Summary Background:  Severe hypophosphataemia associated with refeeding syndrome requires treatment with intravenous phosphate to prevent potentially life‐threatening complications. However, evidence for replacement regimens is limited and current regimens are complex and replace phosphate inadequately. Aim:  To assess the effectiveness and safety of 50 mmol intravenous phosphate infusion, given as a ‘Phosphates Polyfusor’, for the treatment of severe hypophosphataemia in refeeding syndrome. Methods:  Patients with refeeding syndrome and normal renal function received a Phosphates Polyfusor infusion for the treatment of severe hypophosphataemia (< 0.50 mmol/L). The outcome measures were serial serum phosphate, creatinine and calcium concentrations for 4 days following phosphate infusion and adverse events. Results:  Over 2 years, 30 patients were treated. Following treatment, 37% of cases had a normal serum phosphate concentration and 73% had a serum phosphate concentration of > 0.5 mmol/L within 24 h. Ten patients required more than one Phosphates Polyfusor infusion. Within 72 h, 93% of cases had achieved a serum phosphate concentration of ≥ 0.50 mmol/L. No patient developed renal failure. Three episodes of transient mild hyperphosphataemia were recorded. Four patients developed mild hypocalcaemia. Conclusions:  This is the largest published series of the use of intravenous phosphate for the treatment of severe hypophosphataemia (< 0.50 mmol/L), and is the most effective regimen described. All patients had refeeding syndrome and were managed on general wards.

Context:Serum thyroid hormone levels differ between children and adults, but have not been studied longitudinally through childhood.Objective:To assess changes in thyroid-stimulating hormone (TSH) and thyroid hormone levels over childhood and their interrelationships.Design:Cohort study.Setting:The Avon Longitudinal Study of Parents and Children, a population-based birth cohort.Participants:A total of 4442 children who had thyroid function measured at age 7, and 1263 children who had thyroid function measured at age 15. Eight hundred eighty-four children had measurements at both ages.Main Outcome Measures:Reference ranges for TSH, free tri-iodothyronine (FT3), free thyroxine (FT4), their longitudinal stability, and interrelationships.Results:Children at age 7 years had a higher FT3 [6.17 pmol/L, standard deviation (SD) 0.62] than children at age 15 (5.83 pmol/L, SD 0.74); P < 0.0001 with 23.2% of children at age 7 having FT3 above the adult reference range. Higher FT3 levels at age 7 in boys (P = 0.0001) and girls (P = 0.04) were associated with attainment of a more advanced pubertal stage at age 13. TSH was positively associated with FT3 at age 7 and age 15 even after adjusting for confounders. In contrast, TSH was negatively associated with FT4.Conclusions:There are substantial changes in TSH and thyroid hormone levels over childhood, in particular for FT3, which appear to relate to pubertal readiness. Our data provide increased insight into the evolution of the pituitary–thyroid axis over childhood and may have implications for determining optimal ranges for thyroid hormone replacement in children.

GHD was more prevalent in BMT/TBI survivors than expected for the CRT dose in TBI, worsened with time and persisted into adulthood. GHD could not be explained by adiposity. There was no evidence of GH neurosecretory dysfunction or resistance after BMT/TBI.

The development and use of biochemical markers of cardiac damage is in a dynamic state. Creatine kinase (CK), aspartate aminotransferase (AST) and creatine kinase muscle± brain (CK±MB) remain in widespread use, but cardiac-speci®c isoforms of troponin T (cTnT) and troponin I (cTnI) have emerged as sensitive and speci®c indicators of myocardial infarction which are also used for risk strati®cation of patients with acute coronary syndrome. 1 The diagnostic performance of the troponins has been widely evaluated. It is important, however, that other factors, such as analytical performance, interpretation of results, availability out of hours and in vitro stability are considered before any new test is brought into routine use.Most laboratories store routine samples for up to 14 days at 48C. Retrospective analysis of cardiac markers is occasionally requested if the diagnosis of myocardial injury is not initially apparent or if the clinical presentation changes. Published and manufacturers' data on long-term in vitro stability of cardiac markers are limited. This study examines the stability of ®ve cardiac markers, CK, AST, CK±MB, cTnT and cTnI at 48C over 14 days.