Rml. Murray et al., Hypocalcemic and normocalcemic hyperparathyroidism in patients with advanced prostatic cancer, J CLIN END, 86(9), 2001, pp. 4133-4138
PTH and ionized calcium levels were measured in 131 patients with advanced
prostate cancer, all of whom had received at least first-line hormone thera
py. Patients were classified into those in remission, those with stable dis
ease, or those with progressive disease according to their prostate-specifi
c antigen response and their clinical status.
Thirty-four percent of all patients had PTH levels above the upper level of
normal for controls of similar age (7.0 pmol/ liter), and in 44% of these
patients this was associated with a normal ionized calcium. Patients with p
roven bone metastases had significantly higher PTH levels than those withou
t. (7.3 +/- 0.5 vs. 4.3 +/- 0.4 pmol/liter, P < 0.0005).
There was evidence for a difference in the PTH levels between the three res
ponse groups. The PTH levels tended to be higher in patients with progressi
ve disease. Thirty-seven of 65 patients (57%) with both progressive disease
and proven bone metastases had elevated PTH levels. Mean levels of urinary
deoxypyridinoline and cAMP were significantly greater in patients with hig
h PTH than in those with a normal PTH.
Treatment with oral calcium supplements in 32 patients with a high PTH seem
ed to have only a transient effect on elevated PTH or low ionized calcium l
evels.
These data show that secondary hyperparathyroidism occurs frequently in pat
ients with advanced prostate cancer, particularly in those with both progre
ssive disease and bone metastases. The increased PTH levels are associated
with an increase in bone resorption markers. These findings raise important
questions about the role of PTH in progression of prostatic cancer in bone
and the potential limitations of the use of bisphosphonates in patients wi
th a raised PTH or low ser-um calcium.