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In his discussion of paraneoplastic conditions causing dysphagia Dr Camidge does not include paraneoplastic hypercalcaemia (November 2001 JRSM, pp. 567-572). In the hospital population, hypercalcaemia is a common metabolic complication of malignancy. Hypercalcaemia has several recognized effects on the gastrointestinal system, and dysphagia has occasionally been reported1,2. Muscular weakness is a prominent feature which can seem paradoxical from a physiological point of view since calcium ions are responsible for the excitation—contraction coupling in all muscle cells. Calcium ions are involved in neuromuscular transmission and muscular contractions. At the neuromuscular junction, release of acetylcholine is stimulated by the rapid influx of calcium ions into the synapse. In all types of muscle a rise in intracellular calcium promotes contraction. In skeletal muscle, it stimulates interactions between actin and myosin by removing the inhibitory influence of the troponin—tropomyosin complex. In smooth muscle, calcium ions bind to calmodulin which, via activation of a protein kinase, phosphorylates myosin. This phosphorylation is a prerequisite for activation of the actin—myosin complex which leads to muscular contraction. Hypercalcaemia reduces the contractility of smooth muscle, which may explain the pathogenesis of dysphagia in patients with hypercalcaemia.