Three conditions that may occur after consumption of seafood--puffer fish poisoning, ciguatera, and paralytic shellfish poisoning--are caused by a group of poisons that block voltage-gated sodium channels in myelinated and non-myelinated nerves. The conditions cannot be distinguished clinically and so constitute an entity for which the name pelagic paralysis is proposed. Variations in the clinical features can be accounted for by large differences in the amount of toxin present in the seafood.

Recombinant human erythropoietin is a major advance in the management of patients with chronic renal failure. The sustained dose-dependent rise in haematocrit which it produces effectively abolishes symptoms of anaemia, but at the cost of an increase in blood viscosity. This in turn predisposes to increased vascular resistance and the development of hypertension. Over half of all deaths of patients with end-stage renal failure are from cardiovascular disease, notably myocardial infarction, heart failure, and stroke, for which hypertension is a known risk factor. Erythropoietin-related increases in blood pressure are therefore of particular concern, and seem to be most severe in previously hypertensive patients. There is now a need to establish the optimum rate and extent of rise of haematocrit required to alleviate symptoms without incurring undue risk.

The syndrome of humoral hypercalcaemia of malignancy (HHM) is characterised by end-organ manifestations of parathyroid-hormone (PTH)-like effects such as abnormalities of renal tubular calcium and phosphate transport, increased nephrogenous cyclic AMP and 1,25 dihydroxyvitamin D production, and increased osteoclastic bone resorption. Despite this, true ectopic PTH production has seldom been documented in HHM. A number of bone-resorbing factors, including prostaglandins, prostaglandin-stimulating factors, lymphokines, growth factors, and vitamin-D-like sterols, have been implicated as causes of HHM, but none can reproduce the PTH-like biochemical features characteristic of the syndrome. PTH-related peptides have recently been isolated from tumours associated with HHM. These substances are the most likely putative humoral mediators of HHM, since they are structurally similar to PTH in the aminoterminal region and interact with the PTH receptor in vitro. However, the remainder of the molecule is quite distinct from PTH, which accounts for the absence of PTH immunoreactivity in serum and tumour extracts from HHM patients. Since these factors seem to act by binding to the PTH receptor, synthetic PTH antagonists may in the future be a means of treating HHM.