Editorial Comment

Abstract

I would like to commend Carrodeguas et al. [ [1] Carrodeguas L. Kaidar-Person O.K. Szomestein S. Antozzi P. Rosenthal R. Preoperative thiamine deficiency in an obese population undergoing laparoscopic bariatric surgery. Surg Obes Relat Dis. 2005; 1: 517-522 Abstract Full Text Full Text PDF PubMed Scopus (94) Google Scholar ] for publishing the first article dealing with the preoperative quantification of thiamine deficiency in the bariatric surgery population. Postoperative thiamine deficiency has been well described, initially after restrictive procedures by MacLean et al. [ [2] MacLean L.D. Rhode B.M. Shizgal H.M. Nutrition following gastric operations for morbid obesity. Ann Surg. 1983; 198: 347-355 Crossref PubMed Scopus (118) Google Scholar ] and later after gastric bypass operations by the late John Halverson [ [3] Halverson J.D. Metabolic risk of obesity surgery and long-term follow-up. Am J Clin Nutr. 1992; 55: 602S-605S PubMed Google Scholar ]. In addition, the need for bariatric surgeons to realize its significance, as illustrated by Mason [ [4] Mason E.E. Starvation injury after gastric reduction for obesity. World J Surg. 1998; 22: 1002-1007 Crossref PubMed Scopus (66) Google Scholar ], must not go unnoticed. This complex nutritional derangement, with its radiographic [ [5] Doherty M.J. Watson N.F. Uchino K. Hallam D.K. Cramer S.C. Diffusion abnormalities in patients with Wernicke encephalopathy. Neurology. 2002; 58: 655-657 Crossref PubMed Scopus (56) Google Scholar ] and clinicopathologic sequellae [ [6] Nautiyal A. Singh S. Alaimo D.J. Wernicke encephalopathy – an emerging trend after bariatric surgery. Am J Med. 2004; 117: 804-805 Abstract Full Text Full Text PDF PubMed Scopus (34) Google Scholar ], has received a tremendous amount of press in the last 24 months. However, to date, little instruction has been given to bariatric surgeons on its preoperative and postoperative management.