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Nephrogenous cyclic AMP in primary hepatocellular carcinoma patients with or without hypercalcaemia
N S Panesar1, K M Au, N W Leung
1Department of Chemical Pathology, Chinese University of Hong Kong.
Clinical Endocrinology
|December 1, 1991
Summary
Primary hepatocellular carcinoma can cause hypercalcaemia through a parathyroid hormone (PTH)-like factor, leading to elevated nephrogenous cyclic AMP (NcAMP). Some patients also show suppressed PTH levels.
Area of Science:
- Endocrinology
- Oncology
- Nephrology
Background:
- Hypercalcaemia is a potential complication in primary hepatocellular carcinoma (HCC).
- The role of parathyroid hormone (PTH) and related factors in HCC-associated hypercalcaemia requires further investigation.
Purpose of the Study:
- To investigate the relationship between nephrogenous cyclic AMP (NcAMP) excretion and other biochemical parameters in HCC patients.
- To assess PTH-like activity as a potential cause of hypercalcaemia in HCC.
Main Methods:
- Collected blood and urine samples from 55 untreated HCC patients, 14 healthy controls, and 8 cirrhosis patients.
- Measured serum calcium, phosphate, alkaline phosphatase, albumin, creatinine, urinary calcium, creatinine, hydroxyproline, plasma/urine cAMP, and serum PTH.
- Calculated TmP/GFR and NcAMP using established methods.
Main Results:
- Seven percent of HCC patients presented with hypercalcaemia.
- Hypercalcaemic HCC patients exhibited significantly lower phosphate, PTH, and TmP/GFR, with elevated NcAMP compared to controls.
- Elevated hydroxyproline and calcium excretion were observed in hypercalcaemic patients, with bone resorption identified as the primary cause in most cases.
- Twenty-nine percent of normocalcaemic HCC patients showed suppressed PTH levels.
Conclusions:
- A PTH-like humoral factor, possibly PTH-related peptide, is implicated in causing hypercalcaemia in HCC.
- PTH suppression can occur in some normocalcaemic HCC patients.