The present approach to the diagnosis, management and follow‐up of anaphylaxis during anaesthesia varies in the Scandinavian countries. The main purpose of these Scandinavian Clinical Practice Guidelines is to increase the awareness about anaphylaxis during anaesthesia amongst anaesthesiologists. It is hoped that increased focus on the subject will lead to prompt diagnosis, rapid and correct treatment, and standardised management of patients with anaphylactic reactions during anaesthesia across Scandinavia. The recommendations are based on the best available evidence in the literature, which, owing to the rare and unforeseeable nature of anaphylaxis, mainly includes case series and expert opinion (grade of evidence IV and V). These guidelines include an overview of the epidemiology of anaphylactic reactions during anaesthesia. A treatment algorithm is suggested, with emphasis on the incremental titration of adrenaline (epinephrine) and fluid therapy as first‐line treatment. Recommendations for primary and secondary follow‐up are given, bearing in mind that there are variations in geography and resources in the different countries. A list of National Centres from which anaesthesiologists can seek advice concerning follow‐up procedures is provided. In addition, an algorithm is included with advice on how to manage patients with previous suspected anaphylaxis during anaesthesia. Lastly, provides an overview of the incidence, mechanisms and possibilities for follow‐up for some common drug groups.

No abstract

Individual smoking histories of a general population sample and of two groups of workers exposed to occupational allergens were related to serum IgE concentrations and results of radioallergosorbent and prick tests in the workers.The geometric mean IgE concentration was higher in smokers than in non-smokers. The distribution of serum IgE values in the two groups showed an apparent difference, with a bimodal appearance in the smokers.Evidence of sensitisation against occupational allergens was more common in workers who smoked.The adjuvant effect of smoking on IgE antibody production might be due to damage to airways mucosa and supports the mucosal theory of atopy.

IgE-sensitization to SUX, MOR and PHO was detected in Norway but not in Sweden. One possible explanation is the unrestricted use of cough mixtures containing MOR derivatives in Norway.

No abstract

The magnesium status of 22 hemodialysis patients was studied by analyses of serum, skeletal muscle and peripheral blood lymphocyte levels of magnesium. Despite elevated serum magnesium, normal magnesium levels were noted in skeletal muscle and lymphocytes. 12 patients were exposed to a low dialysate magnesium concentration, resulting in normalization of serum magnesium but no changes in muscle or lymphocyte magnesium, which might indicate slow exchange between these intracellular stores and the extracellular fluid. Normalization of serum magnesium was followed by a slight rise in circulating parathyroid hormone levels without noticeable changes in serum calcium or phosphate levels. Since signs of an absolute magnesium excess were not detected, a combination of low dialysate magnesium and the use of an oral magnesium compound as a phosphate binder might be a way to decrease aluminium exposition in hemodialysis patients.

Mouse interleukin 4 (IL-4) has been shown to act on B cells as an induction factor for Ig class switch. We studied the characteristics of IL-4-regulated Ig isotype production in lipopolysaccharide (LPS)-stimulated splenic B-cell cultures with emphasis on the comparison between the IgG1 and IgE responses. The results show that the kinetics for the appearance of IgG1 and IgE isotypes are similar, but that the dose of IL-4 required for the induction of an IgE response is 3-10 times higher than that for an IgG1 response. No requirement for T cells was found for the induction of either isotype. Pre-incubation of cells for 24 h with IL-4 alone was sufficient to induce an IgG1 response when cells were recultured with LPS from days 1 to 6. However, the simultaneous presence of both IL-4 and LPS for at least 24 h was required for a detectable IgE response. For an optimal IgE response, IL-4 needed to be present for more than 72 h in LPS-activated cultures. The possible reasons for the different regulation of IgG1 and IgE responses are discussed.

Summary Three cases are described showing a seasonal exacerbation of their nephrotic syndrome in association with an atopic trait and grass pollen allergy. The first patient has a history of four consecutive seasonal relapses each requiring steroid therapy. Following a course of desensitization injections he has now been free of relapse for 3 consecutive years. The second patient has also had a recurrent steroid‐sensitive nephrotic syndrome often associated with the pollen season and allergic rhinitis. In this patient a course of cyclophosphamide has reduced his tendency to relapse. The third patient who has been on continuous prednisone therapy shows a seasonal increase in proteinuria. Serum changes in the first two patients include: a seasonal rise in total and grass pollen specific IgE; the continued presence of grass pollen specific IgG throughout the year but with a reduction during the pollen season in association with a more pronounced fall in the total IgG level; a depression in the C3 level in association with each major relapse; a mild rise in the I‐K titre and a positive result in the C1q test for circulating complexes. A renal biopsy performed on the first patient when in relapse showed minor histological changes only and IgG. IgM, IgA, IgD, IgE, C3 and fibrinogen were undetectable by immunofluorescent examination. The probable mechanism for the development of proteinuria in these patients is discussed.