SummaryThese guidelines have been prepared by the Standards of Care Committee (SOCC) of the British Society for Allergy and Clinical Immunology (BSACI) and are intended for allergists and others with a special interest in allergy. As routine or validated tests are not available for the majority of drugs, considerable experience is required for the investigation of allergic drug reactions and to undertake specific drug challenge. A missed or incorrect diagnosis of drug allergy can have serious consequences. Therefore, investigation and management of drug allergy is best carried out in specialist centres with large patient numbers and adequate competence and resources to manage complex cases. The recommendations are evidencebased but where evidence was lacking consensus was reached by the panel of specialists on the committee. The document encompasses epidemiology, risk factors, clinical patterns of drug allergy, diagnosis and treatment procedures. In order to achieve a correct diagnosis we have placed particular emphasis on obtaining an accurate clinical history and on the physical examination, as these are critical to the choice of skin tests and subsequent drug provocation. After the diagnosis of drug allergy has been established, communication of results and patient education are vital components of overall patient management.

SUMMARY In iii'o rectal dialysis was used to study rectal mucosal release of immunoreactive prostaglandin E2-like material and its relation to disease activity, rectal electrical potential difference (PD), and treatment in 24 patients with ulcerative colitis. In untreated colitics in remission and in relapse, median values for apparent mucosal prostaglandin E2 (PGE2) release were increased three-fold (P <0.05) and 13-fold (P <0-002) respectively over that found in control subjects. In patients in remission during treatment with sulphasalazine and/or corticosteroids, median apparent PGE2 release was similar to that of controls, but in colitics in relapse, despite treatment, it was greatly increased (p < 0.002). Ulcerative colitis in relapse was associated with a significant reduction in rectal PD (p < 0.002); in patients with quiescent ulcerative colitis, a smaller reduction was found (p <0.05). In nine patients studied serially before and during treatment, there were associations between changes in disease activity assessed sigmoidoscopically, in PD and in apparent mucosal PGE2 release. Furthermore, rectal mucosal PGE2 release and PD were linearly correlated (p < 00 1). These findings indicate that mucosal PGE2 release is markedly enhanced in active ulcerative colitis, and they confirm the value of rectal PD as a guide to disease activity. In addition, they suggest that rectal dialysis may be a useful way of studying rectal prostaglandin metabolism in man.

Prostaglandin E1 is chemotactic at concentrations down to 10 ng/ml for rabbit polymorphonuclear (PMN) leucocytes. Prostaglandins E2 and F2α have little or no chemotactic effect at concentrations up to 10 μg/ml. Washed PMN leucocytes produce a chemotactic agent during phagocytosis, but not in the presence of indomethacin (28 μM). Phagocytosing PMN leucocytes produce up to ten times as much prostaglandin as do resting cells. Some of this is prostaglandin E1 as judged by thin layer chromatography and differential bioassay. This prostaglandin production by PMN leucocytes is abolished by indomethacin (28 μM). Ultrasonicated suspensions of PMN leucocytes produce prostaglandin from arachidonic acid. This synthesis is inhibited by indomethacin. Homogenates of PMN leucocytes which have been pre‐incubated with bacteria for 30 min show more prostaglandin synthetase activity than homogenates from PMN leucocytes which have not been exposed to bacteria. It is concluded that in some forms of inflammation, prostaglandin E1 may play a controlling role in cellular migration. PMN leucocytes may contribute to the generation of prostaglandins found in some inflammatory lesions.

Allergic reactions to Hymenoptera stings are frequently observed all over Europe. Rarely they may induce long-standing morbidity or even be fatal. Several investigations have shown that the emergency treatment given to these patients is often inadequate. Cutaneous symptoms respond well to antihistamines and also to adrenaline. Adrenaline is the mainstay for outside hospital treatment of more severe reactions involving the respiratory tract (bronchial asthma, laryngeal oedema) and the cardiovascular system (anaphylactic shock). Inhaled adrenaline is especially useful in respiratory symptoms, while parenteral application of adrenaline is prefered for shock treatment. All patients with severe respiratory or cardiovascular reactions must be hospitalized, treated under intensive care conditions and observed for at least 24 hr. Emergency medications including adrenaline for inhalation or for self-injection must be given to all patients with a history of systemic allergic reactions to hymenoptera stings. These patients must also get instructions for safety measures to avoid further stings. They should be referred to an allergist in order to evaluate the indication for venom immunotherapy.

The incidence, time course and nature of systemic reactions to injections of bee and wasp venom during immunotherapy have been estimated in an open, prospective, single centre study. One hundred and nine survivors of moderate to severe systemic reactions to stings from hymenoptera, received courses of bee or wasp venom by monthly subcutaneous injection for up to 3 years. Systemic reactions were recorded after 7.5% of 946 weekly venom injections during the initial phase of treatment, and after 2.1% of 1789 monthly maintenance injections. In both phases of treatment, reactions were more frequent after bee (17% of initial phase, 7.8% of maintenance treatment) than after wasp (3% of initial phase, 0.3% of maintenance treatment) venom injections. The percentage of patients experiencing at least one reaction was also higher for bee (46%) than for wasp (14%) sensitive patients. Over 80% of reactions began within 30 min of injection, over 90% within 1 h and only two (2%), between 1 and 2 h, the remaining six (5.5%) starting more than 2 h after injection. Only 0.47% of venom injections produced a systemic reaction which was severe enough to require adrenaline treatment. The female patients experienced more reactions (21% of the wasp, 60% of the bee, sensitive) than the males (5.5% wasp, 20% bee). Age and atopy did not appear to be significant risk factors for systemic reactions. We conclude that wasp and bee venom immunotherapy in a conventional dosage regimen was generally well tolerated.(ABSTRACT TRUNCATED AT 250 WORDS)