Progressively increased serum 1,25-dihydroxyvitamin D2 concentration in a hypoparathyroid patient with protracted hypercalcemia due to vitamin D2 intoxication.
A 76-year-old female patient who had been taking vitamin D2 100,000 U/day for more than 14 years due to hypoparathyroidism following total throidectomy was admitted because of protracted hypercalcemia. On admission, the levels of serum vitamin D2 (99.8 ng/ml) and 25-OHD2 (356 ng/ml) were very high, and 1,25-(OH)2D2 was low (4.0-18.7 pg/ml). Serum D3' 25-OHD3 and 1,25-(OH)2D3 were below the normal range. Despite intensive hydration with saline, intravenous hyperalimentation with phosphate- and calcium-free nutrients, and administration of glucocorticoid and calcitonin, the hypercalcemia persisted, accompanied by hypoproteinemia, edema, pleural effusion and congestive heart failure. The serum D2 and 25-OHD2 concentrations remained high and were accompanied by a gradual increase in 1,25-(OH)2D2 (121 pg/ml), which further increased after the administration of bisphosphonate (pamidronate) to 183 pg/ml. Seventeen months later, serum calcium and 1,25-(OH)2D2 were normalized but serum D2 and 25-OHD2 remained high. The serum 24,25-(OH)2D2/25-OHD2 ratio was relatively constant throughout her clinical course, whereas the low serum 1,25-(OH)2D2/25-OHD2 ratio at admission gradually increased during admission, suggesting that the increase in serum 1,25-(OH)2D2 is due to increased production rather than decreased degradation. The administration of pamidronate further increased serum 1,25-(OH)2D2. These features of the clinical course demonstrate that the 1,25-dihydroxyvitamin D concentration in hypercalcemic patients with protracted vitamin D intoxication may be decreased, normal or increased. Possible factors responsible for a protracted increase in serum 1,25-(OH)2D2 are body weight loss, hypoproteinemia, and phosphate depletion. In addition, some bisphosphonates would certainly promote PTH-independent production of 1,25-(OH)2D2.
Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College, Japan.
K
K
Sato
N
N
Emoto
S
S
Toraya
T
T
Tsushima
H
H
Demura
N
N
Tsuji
S
S
Inaba
A
A
Takeuchi
T
T
Kobayashi
D000368:Aged; D004872:Ergocalciferols / Q000097:blood* / Q000506:poisoning*; D005260:Female; D006801:Humans; D006934:Hypercalcemia / Q000097:blood* / Q000209:etiology; D007011:Hypoparathyroidism / Q000097:blood* / Q000150:complications / Q000188:drug therapy
D004872:Ergocalciferols; C003564:1,25-dihydroxyergocalciferol