Hypercalcaemia associated with cancer is seen not infrequently in hospital practice and can be a source of considerable morbidity. Over the past decade, our understanding of the pathogenesis of this syndrome has advanced, allowing improved treatment protocols. Because one of the principal abnormalities relates to an increase in bone resorption, antiresorptive agents such as calcitonin and the bisphosphonates have been shown to be of value. In the medium to longer term, the bisphosphonates -particularly pamidronic acid[pamidronate;aminohydroxypropylidene bisphosphonate (APD)] and clodronic acid [clodronate; dichloromethyl bisphosphonate (Cl2MDP)]¿ appear to be more efficacious in terms of their calcium-lowering effect than calcitonin, and also appear to be associated with fewer adverse effects than most other agents. However, the importance of energetic re-expansion of the extracellular space with 0.9% sodium chloride before bisphosphonate therapy is extremely important. Cancer-associated hypercalcaemia, especially with squamous cancer, is often associated with the production of parathyroid hormone-related protein (PTHrP). Where this is the case, it usually reflects the presence of more advanced disease with shortened life expectancy, and poorer response to calcium-lowering therapy. Multiple treatments with larger doses of bisphosphonate may be required for these patients.