Summary
Of 155 institutionalized epileptics, 16 (10%) were noted to have suffered from different kinds of fractures when observed over a period of 1 year. The patients with fractures were further investigated with respect to blood and urine chemistry and bone morphology. The serum and urinary calcium values were below the average values for the population. Elevated values for serum alkaline phosphatase and for immunoreactive parathyroid hormone were found in most patients. The values of serum phosphate were distributed close to those of the normal population, while the urinary phosphate values were lower. Examination of bone biopsies revealed a significantly increased amount of osteoid and a significantly increased osteoclastic resorptive activity in epileptics, compared with age-matched controls. Furthermore, a slightly diminished volume of trabecular bone was noted. The high incidence of fractures may be explained by bone disease — a combination of osteoporosis, osteomalacia, and hyperparathyroidism due to chronic treatment with anti-convulsant drugs.
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Almqvist S, Hjern B, Writhed B (1975) The diagnostic value of a radioimmunoassay for parathyroid hormone in human serum. Acta Endocrinol (Copenh) 78:493–509
Christiansen C, Rödbro P, Lund M (1973) Incidence of anticonvulsant osteomalacia and effect of vitamin D: controlled therapeutic trial. Br Med J 4:695–701
Conney AH (1967) Pharmacological implications of microsomal enzyme induction. Pharmacol Rev 19:317–366
Dent CE, Richens A, Rowe DJF, Stamp TCB (1970) Osteomalacia with long-term anticonvulsant therapy in epilepsy. Br Med J 4:69–72
Dymling JF, Johnell O, Lidgren L, Nilsson BE, Wallöe A, Wiklund PE (1979) Bone disease in epileptics. In: Norman AW, Schaffer K, v Herrath D, Grigolet HS, Coburn JW, deLuca AF, Meiwer EB, Sida T (eds) Vitamin D. Basic research and its clinical application. de Gruyter, Berlin New York, p 1193
Hahn TJ, Birge SJ, Scharp CR (1972) Phenobarbital-induced alterations in vitamin D metabolism. J Clin Invest 51:741–748
Hahn TJ, Hendin BA, Scharp CR, Boisseau VC, Haddad JG (1975) Serum 25-hydroxycalciferol levels and bone mass in children on chronic anticonvulsant therapy. N Engl J Med 292:550–554
Hunter J, Maxwell JD, Stewart DA, Parson V, Williams R (1971) Altered calcium metabolism in epileptic children on anticonvulsants. Br Med J 4:202–204
Lindholm TS, Eriksson SA, Lindholm TC (1984) Results of long-term treatment of osteoporosis with la-hydroxyvitamin D3 and calcium. Int J Orthop Traumatol 10:187–201
Livingston S, Berman W, Pauli LL (1978) Anticonvulsant drugs and vitamin D metabolism. JAMA 224:1634–1635
Melsen F, Melsen B, Mosekilde L, Bergman S (1978) Histomorphometric analysis of normal bone from the iliac crest. Acta Pathol Microbiol Immunol Scand [A] 86:70–81
Meunier P (1971) La dynamique du remaniement osseux etudiée par lecture quantitative de la biopsie osseuse. Dissertation, Université de Lyon
Mosekilde L, Melsen F (1976) Anticonvulsant osteomalacia determined by quantitative analysis of bone changes. Acta Med Scand 199:349–355
Richens A, Rowe DJF (1970) Disturbance of calcium metabolism by anticonvulsant drugs. Br Med J 4:73–76
Schmid F (1967) Osteopathien bei antiepileptischer Dauerbehandlung. Fortschr Med 85:381
Sotaniemi EA, Hakkarainen HK, Puranen JA, Lahti RO (1972) Radiological bone changes and hypocalcemia with anticonvulsant therapy in epilepsy. Ann Intern Med 77: 389–394
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Nilsson, O.S., Lindholm, T.S., Elmstedt, E. et al. Fracture incidence and bone disease in epileptics receiving long-term anticonvulsant drug treatment. Arch. Orth. Traum. Surg. 105, 146–149 (1986). https://doi.org/10.1007/BF00433931
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DOI: https://doi.org/10.1007/BF00433931