As an alternative to corticosteroids, evidence supports enteral nutrition to induce disease remission. Food re-introduction diets provide structure to food re-introduction and help maintain disease remission. These guidelines aim to reduce variation in clinical practice.

Background: Refeeding syndrome (RS) is a potentially fatal condition that can occur following the re-introduction of nutrition after a period of starvation. Hypophosphataemia following the reintroduction of nutrition is often the only reliable biochemical marker of RS. Refeeding index (RI) generated from baseline insulin-like growth factor-1 (IGF-1) and leptin has been proposed as a useful biochemical marker for the identification of patients at risk of developing refeeding hypophosphataemia (RH). Methods: A prospective study included 52 patients referred for parenteral nutrition (PN). The sensitivity and specificity of IGF-1 measured using a sensitive assay was compared to the RI in predicting the development of RH (a 530% drop in PO 4 during the first 36-h of PN administration). Leptin and IGF-1 were analysed on baseline samples using a quantitative enzyme-linked immunoassay. Daily blood samples were collected from all patients for routine biochemistry for the full duration of PN administration. Results: High sensitivity IGF-1 measurement alone was comparable with the RI, using receiver-operating characteristic (ROC) curve analysis, with areas under the curve being 0.79 and 0.80, respectively, and superior to leptin alone (0.72) for predicting 530% drop in PO 4 . The cut-off value for IGF-1 that gave best sensitivity (91% [95% CI 75-98%]) and specificity (65% [95% CI 41-85%]) was 63.7 mg/L, with a likelihood ratio of 2.59. Conclusion: Baseline IGF-1 is an objective, sensitive and specific biochemical marker in identifying patients who are at high risk of developing RH prior to PN administration and therefore may have a role in clinical practice.

We present the case of a 62-year-old man on the intensive care unit with pancreatitis. Since early in his admission, and for the remainder of his prolonged stay in intensive care, he has received parenteral nutrition for intestinal failure. The whole blood manganese concentration was significantly increased after 2½ months of parenteral nutrition (PN). Three months into his stay, he developed a resting tremor and extra-pyramidal dyskinesia. In the absence of other neurological symptoms, and with no history of essential tremor, Parkinsonism or cerebral signs, hypermanganesaemia was presumed to be the cause. We review manganese metabolism and toxicity in patients who are fed with parenteral nutrition and review the current recommendations and guidelines.

Dear Sir,We have recently reported on a case of presumed manganese (Mn) toxicity in a patient requiring longterm parenteral nutrition (PN) for intestinal failure associated with acute pancreatitis and hepatobiliary failure.1 The report highlighted the non-specific symptoms associated with manganaemia and discussed accumulation within the brain with neurological manifestations. It also highlighted that toxicity can occur in critically ill patients given manganesesupplemented PN, deficiency is rarer than toxicity in critically ill patients, and that the current recommendations may over-estimate daily parenteral requirements.Manganese distributes very rapidly into tissues and eliminates rapidly from the blood compartment. Total body elimination half-life in humans is reported as 34 (females) to 48 (males) days, 2 predominantly via the hepatobiliary system. However, there are limited data on manganese elimination in patients with impaired hepatobiliary function.In this reported case, total blood manganese concentration was measured at regular intervals over several months, after the Mn had been removed from the PN.1 These results were modelled using a PK program (Excel, MS Office 2015). A semi-log plot showed good correlation (r ¼ À0.93), suggesting first-order elimination (Figure 1). The elimination half-life was calculated to be 153.3 days, 3.1-fold greater than in patients with normal liver function.These data are consistent with previous findings suggesting that elimination of manganese is significantly impaired in the patient with concomitant hepatobiliary dysfunction.