Refeeding syndromeBMJ 2004; 328 doi: https://doi.org/10.1136/bmj.328.7445.908 (Published 15 April 2004) Cite this as: BMJ 2004;328:908
- Stephen D Hearing, consultant gastroenterologist (firstname.lastname@example.org)
- >Department of Gastroenterology, Staffordshire General Hospital, Weston Road, Stafford ST16 3SA
Is underdiagnosed and undertreated, but treatable
Refeeding syndrome was first described in Far East prisoners of war after the second world war.1 Starting to eat again after a period of prolonged starvation seemed to precipitate cardiac failure. The pathophysiology of refeeding syndrome has now been established.2 In starvation the secretion of insulin is decreased in response to a reduced intake of carbohydrates. Instead fat and protein stores are catabolised to produce energy. This results in an intracellular loss of electrolytes, in particular phosphate. Malnourished patients' intracellular phosphate stores can be depleted despite normal serum phosphate concentrations. When they start to feed a sudden shift from fat to carbohydrate metabolism occurs and secretion of insulin increases. This stimulates cellular uptake of phosphate, which can lead to profound hypophosphataemia.3 This phenomenon usually occurs within four days of starting to feed again.
Phosphate is necessary for the generation of adenosine triphosphate from adenosine diphosphate and adenosine monophosphate and other crucial phosphorylation reactions. Serum phosphate concentrations of less …
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