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Abstract
Background: Hypercalcaemia of malignancy is well recognised, but hypocalcaemia in cancer patients is not, although it is increasingly encountered.
Methods: Analysis of an exemplary case and a narrative review of the literature based on the search terms cancer and hypocalcaemia.
Results: Hypocalcaemia may affect as many as 10% of hospitalised cancer patients. We identified 12 different potential mechanisms of hypocalcaemia of malignancy. Identifying the pathogenesis is essential for the correct treatment and can usually be performed at the bedside, based on serum parathyroid hormone (PTH) levels, creatinine, phosphate, magnesium, creatine kinase, liver enzymes and 25(OH)D. Essentially, decreased or normal PTH hypocalcaemia is seen after removal or destruction of its source, hypomagnesaemia, or cinacalcet treatment. In all other cancer-associated hypocalcaemia, PTH is elevated, including significant renal impairment, critically ill patients, extensive cell destruction (rhabdomyolysis, tumour lysis, haemolysis), acute pancreatitis, adverse drug reactions, cancer or cancer treatment-related malabsorption syndromes, vitamin D deficiency, or osteoblastic metastases. Different mechanisms may often operate in tandem. Pathogenesis determines treatment and affects prognosis. However, hypocalcaemia of malignancy as such did not imply a worse prognosis, in contrast with
hypercalcaemia.
Conclusion: Hypocalcaemia in cancer patients is commonly encountered, particularly in hospitalised patients, may be mediated by diverse mechanisms and should be better recognised.
