The Clinical and Laboratory Characteristics of Vitamin D Intoxication in Children


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Döneray H., Ozkan B., Ozkan A., Kosan C., Orbak Z., Karakelleoglu C.

TURKISH JOURNAL OF MEDICAL SCIENCES, sa.1, ss.1-4, 2009 (SCI-Expanded) identifier

  • Yayın Türü: Makale / Tam Makale
  • Basım Tarihi: 2009
  • Doi Numarası: 10.3906/sag-0805-54
  • Dergi Adı: TURKISH JOURNAL OF MEDICAL SCIENCES
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, TR DİZİN (ULAKBİM)
  • Sayfa Sayıları: ss.1-4
  • Atatürk Üniversitesi Adresli: Evet

Özet

Aim: In this retrospective study, patients with vitamin D intoxication (VDI) were evaluated with respect to clinical and laboratory characteristics. treatment protocols and complications. Materials and Methods: The medical records of 27 children with VDI between 2003 and 2008 were investigated. Data included age. gender. nutritional status, dose and duration of prophylactic/therapeutic vitamin D, the reasons for vitamin D therapy prescription, clinical signs and symptoms, laboratory findings, therapy protocol for VDI, and complications. Results: The mean dose of vitamin D prescribed to the patients was 600.000 U (range: 300,000-1.200.000 U), The most prominent reason (80.9%) for physician prescription of vitamin D therapy was delay in achievement of developmental milestones. which may also be seen in vitamin D-deficient rickets (VDDR). Clinical manifestations of the patients with VDI were vomiting (85.7%). anorexia (57.1%), weight loss (47.6%), dehydration (42.8%), polyuria/polydipsia (38%), and constipation (33.3%). Biochemical parameters of the patients at admission were as follows: mean serum total calcium 12.1 +/- 2.8 mg/dl, phosphorus 6.1 +/- 1.2 mg/dl, alkaline phosphatase 351 +/- 224 IU/L, 25 hydroxyvitamin D (25[OH]D) 247 +/- 117.8 ng/ml, intact parathyroid hormone (PTH) levels 15 +/- 9.2 ng/ml, and urine calcium/creatinine ratio 2.47 +/- 1.03. There was negative correlation between the serum 25[OH]D and PTH levels (r = -0.84, P < 0.001). Six patients with severe hypercalcemia (serum total calcium: > 15 mg/dl) were controlled with bisphosphonate therapy. Nephrocalcinosis developed in seven patients (25.9%). All patients were followed up at three-month intervals for 1.3 years after treatment. Hypercalcemia did not recur and nephrocalcinosis persisted in all except one case. Conclusions: The diagnosis of VDDR without checking serum 25[OH]D level may cause redundant treatment that leads to VDI. All patients who are clinically suspected of VDDR should be checked for serum vitamin D status and questioned for previous vitamin D administration before starting vitamin D therapy.