ESPE Abstracts (2018) 89 P-P3-035

ESPE2018 Poster Presentations Bone, Growth Plate & Mineral Metabolism P3 (40 abstracts)

Our Treatment Experience with Nocturnal Continuous Enteral Calcium Infusion in a Case with Vitamin D Resistance Rickets Type II

Berna Eroğlu Filibeli a , Özgür Kırbıyık b & Bumin Nuri Dündar b

aDepartment of Pediatric Endocrinology, Tepecik Training and Research Hospital, Izmir, Turkey; bDepartment of Medical Genetics, Tepecik Training and Research Hospital, Izmir, Turkey; cDepartment of Pediatric Endocrinology, Katip Celebi University, Izmir, Turkey

Introduction: Vitamin D resistant rickets type II (VDDR-II) is a disease with a difficult treatment developed as a result of mutations in VDR gene. Despite high dose active vitamin D and oral calcium treatments, sufficient recovery cannot be achieved mostly. Successful results with intravenous calcium infusion that is an alternative treatment have been reported; however, serious restrictions and complications such as hospitalization, catheter infection, thrombosis, skin necrosis.

Aim: It presents the results of nocturnal-continuous enteral calcium infusion in a case not responding to conventional treatment.

Case: A 19-month-old male patient was guided with findings; caput quadratum, rachitic beads, enlargement in wrists and O-leg deformity. The height of patient whose parents are relatives was −3,2 SDS, weight was −1,47 SDS; he had no alopecia. Biochemical and radiological findings were compatible with stage 3 rickets. VDDR-II was considered when not having response to stoss therapy applied with nutritional rickets diagnosis and determining high 1,25 (OH)2D3 level. R158L (c.473>T) homozygote response mutation was identified in VDR gene. Upon not having response to conventional treatment, nocturnal-continuous enteral calcium gluconate infusion (100 mg/kg/12 hour with naso-gastric catheter) was initiated by taking consent to avoid complications of intravenous calcium treatment. 20 days later, he applied to us with brain fog and severe metabolic acidosis with increased anion gap. Despite all examinations carried out, the cause of acidosis could not be clarified. Dialysis was applied to the patient who did not respond to NaHCO3. After being discharged from the hospital, the patient referred to us on the 30th day of the treatment with consciousness change. Scan tests performed in terms of neurometabolic diseases were normal. Metabolic acidosis attacks of the patient recovered with support treatment did not recur after discontinuation of enteral calcium gluconate treatment. The patient is still 4 years old and he periodically receives intravenous calcium gluconate treatment.

Conclusion: Difficulties experienced in the treatment of cases with VDDR-II direct physicians to alternative treatment search. A case with severe metabolic acidosis thought to be related to enteral calcium gluconate infusion was presented in this case report. While calcium gluconate treatment does not lead to metabolic acidosis when applied intravenously, it is unclear why it causes this situation when applied enterally.

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