Residential fires may cause cyanide poisoning. At the time of a patient's hospital admission, an elevated plasma lactate concentration is a useful indicator of cyanide toxicity in fire victims who do not have severe burns.

1 A non-exponential mathematical equation was used to extrapolate the 'predictive line' for plasma paraquat concentrations beyond 24 h. Plasma paraquat concentrations were measured in 30 patients who were admitted more than 24 h after overdose. The extrapolated line accurately predicted the outcome in 27 of these 30 patients. 2 Urine paraquat concentrations were measured in 53 patients. All patients with urine paraquat concentrations of less than 1 mg/l (colourless or light blue test result using the colorimetric test) within 24 h of overdose survived. In contrast, patients with urine paraquat concentrations of more than 1 mg/l had a high probability of death. 3 Even if plasma paraquat concentrations have a higher predictive value, urine data may contribute to a more rapid evaluation of prognosis.

It has been suggested that in uremic bone, aluminum interferes with normal mineralization. Aluminum content and aluminum localization were studied in iliac crest biopsies of two groups of patients on regular hemodialysis; one group had histologic osteomalacia, and little or no bone resorption (group 1); the other, osteitis fibrosa and no mineralization defect (group 2). Group 1 patients had significantly higher plasma aluminum concentrations than those of group 2. No difference was found in bone aluminum content, which was above normal in both groups. In the bone samples of the osteomalacic subjects, aluminum was mainly localized at the limit between osteoid and calcified tissue, the site where the bone mineral is normally first deposited. Osteomalacia could not be related to hypocalcemia or to phosphate depletion. Active vitamin D derivatives (25-hydroxycholecalciferol and 1alpha-hydroxycholecalciferol) failed to prevent or to improve the bone disease. In the bone samples of group 2 subjects, aluminum could not be localized by the methods used, except in the two cases with greatly elevated bone aluminum, where it was mainly localized on cement lines. In group 2 subjects, immunoreactive parathyroid hormone plasma concentration, osteoclast surface, and marrow fibrosis were significantly higher than they were in group 1 subjects. It is concluded that in bone from uremic patients on regular dialysis, aluminum can induce a particular form of osteomalacia, resistant to the vitamin D active derivatives. The bone disease is only observed in the absence of severe secondary hyperparathyroidism. This suggests that parathyroid hormone may be involved in the development of the aluminum-induced mineralization defect.

1 The toxicokinetics of paraquat were studied in 18 cases of acute human poisoning using a specific radioimmunoassay. Plasma paraquat concentration exhibited a mean distribution half-life ( t½ α) of 5 h and a mean elimination half-life ( t½ β) of 84 h. Cardiovascular collapse supervened early during the course of the intoxication and was associated with the distribution phase. Death related to pulmonary fibrosis occurred late and was associated with the elimination phase. 2 Pharmacokinetic analysis of urine paraquat excretion confirmed the biphasic decline of paraquat. Moreover, renal paraquat and creatinine clearances were not correlated but renal paraquat clearance was never higher than the renal creatinine clearance. 3 Tissue paraquat distribution was ubiquitous with an apparent volume of distribution ranging from 1.2 to 1.6 l/kg. Muscle could represent an important reservoir explaining the long persistence of paraquat in plasma and urine for several weeks or months after poisoning.