Metabolic bone disease (anticonvulsant osteomalacia) and renal tubular acidosis in tuberous sclerosis

Intern Med. 1993 Jul;32(7):574-9. doi: 10.2169/internalmedicine.32.574.

Abstract

The characteristics triad of tuberous sclerosis-adenoma sebaceum, mental deficiency and epilepsy-associated with distal-type renal tubular acidosis was combined with anticonvulsant osteomalacia in a 41-year-old woman. In addition to the specific bone lesions of tuberous sclerosis, the bone disease was caused by an adverse effect of a drug and possibly also by the renal disorder leading to significant musculoskeletal disability. In response to calcium carbonicum and 1-25-dihydroxyvitamin D therapy the musculoskeletal disability healed and the abnormal biochemical markers of anticonvulsant osteomalacia disappeared. The present observation draws attention to the increased hazard threatening patients on chronic anticonvulsant therapy simultaneously suffering from renal diseases.

Publication types

  • Case Reports
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acidosis, Renal Tubular / chemically induced*
  • Adult
  • Back Pain / etiology
  • Bicarbonates
  • Bone and Bones / drug effects
  • Bone and Bones / metabolism
  • Calcitriol / therapeutic use
  • Calcium / metabolism
  • Calcium Carbonate / therapeutic use
  • Drug Therapy, Combination
  • Epilepsy / drug therapy
  • Epilepsy / etiology
  • Female
  • Humans
  • Intestinal Absorption / drug effects
  • Neural Conduction
  • Osteomalacia / chemically induced*
  • Osteomalacia / drug therapy
  • Phenytoin / administration & dosage
  • Phenytoin / adverse effects*
  • Phenytoin / therapeutic use
  • Primidone / administration & dosage
  • Primidone / adverse effects*
  • Primidone / therapeutic use
  • Tuberous Sclerosis / complications*

Substances

  • Bicarbonates
  • Primidone
  • Phenytoin
  • Calcitriol
  • Calcium Carbonate
  • Calcium