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  4. Plasma PTH and PTH-rP levels and clodronate therapy in cancer patients with hypercalcemia
 
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Plasma PTH and PTH-rP levels and clodronate therapy in cancer patients with hypercalcemia

Journal
Journal of the Formosan Medical Association
Journal Volume
92
Journal Issue
11
Pages
977-982
Date Issued
1993
Author(s)
Su R.-J.
Chang C.-C.
KEH-SUNG TSAI  
URI
https://scholars.lib.ntu.edu.tw/handle/123456789/551566
Abstract
To investigate the roles of parathyroid hormone (PTH) and parathyroid hormone-related peptide (PTH-rP) in hypercalcemia patients with various malignancies, we measured the plasma levels of intact PTH and intact PTH-rP in five hypercalcemic patients with hematologic malignancies and 29 hypercalcemic patients with solid cancers. Ten eucalcemic cancer patients with either hepatocellular carcinoma or squamous cancer of the lung served as controls. The results showed a suppressed PTH level in all of the 34 hypercalcemic cancer patients. The PTH-rP levels were within normal limits (<2.5 pg/mL) for all of the eucalcemic cancer controls, all of the five hematologic cancer patients with hypercalcemia, and only two out of the 29 hypercalcemic patients with solid cancers. The PTH-rP level was elevated in nearly all (27/29) hypercalcemic patients with or without bony metastasis. There was a good correlation between the corrected total serum calcium level and the natural log of PTH-rP level in 39 patients (10 eucalcemic and 29 hypercalcemic) with solid cancers (r = 0.75, p < 0.001). These results suggest that PTH-rP plays an important role in the hypercalcemia of patients with solid cancers, but this was not the case in our patients with hematologic malignancies. True ectopic secretion of PTH is unlikely in most of these patients. The mean serum total calcium levels of 17 hypercalcemic patients (13 solid cancers, four hematologic malignancies) dropped significantly after the third day of treatment with a new-generation bisphosphonate-clodronate product. This treatment consisted of 300 mg daily intravenous infusion for seven days, followed by oral administration (800 mg, bid) for the following three weeks. The nadir was on the seventh day of treatment. The response rate for the intravenous infusion was 100% (17/7), and 81% (9/11) for the oral administration period, if a calcium level of below 2.75 mmol/L was used to define the responsiveness. Seven patients survived long term and received a second course of treatment using the same protocol when they developed hypercalcemia again. Six of those patients responded to the intravenous injection. The elevated creatinine levels decreased with this treatment and there was no noticeable untoward effect in the patients. These results show that clodronate therapy is safe and effective regimen for hypercalcemia of malignant disorders.
Subjects
clodronate; hypercalcemia of malignancy; parathyroid hormone; parathyroid hormone-related peptide
SDGs

[SDGs]SDG3

Other Subjects
clodronic acid; furosemide; parathyroid hormone; article; cancer; clinical article; controlled study; human; hypercalcemia; intravenous drug administration; liver cell carcinoma; lung cancer; oral drug administration; parathyroid hormone blood level; Clodronic Acid; Human; Hypercalcemia; Neoplasms; Parathyroid Hormones; Proteins; Support, Non-U.S. Gov't
Type
journal article

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