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SUDDEN DEATH IN INFANCY SYNDROME

SIR: The recent article by Dr Rainsford and Dr Brune (Journal, June 5) presents the hypothesis that the parietal cell is the major site of damage after peroral aspirin. The authors cite a number of studies which support this hypothesis, but unfortunately ignore other studies which do not. For instance, aspirin-induced erosions do develop in the non acid-secreting antral mucosa, both in the experimental animal and man.' 2 3 Also, Hingson and Ito have found that the initial damage (assessed by electron microscopy) involves the surface mucous cells, not the parietal cells." A further criticism is that the authors leap from their as yet unproven hypothesis to a recommendation for clinical practice-r-that aspirin "should not be taken on an empty stomach". Gastric acid is undoubtedly important in the pathogenesis of aspirin-induced erosions. 5 Even so, predictions about the effects of food on the extent of aspirin damage must take into consideration several factors including: (i) alterations in the rate of gastric emptying; (ii) buffering by food; and (iii) stimulation of gastric acid secretion by food. Indeed, in a recent symposium in Canberra, Leonards suggested that aspirin might cause more damage if taken soon after meals." While direct information about the effects of food on aspirin damage is difficult to obtain in man, indirect evidence (provided by measurement of faecal blood loss after aspirin ingestion) is available. Aspirininduced blood loss has been found to be the same, irrespective of whether the drug is administered before meals or with milk or food. 7 8 Therefore, at present, the recommendation to avoid aspirin "on an empty stomach" cannot be justified.