Disordered calcium homeostasis of sepsis: association with calcitonin precursors

Citation
B. Muller et al., Disordered calcium homeostasis of sepsis: association with calcitonin precursors, EUR J CL IN, 30(9), 2000, pp. 823-831
Citations number
56
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research General Topics
Journal title
EUROPEAN JOURNAL OF CLINICAL INVESTIGATION
ISSN journal
00142972 → ACNP
Volume
30
Issue
9
Year of publication
2000
Pages
823 - 831
Database
ISI
SICI code
0014-2972(200009)30:9<823:DCHOSA>2.0.ZU;2-D
Abstract
Background Hypocalcemia and increased serum levels of calcitonin precursors are common in critically HI patients, especially in those with sepsis. We investigated calcium homeostasis in such patients. Patients and methods Serum concentrations of total and ionized calcium and known factors influencing or reflecting calcium homeostasis were measured i n 101 consecutive patients of a medical intensive care unit. Calcitonin pre cursor levels were determined using a highly sensitive radioimmunoassay. Results Critical illness per se was associated with decreased serum total a nd ionized calcium levels, which correlated with the severity of the underl ying disease as measured by the APACHE II score. In addition, total and ion ized hypocalcemia was more pronounced with increasing severity of infection (P < 0.02), and occurred in parallel with a marked increase of calcitonin precursors (P < 0.001). Mature calcitonin levels, however, remained normal. Changes of serum ionized calcium concentrations from admission to discharg e correlated significantly with changes in the serum calcitonin precursor c oncentration (r(2) = -0.14, P < 0.001). Circulating vitamin D levels, parat hyroid hormone levels and other markers reflecting calcium homeostasis did not correlate with the severity of infection. Conclusions In critically ill patients with sepsis, markedly elevated circu lating calcitonin precursors might play a role in the development of the pr onounced hypocalcemia. The specific calcitonin precursor(s) responsible for this effect and the pathophysiological mechanism remain to be elucidated.