AI Summary & Key Takeaways
AI InsightAll 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.
📌 3 Key Takeaways
Abstract
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.
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.