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Altered epigenetic clock in children exposed to maltreatment

at 4.1 mg/dL from blood drawn at 06.00 hours on the second hospital day. Her hands and feet went numb for 30 min at approximately 20.00 hours, so we collected blood. We confirmed a significant decrease in her serum phosphorus concentration to 1.1 mg/dL. We believed it to be refeeding syndrome and administered phosphorus to protect against hypophosphatemia by giving her 200 mg of sodium dihydrogen phosphate along with 620 mg of sodium phosphate via intravenous drip. Her serum phosphorus concentration recovered to 4.9 mg/dL according to a blood test taken 4 hours later (Fig. 1), with much less numbness. Her serum potassium was mildly low at 2.9–3.2 mmol/L during the course of treatment but there was no significant change. The preserved samples were tested again in order to confirm the accuracy of the test results; however, the same results were indicated. We wondered about the rapid recovery of phosphorus, which normally cannot be seen in refeeding syndrome. Regarding respiratory alkalosis, there are reports indicating that decreased serum phosphorus improved in 30 min to 2 h once breathing was stabilized. A decline in PaCO2 due to hyperventilation leads to an increase in pH within the cells, with phosphorus moving inside the cell along with H movement, leading to hypophosphatemia. When hyperventilation disappears and respiratory alkalosis is corrected, phosphorus immediately moves out of the cells and the blood phosphorus concentration rises. The above are the mechanisms of onset and recovery of hypophosphatemia due to respiratory alkalosis. In this case, the period from the decrease in serum phosphorus to the recovery thereof was short. There was no decrease in magnesium and potassium, which are seen with refeeding syndrome. The risk factors for refeeding hypophosphatemia developing in AN patients has been previously reported. In this patient, lower BMI (14.7 kg/m) applied as a risk factor, however the other factors are not associated with an increased risk of refeeding hypophosphatemia, the patient was young, and her blood urea nitrogen and creatinine levels on the first day of hospitalization were normal, at 15 and 0.59 mg/dL, respectively. Although no one observed hyperventilation seizures on the second hospital day, based on the fact that mild hyperventilation was observed on the first hospital day, we believe that this patient suffered from hypophosphatemia due to respiratory alkalosis. A blood gas analysis is useful for accurately diagnosing respiratory alkalosis. We did not know that respiratory alkalosis could cause hypophosphatemia at that time and as a result we did not perform a blood gas analysis. When hypophosphatemia occurs while supplying nutrition, it is necessary to consider the possibility of respiratory alkalosis as well as refeeding syndrome. We recommend that serum phosphate levels be carefully monitored even when such patients show no hyperventilation. The patient provided her permission for the publication of these features of her case and her anonymity has been preserved. Disclosure statement The authors declare no conflict of interest.