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Recurrent lead poisoning in a child with immobilization osteoporosis
1Division of Clinical Pharmacology/Toxicology, Children's Hospital, Boston, MA.
Insights
Bone lead can re-enter circulation, causing recurrent lead poisoning in children with osteoporosis. This case highlights bone as a lead reservoir during conditions of accelerated resorption.
Area of Science:
- Pediatric toxicology
- Metabolic bone disease
Background:
- Lead poisoning can cause osteoporosis, but the bone's role as a lead source is poorly understood.
- Recurrent lead elevations in previously poisoned patients are rarely documented.
Observation:
- A 4-year-old child with prior lead poisoning developed recurrent high blood lead levels after transverse myelitis.
- No external lead sources were identified; the child had osteoporosis and low vitamin D levels.
Findings:
- Metabolic studies showed negative calcium balance and high urinary calcium excretion.
- Radiographs confirmed progressive osteoporosis without foreign bodies, suggesting bone resorption released lead.
Implications:
- Bone can act as an endogenous source of lead during conditions of accelerated bone resorption.
- This mechanism may explain recurrent lead poisoning in patients with compromised bone health.
Abstract:
Lead poisoning associated with progressive osteoporosis in patients who have been previously lead poisoned has been described but poorly documented. We managed a 4-year-old child with a prior history of plumbism who developed recurrent blood lead elevations (as high as 70 mcg/dl), requiring multiple courses of EDTA, after acute paraplegia from transverse myelitis. The patient was hospitalized throughout these periods of chelation. No exogenous sources of lead were found. Calcium, phosphate, magnesium, alkaline phosphatase and parathyroid hormone levels remained normal while vitamin D levels were depressed. Metabolic studies revealed negative calcium balance with an elevated urinary calcium:creatinine ratio. Long-bone radiographs were remarkable for progressive osteoporosis with no evidence of metallic foreign bodies. This case illustrates that bone, the major repository of lead, can become a source of significant lead level elevations in conditions associated with accelerated resorption.