Colonic Hyponatraemia: Where Has the Salt Gone?Tran, Huy A. FACE, FRCPA, FRACPAuthor Information Director of Clinical Chemistry and Associate Professor, Hunter Area Pathology Service, John Hunter Hospital and University of Newcastle, Newcastle, New South Wales, Australia. The author has disclosed that he has no significant relationships with or financial interests in any commercial company that pertains to this educational activity. Lippincott Continuing Medical Education Institute, Inc. has identified and resolved all faculty conflicts of interest regarding this educational activity. Reprints: Huy A. Tran, Department of Clinical Chemistry, Hunter Area Pathology Service, John Hunter Hospital, New South Wales 2310, Australia. E-mail: firstname.lastname@example.org. Chief Editor’s Note: This article is the 4th of 36 that will be published in 2007 for which a total of up to 36 AMA PRA Category 1 Credits™ can be earned. Instructions for how credits can be earned precede the CME Examination at the back of this issue. The Endocrinologist: January/February 2007 - Volume 17 - Issue 1 - pp 46-49 doi: 10.1097/01.ten.0000255883.83478.c8 Buy Take the CME Test Metrics Abstract Hyponatraemia is a common condition in the hospitalized population with the syndrome of inappropriate antidiuretic hormone secretion being the most common cause. The assessment of such a biochemical condition necessitates a careful clinical evaluation of hydration status. It is important that the source of sodium loss is identified to ensure correct management. The following case illustrates how a careful clinical and biochemical evaluation can reveal the gastrointestinal tract as a source of sodium loss, in this case a recto-sigmoid adenocarcinoma being the cause of hyponatraemia. Fluid extracted from the colonic adenoma was analyzed biochemically providing a unique opportunity and insight into the pathogenesis of adenomatous-associated hyponatraemia. © 2007 Lippincott Williams & Wilkins, Inc.