A CASE OF TEMPORARY SEVERE DISEQUILIBRIUM HYPERCALCEMIA

Citation
K. Kogawa et al., A CASE OF TEMPORARY SEVERE DISEQUILIBRIUM HYPERCALCEMIA, Mineral and electrolyte metabolism, 20(3), 1994, pp. 163-168
Citations number
17
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
03780392
Volume
20
Issue
3
Year of publication
1994
Pages
163 - 168
Database
ISI
SICI code
0378-0392(1994)20:3<163:ACOTSD>2.0.ZU;2-M
Abstract
We report a rare case of temporary and severe hypercalcemia: the patie nt, a 69-year-old woman, was admitted to Osaka City University Hospita l on July 25, 1992, for severe hypercalcemia. The laboratory data on a dmission revealed severe hypercalcemia (14.9 mg/dl) and renal dysfunct ion with increased serum creatinine level (2.9 mg/dl). The urinary exc retion of pyridinoline and deoxypyridinoline was increased, and serum levels of parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D were d ecreased. The data suggested that increased bone resorption was a prob able main factor in the development of the hypercalcemia. The developm ent of hypercalcemia seemed to be of acute onset because of (1) her se vere symptoms caused by hypercalcemia and (2) impaired renal function which was improved after normalization of serum calcium level. Combina tion therapy with saline infusion and furosemide was administered, and there was a gradual decrease and subsequent normalization of serum ca lcium level along with serum creatinine. Even 8 months after discontin uation of the therapy for hypercalcemia, the serum calcium level remai ned within the normal range. The measured values of serum factors whic h are suspected to have a hypercalcemic effect, such as PTH, parathyro id hormone-related peptide and the cytokines (interleukin-1 alpha, int erleukin-1 beta, interleukin-2, interleukin-6 and tumor necrosis facto r-alpha) were all within the normal range. In summary, the hypercalcem ia in this patient was regarded to be a type of disequilibrium hyperca lcemia due to a combination of increased bone resorption and decreased renal capacity to excrete calcium. Furthermore, since it was temporar y and did not recur even in the absence of treatment, the hypercalcemi a was concluded to have developed due to an imbalance in calcium regul ation rather than as a result of organic disease.