Hypocalcaemia of malignancy.

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.

Response to experimental implantation of autologous iris tissue and to iris injuries.

Autoimmune disease has been suspected in some cases of human uveitis. The initiating event has been thought to be injury and/or infection. To investigate the effect of injury on the uvea and on the immune apparatus rabbits and guinea pigs were subjected to various repeated iris insults, including implantation of autologous iris tissue into the anterior chamber of the contralateral eye. Of the procedures employed only iridectomy and insertion of iris produced some anterior chamber clouding, which was only slightly increased on repetition of the procedure; 76% of these animals failed to produce circulating CF antibodies. No local CF antibodies in the anterior chamber fluid nor increases in fluorescent antibodes in sections of the eyes could be detected. None of the animals tested developed skin hypersensitivity to homologous uveal antigen. None of the other traumatic procedures, which included repeated insertions of plastic into the anterior chamber, produced uveitis manifested clinically or by histological examination, circulating or local humoral antibodies, nor increases in fluorescent antibodies in the tissues of the eye. Introduction of antiuveal antibody into the anterior chamber also failed to produce uveitis. It can be concluded from these experiments that simple, repeated injury to the iris is not sufficient to elicit an autoimmune response under the conditions tested.