Renal tubular acidosis and skeletal demineralization in patients on long-term anticonvulsant therapy.
Three children ranging from seven to 12 years of age from unrelated families were given long-term anticonvulsant therapy including acetazolamide (Diamox). These children had rickets and renal tubular acidosis. Investigations have suggested (1) secondary hyperparathyroidism due to hypocalcemia of rickets and (2) prolonged acetazolamide therapy were responsible for acidosis as a result of reduction of bicarbonate reabsorption in the kidney. A clear-cut recovery from acidosis and rickets was seen in two patients following medication with high doses of vitamin D, an oral supplement of phosphorus, and discontinuance of acetazolamide therapy.
D000086:Acetazolamide / Q000009:adverse effects / Q000627:therapeutic use; D000141:Acidosis, Renal Tubular / Q000139:chemically induced*; D000643:Ammonium Chloride; D000927:Anticonvulsants / Q000009:adverse effects*; D001639:Bicarbonates / Q000097:blood; D001842:Bone and Bones / Q000000981:diagnostic imaging; D002118:Calcium; D002648:Child; D005260:Female; D005942:Gluconates; D006225:Hand / Q000000981:diagnostic imaging; D006801:Humans; D006863:Hydrogen-Ion Concentration; D006962:Hyperparathyroidism, Secondary / Q000175:diagnosis; D007003:Hypoglycemia / Q000188:drug therapy; D007677:Kidney Function Tests; D008297:Male; D010710:Phosphates / Q000627:therapeutic use; D011859:Radiography; D012279:Rickets / Q000139:chemically induced* / Q000188:drug therapy; D014807:Vitamin D / Q000627:therapeutic use; D014953:Wrist / Q000000981:diagnostic imaging
D000927:Anticonvulsants; D001639:Bicarbonates; D005942:Gluconates; D010710:Phosphates; D000643:Ammonium Chloride; D014807:Vitamin D; D000086:Acetazolamide; D002118:Calcium