In two of those cases the mechanism of hypercalcemia was thought to be related to overproduction of calcitriol, in one case the production of PTH-rP
was the cause, and in the remaining two cases no mechanism was identified.
During the second trimester the calcium intake increased (930.6 [+ or -] 300.7 mg/day to 1195 [+ or -] 467 mg/day, p<0.001) and PTH decreased without changes on PTH-rp
, endothelin and nitrite-nitrate levels (Table 2).
It is now clear that PTH-rP has a pathophysiological role not just in hypercalcemia but also in local osteolysis.
The physiological role of the PTH-rP remains unclear.
These include the effects of PTH-rP on this receptor and whether these are identical to those of PTH, whether this receptor can explain some of the controversial non-bone effects of PTH that have been described for many years such as those on the vascular system, what the signal transduction pathway that is connected to this receptor is, and finally whether this receptor is related to the anabolic response of PTH.
 Nonstandard abbreviations: ECF, extracellular fluid; PTH, parathyroid hormone; 1,25[(OH).sub.2][D.sub.3], 1,25-dihydroxyvitamin D; and PTH-rP, PTH-related protein.
In addition, the serum PTH-rP concentration was 13.7 pmol/mL, which well exceeded the normal range (<1.1 pmol/mL).
In the present case, the serum PTH-rP and G-CSF concentrations were markedly elevated in a patient with a pancreatic adenocarcinoma.
PTH-rP is a single-chain peptide with an amino terminal domain that is very similar to that of PTH.
These findings suggest that inflammatory cytokines played a key role in the production of PTH-rP by cancer cells and the high serum G-CSF concentration.