PubMed · 5333819
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G Milhaud. 1967-01-14. [Thyrocalcitonin].. https://pubmed.ncbi.nlm.nih.gov/5333819/
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INTRODUCTION: Hypercalcaemia is a relatively common clinical problem with a wide spectrum of presentations. This review provides an overview of the diagnosis and management of hypercalcaemia, and recent developments in drug therapy. METHODS: A non-systematic review of the English-language literature on various aspects in the management of hypercalcaemia was conducted. RESULTS: Increasingly, more patients with asymptomatic or minimally symptomatic disease are being detected. Appropriate evaluation of hypercalcaemia requires a careful elucidation of the underlying causes, the commonest being primary hyperparathyroidism and malignancy. The decision to treat and extent of treatment depends on factors such as the degree of hypercalcaemia, severity of symptoms, and the underlying cause. Several options are readily available to lower serum calcium levels. In the setting of acute, symptomatic hypercalcaemia, general measures such as saline rehydration and loop diuretics, and more specific measures including bisphosphonates (e.g. clodronate, pamidronate, ibandronate and zoledronate), calcitonin, mithramycin, gallium, glucocorticoids and dialysis, could be utilised. Definitive correction of the underlying cause, such as surgery for primary hyperparathyroidism or anti-tumour therapy, is important in controlling chronic hypercalcaemia. Medical therapy (estrogen, alendronate and raloxifene) is available to control bone sequelae in asymptomatic, mild hyperparathyroidism where surgery is not indicated. CONCLUSION: The therapeutic approach to hypercalcaemia should be tailored to the clinical setting. Developments in the understanding of the pathophysiological processes and the increasing availability of more powerful therapeutic options would help in achieving good outcomes in the management of acute and chronic hypercalcaemia.
Procalcitonin (PCT), a precursor of calcitonin is a useful indicator of severe systemic infection and sepsis. For a better understanding of the pathophysiological background of PCT induction, a study was made of the intracellular expression of PCT in various human white blood cell populations-i.e. monocytes and polymorphonuclear granulocytes (PMNs)-and the role of TNF-alpha in the stimulation of their PCT production. The expression of PCT was investigated by flow cytometric analysis with intracellular staining with antibodies to the PCT components calcitonin (CT) and katacalcin (KC). Both human peripheral monocytes and granulocytes expressed PCT, and increased intracellular amounts of the PCT components were demonstrated after stimulation with Staphylococcus aureus as TNF-alpha inducer. The S. aureus induced stimulation of PCT production was inhibited by anti-TNF-alpha monoclonal antibodies. The monocytic cell line U937 expressed considerable intracellular PCT, but S. aureus failed to induce an increase in PCT expression. The determination of intracellular PCT by flow cytometry is a promising and a sensitive method for further investigation of the effects of various cytokines and cytokine-inducing agents in PCT synthesis of human monocytes and granulocytes.