CORRESPONDENCE Alendronate for the treatment of hypercalcaemia due to neonatal subcutaneous fat necrosis Nilay Hakan & Mustafa Aydin & Ayşegul Zenciroglu & Nihal Demirel & Nurullah Okumus & Semra Cetinkaya & Mehmet Sah Ipek Received: 21 February 2011 /Accepted: 29 March 2011 # Springer-Verlag 2011 Dear Editor, We read with great interest the article by Mitra et al. [3] who described subcutaneous fat necrosis (SCFN) in a preterm infant after severe perinatal hypoxic injury complicated by hypercalcaemia. Mitra et al. [3] state that significant SCFN can develop in both preterm and term infants and preterm infants also develop significant complications including hypercalcaemia. Most patients can be treated successfully by hyperhydration, furosemide, corticosteroids, and also by citrate, calcitonin, and bisphosphonates [4, 5]. Among the bisphosphonates, both etidronate [4] and pamidronate [2] have been used in the treatment of hypercalcaemia due to SCFN of the newborn. However, the use of alendronate for this purpose has not been reported yet, as far as we know. Alendronate as a bisphosphonate is a potent inhibitor of osteoclast-mediated bone resorption. Previously, it has been used safely in patients with hypercalcaemia associated with vitamin D intoxication [1]. Recently, we successfully treated with alendronate sodium a patient with hypercalcaemia associated with SCFN after a severe perinatal asphyxic event. In our patient, the indurated erythematous plaques and nodules appeared on the back, upper arm and gluteal areas by postnatal day 7 (Fig. 1). When the lesions had almost disappeared on postnatal day 30, serum calcium level still reached a peak of 11.5 mg/dL with a urine calcium/urine creatinine ratio of 0.74 mg/mg. Laboratory testing showed serum parathyroid hormone level of 7.5 pg/mL (normal range, 15–65 pg/mL) and serum 25-hydroxyvitamin D level of 38.5 ng/mL (normal range, 10–40 ng/mL). Because of the clear clinical findings, a histopathological examination was not required. Renal ultrasonography showed bilaterally punctiform renal medullary hyperechogenicities. Despite adequate hydration, the patient’ s serum calcium level remained high. Because the degree of hypercalcaemia was mild and there was nephrocalcinosis, furosemide treatment was not chosen in our patient. Moreover, corticosteroids were not considered because of their potential side effects. Hence, the bisphosphonate treatment was intended and then, because availability of oral preparation, the patient was given oral alendronate at a dosage of 5 mg/day. Oral alendronate treatment was discontinued on postnatal day 50 when the serum calcium level and urinary calcium/ creatinine ratio had returned to normal. During the alendronate therapy, no side effects were observed. In conclusion, patients with SCFN should be closely monitored for developing metabolic problems like hyper- calcaemia. Moreover, alendronate can be used safely and effectively in the treatment of hypercalcaemia associated with SCFN. N. Hakan : M. Aydin (*) : A. Zenciroglu : N. Demirel : N. Okumus : M. S. Ipek Department of Neonatology, Dr. Sami Ulus Maternity and Children’ s Hospital, Babur Street, no: 44 (06080) Altındag, Ankara, Turkey e-mail: dr1mustafa@hotmail.com S. Cetinkaya Department of Pediatric Endocrinology, Dr. Sami Ulus Maternity and Children’ s Hospital, Ankara, Turkey Eur J Pediatr DOI 10.1007/s00431-011-1468-8