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Four patients suffered from chronic or recurrent angioedema, of sudden onset in adult life, associated with visceral pain and impossible to control by dietary means. In spite of normal complement function they respond very well to tranexamic acid therapy. Antiprotease drugs need not be restricted to cases of ClsINH deficiency.

One hundred patients who reacted adversely to one or more specific foods were studied. In 93 the food induced symptoms included asthma, eczema, angioedema, urticaria, rhinorrhoea, or a combination of one or more of these with gastrointestinal symptoms. The remaining seven had gastrointestinal symptoms only. The diagnosis of food allergy was made on the on the basis of a definite, immediate allergic reaction to specific foods or a reaction that was suggestive of allergy, supported by a corresponding positive skin prick or radioallergosorbent test. In the absence of such evidence, the less specific diagnosis of 'food intolerance' seemed preferable. Test materials appeared to differ in their diagnostic usefulness. A high proportion (c. 75 per cent) of patients who were intolerant to egg, fish or nuts had positive test results. In contrast, only 30 per cent of patients with milk intolerance had positive tests, suggesting inadequate test methods or a non-allergic cause for many patients' milk intolerance. Nevertheless, five milk intolerant patients with negative tests had milk-induced asthma.

Prophylactic doses of aspirin, indomethacin, or ibuprofen prevented symptoms of food intolerance in five out of six patients who on several occasions had had acute gastrointestinal symptoms after the ingestion of specific foodstuffs. Blood and stool prostaglandin E2 and F2alpha concentrations during unprotected challenge were consistent with the idea that these symptoms were mediated through prostaglandin release. Prostaglandin-synthetase inhibitors may benefit some patients with specific food intolerance who are unable or unwilling to avoid the offending food.

Skin test materials vary in their potency and specificity. Although 3 mm reactions are often regarded as diagnostic of a type 1 allergy, a study based on 100 allergy clinic patients with food intolerance showed that thirteen out of fifteen patients with a 3 mm reaction to common inhalant allergens had no RAST-detectable allergen-specific IgE. Three millimetre reactions were significant for milk and egg extracts. Food intolerance was clinically demonstrable in six out of seven patients giving a 4 mm skin reaction and in ten out of thirteen with a 3 mm reaction. There was, however, a "clinically false positive" reaction of 3 mm or more in 3.8% of allergy clinic patients for milk and 2.8% for egg. In fifteen out of nineteen patients with a clinical diagnosis of fish allergy, the diagnosis was supported by a skin test reaction of 5 mm or more. However, seven patients with no history of intolerance to fish gave a 4 mm reaction to the same extract. Reactions of less than 5 mm were thus unhelpful clinically.

Cow's milk allergy was diagnosed in 79 patients, all of whom had signs and symptoms of allergies other than milk intolerance. In addition to difficulties with infant feeding and diarrhoea, clinical features included constipation, vomiting, intestinal colic, growth retardation, and psychological disturbance, as well as eczema and asthma. All were reversible after milk withdrawal, which suggests that the allergic basis of such symptoms may have been underestimated. In most cases, one or both parents were atopic and the child had been bottle-fed from birth. There were no breast-fed children of non-atopic parents in this series.

12 patients with adverse reactions to foods are discussed, including 1 with biopsy-proven ulcerative proctitis. 10 had predominantly gastrointestinal symptoms (diarrhoea, abdominal pain, vomiting) and two had rhinitis and headache. Skin tests (in all but two) and radioallergosorbent tests (RAST) in some patients were negative. All of the patients were challenged in hospital with the offending food, either alone or preceded by a prostaglandin synthetase-inhibiting drug (aspirin, indomethacin or Ibuprofen). In 11 of the 12 patients this premedication prevented both the gastrointestinal and the more remote symptoms. Blood and stool prostaglandin measurements (PGE2 and PGF2 alpha) showed changes which correlated with clinical symptoms and did not occur if one of the inhibiting drugs had been given prior to challenge.