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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    European journal of pediatrics 133 (1980), S. 151-156 
    ISSN: 1432-1076
    Keywords: Calcitonin ; Parathyroid hormone ; Anticonvulsant bone disease ; Urinary cyclic AMP ; Urinary hydroxyproline
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Serum calcitonin (CT) levels and other aspects of calcium metabolism were investigated in 40 epileptic children receiving long-term treatment with phenytoin and/or other anticonvulsant drugs, and in 38 age-matched controls. In the patients CT levels were significantly lower. Immunoreactive parathyroid hormone (iPTH) was significantly elevated exceeding the upper limit of controls in 11 patients. We also observed a highly significant correlation between iPTH and urinary cyclic AMP (cAMP) excretion but a lack of such a correlation with the renal handling of phosphate; this indicates to us a dissociation between cAMP production and phosphaturia. A significant correlation between iPTH levels and urinary hydroxyproline excretion points to a normal action of PTH on bone in the patients. The low CT levels are not due to hypocalcemia and may be directly attributed to the effects of anticonvulsant drugs. As the primary effect of CT is a direct inhibition of PTH induced calcium loss from bone, the drug-related low CT levels in association with secondary hyperparathyroidism possibly is an additional factor in anticonvulsant bone disease.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    European journal of pediatrics 138 (1982), S. 202-205 
    ISSN: 1432-1076
    Keywords: Anticonvulsant bone disease ; Antiepileptic drugs ; Calcitonin ; Calcium metabolism ; Vitamin D metabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Conclusion Recent investigations have illuminated the pathogenesis of anticonvulsant-drug-induced alterations of calcium metabolism. Antiepileptic drugs may provoke renal conservation of calcium and phosphate and possibly compensate partly other of the above mentioned negative effects on calcium and bone metabolism. This may explain the relatively low incidence of manifest rickets or osteomalacia despite long-term treatment with drugs that are now well known to interfere with so many improtant factors of calcium homeostasis.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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