Mechanism for bone disease found in inhabitants environmentally exposed to cadmium: decreased serum 1 alpha, 25-dihydroxyvitamin D level.
To investigate the mechanism for bone disease caused by exposure to cadmium serum samples were collected from 5 itai-itai disease patients, 36 Cd-exposed residents with renal tubular damage and 17 non-exposed individuals and analyzed for 1 alpha,25-dihydroxyvitamin D[1 alpha,25(OH)2D], parathyroid hormone, beta 2-microglobulin, calcium and inorganic phosphorus. Measurement of percentage tubular reabsorption of phosphate (%TRP) were performed only on the Cd-exposed subjects. Serum 1 alpha,25(OH)2D levels were lower in itai-itai disease patients and cadmium-exposed subjects with renal damage than in non-exposed subjects. Parathyroid hormone and beta 2-microglobulin concentrations in serum were higher in the Cd-exposed subjects. Decrease in serum 1 alpha,25(OH)2D levels were closely related to serum concentrations of parathyroid hormone, beta 2-microglobulin and %TRP. This study suggests that cadmium-induced bone effects were mainly due to a disturbance in vitamin D and parathyroid hormone metabolism, which was caused by the cadmium-induced kidney damage.
D000368:Aged; D001847:Bone Diseases / Q000139:chemically induced*; D002104:Cadmium / Q000633:toxicity*; D002117:Calcitriol / Q000097:blood*; D002118:Calcium / Q000097:blood; D004781:Environmental Exposure; D005260:Female; D006801:Humans; D007668:Kidney / Q000187:drug effects; D008297:Male; D008875:Middle Aged; D010281:Parathyroid Hormone / Q000097:blood
D010281:Parathyroid Hormone; D002104:Cadmium; D002117:Calcitriol; D002118:Calcium