30-50 mg of thiamine, body stores will possibly be depleted in 4-6 weeks. [6] One week after the stores are depleted, the blood brain barrier is disrupted with local hypo-perfusion leading to signs of Wernicke encephalopathy.[7] This explains the development of Wernicke encephalopathy 4-12 weeks after gastric bypass surgery.
References
6. Thomson AD, Marshall EJ. The Natural History and Pathophysiology of Wernicke's Encephalopathy and Korsakoff's Psychosis. Alcohol Alcohol 2006;41:151-158.
7. Heye N, Terstegge K, Sirtl C, Mc Monagle U, Schreiber K, Meyer-Gebner M. Wernicke encephalopathy causes to consider. Intensive Care Med 1994;20 282-286.
Disclosure: The authors report no conflicts of interest.