A patient with paraneoplastic hypercalcemia from metastatic neuroendocrine pancreatic neoplasia shows very high levels of both procalcitonin and calcitonin, in the absence of clinical and lab findings of sepsis. Does anyone have an explanation for this situation?
Procalcitonin is normally an intermediate product in calcitonin synthesis; secretion of calcitonin is stimulate by increase of plasmatic levels of gastrin and pentagastrin.
Pancreatic neuroendocrine tumors may be nonfunctional or functional and make extra amount of hormones such gastrin and others. So it's possible to observe high procalcitonin and calcitonin levels without sepsis.
PCT is a relatively specific marker of bacterial disease and may be produced by various organs including the thyroid, liver, testis, lung, prostate, kidney, and small intestine, but the secretion of PCT by a tumour has mainly been reported in small-cell
lung carcinoma and medullary thyroid carcinoma or neuroendocrine neoplasia.