Rickets anticonvulsants

Anticonvulsant treatment Fibrogenes imperfecta ossium Osteitis fibrosa cystica Osteomalacia Osteoporosis Osteopenia Osteosclerosis Renal osteodystrophy Rickets... 

Osteomalacia and rickets have been reported with long-term anticonvulsant therapy additional risk factors for these conditions (e.g., poor sunlight exposure) increases risk... 

Morijiri Y, Sato T. Factors causing rickets in institutionalised handicapped children on anticonvulsant therapy. Arch Dis Child 1981 56(6) 446-9. 

Serum alkaline phosphatase elevation and other indices, both biochemical and radiological, of rickets and osteomalacia are more common in patients receiving anticonvulsant drugs than in control subjects (B13, C16, C37, R16, TIO). The severity of these abnormalities has been reported to relate directly to the duration of therapy (K35, TIO), to the... 

C37. Crosley, C. J., Chee, C., and Berman, P. H., Rickets associated with long-term anticonvulsant therapy in a pediatric outpatient population. Pediatrics 56, 52-57... 

L14. Lifshitz, F., and Maclaren, N. F., Vitamin D-dependent rickets in institutionalized, mentally retarded children receiving long-term anticonvulsant therapy. I. A survey of 285 patients. J. Pediatr. 83, 612-620 (1973). 

Some drugs, for example anticonvulsants phenytoin, phenobarbital and corticosteroids can lead to osteomalacia and rickets by depressing vitamin D dependent calcium uptake in the intestine. 

In addition to the classical environmental or nutritional cause of these diseases, both osteomalacia and rickets can have a pharmacological origin via chronic treatment with anticonvulsants (phenobarbital and phenytoin) or glucocorticoids. These agents interfere with intestinal absorption of calcium and, thereby, cause pseudohyperparathyroidism. As a result, an increase in bone turnover and a decrease in the formation of appropriately mineralized bone is observed. In these patients, treatment with vitamin D improves calcium absorption, ultimately enhancing mineralization of the bone. 

Maclaren N, Lifshitz F. Vitamin D-dependency rickets in institutionalized, mentally retarded children on long term anticonvulsant therapy. II. The response to 25-hydro> cholecalciferol and to vitamin D2. PecSatrRes( 973) 7, 914-22. 

A deficiency of vitamin D results in rickets in children and osteomalacia in adults. It can occur as a result of malnutrition, or malabsorption. Deficiency can also occur when there is a failure to hydroxylate vitamin D. This is thought to occur in some types of renal disease and as a result of treatment with particular anticonvulsant drugs. These drugs are thought to stimulate liver enzymes which oxidize vitamin D to inactive metabolites. 

Anticonvulsants—Epileptic patients given these drugs for the prevention of seizures have sometimes developed softening and distortion of their lx>nes which may lead to rickets in children, or to softening of the lx>nes (osteomalacia) in adults. 0 Apparently, the drugs produce their harmful effects on the bones by provoking increased rates of destruction of vitamin D and its active metabolites, so that the absorption and utilization of dietary calcium is reduced. Sometimes, their effects have been overcome by... 

Calcium absorption was studied in 28 adult male epileptics on chronic anticonvulsant therapy. In 16 patients on phenytoin alone calcium absorption was abnormal in 9. In 12 patients on both phenytoin and phenobarbitone calcium absorption was abnormal in 3. Hypocalcaemia (<8.5 mg/ 100 ml) occurred in only 2 patients, while serum alkaline phosphatase was elevated in 7 patients. The findings support the suggestion that rickets and osteomalacia reported in patients on chronic anticonvulsant therapy results from reduced calcium absorpion. The effect of these drugs appear to be the increased metabolism of vitamin D via enzyme induction, and an increase in the excretion of polar metabolites 25-hydroxycholecalciferol and 1,25-dihy-droxycholecalciferol which are necessary for normal calcium absorption (40 ). 

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