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Seizures as the presenting feature of rickets in an infant

Graeme H Johnson and Francis Willis
MJA 2003; 178 (9): 467

To the Editor: An 8-month-old girl, born in Perth, Western Australia, who received only breast milk feeds for her first six months of life, was referred urgently to Princess Margaret Hospital for Children (the tertiary paediatric hospital in Western Australia) for investigations of seizures. Her parents described the seizures as episodic, involving all limbs, lasting less than five minutes and occurring over the 10 days before presentation.

At presentation, the infant had carpopedal spasm. She was afebrile, and a septic screen gave negative results. Venous blood gas analysis showed a low ionised serum calcium level of 0.71 mmol/L (reference range [RR], 1.13–1.32 mmol/L). An x-ray film of her wrists showed signs of rickets, with cupping and fraying of the distal metaphyses of both radius and ulna. Other blood tests revealed elevated parathyroid hormone levels of 8.6 pmol/L (RR, 0.80–8.00 pmol/L), an elevated alkaline phosphatase level of 523 U/L (RR, 100–350 U/L), and an extremely low level of serum 25-hydroxyvitamin D3 (25OHD3) of 5 nmol/L (RR, 30–150 nmol/L).

The infant responded to treatment with an infusion of 0.5 mg/kg of calcium gluconate and a 4-month oral course of 0.2 μg calcitriol daily. After treatment commenced, she did not have any further seizures. Radiogaphy performed 4 months later showed increasing calcium deposition at the distal metaphyses of the radius and ulna.

Seizures are described as a presenting feature of hypocalcaemia in vitamin D deficiency rickets.1,2 Ultraviolet radiation and/or dietary vitamin D are required to prevent rickets in children. Perth, Western Australia, located at latitude 32° South has an average daily sunshine duration of at least five hours per day. However, even with this amount of sunshine, vitamin D deficiency can still occur in people who, for various reasons, receive little or no sun exposure, especially if their skin is darkly pigmented, and who have an inadequate dietary intake of vitamin D. The girl's mother, who wore a veil and clothing which protected her body from exposure for religious reasons, had a serum 25OHD3 level of 7 nmol/L. Breast milk is a poor source of dietary vitamin D, especially when the lactating woman is vitamin D deficient.3

In Australia, vitamin D deficiency rickets in infants of parents who have migrated from Mediterranean, African, Middle Eastern and southern Asian regions has been reported since the 1960s.4,5 Education of healthcare providers and their patients about the requirement for sunlight exposure or dietary supplementation to prevent vitamin D deficiency rickets needs to continue.

  1. Bachrach S, Fisher J, Parks JS. An outbreak of vitamin D deficiency rickets in a susceptible population. Pediatrics 1979; 64: 871-877. <PubMed>
  2. Hoecker CC, Kaneyage JT. Recurrent febrile seizures: an unusual presentation of nutritional rickets. J Emerg Med 2002; 23: 367-370. <PubMed>
  3. Welch TR, Bergstrom WH, Tsang RC. Vitamin D deficient rickets: the reemergence of a once conquered disease. J Pediatr 2000; 137: 143-145. <PubMed>
  4. Lipson T. Epidemic rickets in migrant families in Melbourne and Sydney. J Pediatr Child Health 1995; 31: 483-484.
  5. Nozza JM, Rodda CP. Vitamin D deficiency of infants with rickets. Med J Aust 2001; 175: 253-255. <eMJA full text> <PubMed>

(Received 15 Oct 2002, accepted 13 Mar 2003)

Princess Margaret Hospital for Children, Subiaco, WA.

Graeme H Johnson, Resident Medical Officer, Department of General Paediatrics; Francis Willis, Paediatrician, Emergency Department.

Correspondence: Dr Graeme H Johnson, Acting Public Health Medical Officer, Kimberley Population Health Unit, Derby, WA 6728. graeme.johnsonAThealth.wa.gov.au

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©The Medical Journal of Australia 2003 www.mja.com.au Print ISSN: 0025-729X Online ISSN: 1326-5377

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