Given the recent spate of reports of vitamin D deficiency, there is a need to reexamine our understanding of natural and other sources of vitamin D, as well as mechanisms whereby vitamin D synthesis and intake can be optimized. This state-of-the-art report from the Drug and Therapeutics Committee of the Lawson Wilkins Pediatric Endocrine Society was aimed to perform this task and also reviews recommendations for sun exposure and vitamin D intake and possible caveats associated with these recommendations.
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Chapters Views & News
Copyright © 2008 by the American Academy of Pediatrics
2008
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Hypocalcemia due to vitamin D deficiency: is calcitriol treatment really required?
To the Editor:
We read with great interest the review article in Pediatrics by Misra et al. (1) on the management and treatment of vitamin D deficiency. The authors reported that simptomatic hypocalcemia with tetany or convulsions should be treated with i.v. 10% calcium gluconate associated, if necessary, with calcitriol until serum calcium levels normalize.
Recently, a 10-month-old boy with generalized seizure (duration approximately 3 minutes) with normal temperature was admitted to our hospital. Clinical examination showed a large anterior fontanelle, frontal bossing with no dysmorphic features, craniotabes, and hypotonia. Laboratory results revealed severe hypocalcemia (4.3 mg/dL), hypophosphatemia (3.1 mg/dL), increased alkaline phosphatase (2031 U/L; normal values 80-645 U/L), parathyroid hormone (189 pg/mL, normal values 10-65 pg/mL), and 1,25-dihydroxyvitamin D (181.8 pg/mL; normal values 20- 80 pg/mL) levels, and reduced 25-hydroxyvitamin D levels (12.8 ng/mL; "desiderable levels" > 20 ng/mL) (2). The child had immigrated to Italy from North Africa, and he was exclusivey breast-fed with no vitamin D supplementation. Radiographs of wrist and knee confirmed vitamin D deficiency rickets. The administration of i.v. 10% calcium gluconate (at admission, 1440 mg; 24h, 1250 mg; 48h, 960 mg; expressed as elemental calcium per day) followed by oral calcium as carbonate (48h, 500 mg; 72h, 1000 mg; expressed as elemental calcium per day) associated with cholecalciferol treatment (5000 IU per day, started from 24h) quickly restored normocalcemia (24h, 6.8 mg/dL; 48h, 7.6 mg/dL; 72h, 8.6 mg/dL). After nine days of treament, parathyroid hormone and 25-hydroxyvitamin D levels normalize (31.4 pg/mL and 50.7 ng/mL, respectively).
In our opinion, vitamin D metabolites, such as calcitriol, should be used if a defect in vitamin D metabolism or an hypoparathyroid state is present; their use in vitamin D deficiency rickets may be a medical error (3, 4). Our data clearly showed the efficacy of cholecalciferol in restoring normocalcemia and a normal vitamin D status. In fact, as also suggested by Holick (4), calcitriol enhances the 25-hydroxyvitamin D-24- hydroxylase (CYP24R) activity with increased degradation of both 25- hydroxyvitamin D and 1,25-dihydroxyvitamin D.
Therefore, cholecalciferol treatment is efficacious and cost- effective to normalize hypocalcemia due to vitamin D deficiency, and there is not a clear indication to the use of calcitriol in this form of rickets.
Giampiero Igli Baroncelli, M.D. Department of Pediatrics, S. Chiara University Hospital Via Roma, 67 56126 Pisa, Italy [email protected]
Silvano Bertelloni, M.D. Department of Pediatrics, S. Chiara University Hospital Via Roma, 67 56126 Pisa, Italy
Francesco Vierucci, M.D. Department of Pediatrics, S. Chiara University Hospital Via Roma, 67 56126 Pisa, Italy
References
1.Misra M, Pacaud D, Petryk A, Collett-Solberg PF, Kappy M; Drug and Therapeutics Committee of the Lawson Wilkins Pediatric Endocrine Society. Vitamin D deficiency in children and its management: review of current knowledge and recommendations. Pediatrics. 2008;122(2):398-417
2.Wagner CL, Greer FR; American Academy of Pediatrics Section on Breastfeeding; American Academy of Pediatrics Committee on Nutrition. Prevention of rickets and vitamin D deficiency in infants, children, and adolescents. Pediatrics. 2008;122(5):1142-1152
3.Wharton B, Bishop N. Rickets. Lancet. 2003;362(9393):1389-1400
4.Holick MF. Vitamin D deficiency. N Engl J Med. 2007;357(3):266-281
Conflict of Interest:
None declared
Hypocalcemia due to vitamin D deficiency: is calcitriol treatment really required?
To the Editor:
We read with great interest the review article in Pediatrics by Misra et al. (1) on the management and treatment of vitamin D deficiency. The authors reported that simptomatic hypocalcemia with tetany or convulsions should be treated with i.v. 10% calcium gluconate associated, if necessary, with calcitriol until serum calcium levels normalize.
Recently, a 10-month-old boy with generalized seizure (duration approximately 3 minutes) with normal temperature was adimitted to our hospital. Clinical examination showed a large anterior fontanelle, frontal bossing with no dysmorphic features, craniotabes, and hypotonia. Laboratory results revealed severe hypocalcemia (4.3 mg/dL), hypophosphatemia (3.1 mg/dL), increased alkaline phosphatase (2031 U/L; normal values 80-645 U/L), parathyroid hormone (189 pg/mL, normal values 10-65 pg/mL), and 1,25-dihydroxyvitamin D (181.8 pg/mL; normal values 20- 80 pg/mL) levels, and reduced 25-hydroxyvitamin D levels (12.8 ng/mL; "desiderable levels" > 20 ng/mL) (2). The child had immigrated to Italy from North Africa, and he was exclusivey breast-fed with no vitamin D supplementation. Radiographs of wrist and knee confirmed vitamin D deficiency rickets. The administration of i.v. 10% calcium gluconate followed by oral calcium as carbonate associated with cholecalciferol treatment (5000 IU per day) quickly restored normocalcemia (Table). After nine days of treament, parathyroid hormone and 25-hydroxyvitamin D levels normalize (31.4 pg/mL and 50.7 ng/mL, respectively).
In our opinion, vitamin D metabolites, such as calcitriol, should be used if a defect in vitamin D metabolism or an hypoparathyroid state is present; their use in vitamin D deficiency rickets may be a medical error (3, 4). Our data clearly showed the efficacy of cholecalciferol in restoring normocalcemia and a normal vitamin D status. In fact, as also suggested by Holick (4), calcitriol enhances the 25-hydroxyvitamin D-24- hydroxylase (CYP24R) activity with increased degradation of both 25- hydroxyvitamin D and 1,25-dihydroxyvitamin D.
Therefore, cholecalciferol treatment is efficacious and cost- effective to normalize hypocalcemia due to vitamin D deficiency, and there is not a clear indication to the use of calcitriol in this form of rickets.
Giampiero Igli Baroncelli, M.D. Department of Pediatrics, S. Chiara University Hospital Via Roma, 67 56126 Pisa, Italy [email protected]
Silvano Bertelloni, M.D. Department of Pediatrics, S. Chiara University Hospital Via Roma, 67 56126 Pisa, Italy
Francesco Vierucci, M.D. Department of Pediatrics, S. Chiara University Hospital Via Roma, 67 56126 Pisa, Italy
References
1.Misra M, Pacaud D, Petryk A, Collett-Solberg PF, Kappy M; Drug and Therapeutics Committee of the Lawson Wilkins Pediatric Endocrine Society. Vitamin D deficiency in children and its management: review of current knowledge and recommendations. Pediatrics. 2008;122(2):398417
2.Wagner CL, Greer FR; American Academy of Pediatrics Section on Breastfeeding; American Academy of Pediatrics Committee on Nutrition. Prevention of rickets and vitamin D deficiency in infants, children, and adolescents. Pediatrics. 2008;122(5):11421152
3.Wharton B, Bishop N. Rickets. Lancet. 2003;362(9393):13891400
4.Holick MF. Vitamin D deficiency. N Engl J Med. 2007;357(3):266281
Table. Serum calcium levels at admission and during treatment in the patient.
At admission 24 h 48 h 72 h Calcium levels, mg/dL 4.3 6.8 7.6 8.6 i.v. 10% calcium gluconate* 1440 1250 960 - Oral calcium as carbonate* - - 500 1000 Oral cholecalciferol° - 5000 5000 5000
*Expressed as elemental calcium, mg per day; °IU per day.
Conflict of Interest:
None declared