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Of the seven patients that developed peripheral oedema, diglyceride only one patient also developed mild hypomagnesaemia (0.66?mmol/L). The remaining six patients developed peripheral oedema in the absence of any electrolyte derangement. Due to the small number of observed cases of patients developing hypophosphatemia (n = 1) or hypokalaemia (n = 3), statistical analysis was not completed due to the sample size selleck compound 7], particularly in the first week of inpatient refeeding. Prophylactic phosphate supplementation was provided, and mild electrolyte derangements were corrected with oral replacement. No incidence of RFS occurred. The principal concept for the development of RFS is due to the switch from the catabolic state to the anabolic state upon refeeding, causing electrolyte shifts, particularly when reintroducing carbohydrate. Due to the importance of phosphate in glucose metabolism, close monitoring of serum phosphate is important to prevent the occurrence of RFS [24, 25]. In the present study, patients received prophylactic phosphate supplementation before commencing a nutritional regimen, which may explain the low rate of patients developing hypophosphatemia during nutritional rehabilitation (1%). Other studies had similarly reported that patients prescribed with prophylactic phosphate before commencing refeeding did not develop hypophosphatemia click here or RFS when started on 1500?kcal�C2400?kcal [18, 21]. In contrast, studies that did not provide routine prophylactic phosphate supplementation observed higher rates of hypophosphatemia in up to 45% of study participants despite starting on lower caloric intakes compared with the current study, in the range of 1200�C2200?kcal/day [19, 22, 23]. Clinical cases of RFS have been reported when routine phosphate supplementation was not prescribed. Rio et al. [16] reported three cases of RFS out of 243 hospitalised adults who started on artificial nutrition support.