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Background: Awareness of the clinical features of anaphylaxis and its causative triggers is important if recurrent episodes are to be avoided. The incidence of anaphylaxis in the general population is often underreported, and epidemiologic studies are few. Because an accurate profile of anaphylaxis could heighten awareness of this problem, we investigated the epidemiology of anaphylaxis in the general population of Olmsted County, Minn., Objective: The purpose of this study was to describe the epidemiology of anaphylaxis in Olmsted County residents from 1983 through 1987., Methods: This was a retrospective population-based cohort study. The medical records of 1255 Olmsted County residents identified by computer-linked, medical diagnostic indices (the Rochester Epidemiology Study) were reviewed retrospectively to identify residents whose clinical episodes met the criteria for anaphylaxis. We determined the incidence and rate of occurrence of anaphylaxis, rate of recurrence, prevalence of atopy, cause of anaphylaxis, frequency of referral to an allergy specialist, hospital admission rate, and case-fatality rate., Results: There were 133 residents who experienced 154 anaphylactic episodes during the 5-year period: 116 residents had 1 episode of anaphylaxis, 13 residents had 2 episodes, and 4 residents had 3 episodes. The anaphylaxis occurrence rate was 30 per 100,000 person-years (95% confidence interval, 25-35). There were 110 residents who had a first lifetime episode of anaphylaxis (that was medically evaluated) during the years 1983 to 1987. The average annual incidence rate of anaphylaxis was 21 per 100,000 person-years (95% confidence interval, 17-25). Atopy was present in 53% of the cohort, and allergy consultation was obtained in 52%. A suspect allergen was identified in 68% of the cohort, most frequently a food, medication, or insect sting. The hospitalization rate was 7%, and 1 patient died., Conclusion: The incidence of anaphylaxis is less than 1%, and death rarely occurs. People with atopy experience anaphylaxis more frequently than people without atopy. Anaphylaxis frequently is not recognized by patients and physicians.

Objective: To report the clinical responses and mediator-release profiles of an aspirin-sensitive man with systemic mast cell disease during aspirin desensitization., Material and Methods: We quantified the release of six mediators during aspirin desensitization., Results: Although aspirin was administered cautiously with an initial dose of 20 mg, successful aspirin desensitization necessitated complete monitoring and resuscitation capabilities of a medical intensive-care unit for 4.5 days because of frequent, severe anaphylactoid responses. To our knowledge, this is the first report of a pronounced increase in plasma levels of the vasodilator peptide calcitonin gene-related peptide during episodes of aspirin-induced hypotension. Increases in plasma levels of calcitonin and serum levels of tryptase paralleled those of calcitonin gene-related peptide, but plasma levels of calcitonin remained increased for up to 18 hours. Urinary excretion of histamine and 1-methyl-4-imidazoleacetic acid also showed precipitous, although delayed, increases. Excretion of the prostaglandin D2 metabolite 11 beta-prostaglandin F2 alpha followed a bimodal pattern during aspirin desensitization; after severe hypotensive responses, the maximal value was more than 490,000 pg/mL, but the level decreased to less than 100 pg/mL after therapeutic serum levels of salicylate were attained., Conclusion: These data suggest that the hypotensive responses to aspirin in some patients with systemic mast cell disease may result from the combined effects of several mediators.

Aspirin therapy for patients with systemic mast cell disease (SMCD) decreases the production of prostaglandin D2, which is thought to be a major mediator of flushing. Paradoxically, in 5 to 10% of patients with SMCD, administration of aspirin causes massive mediator release and an anaphylactoid reaction. We attempted aspirin desensitization in a 34-year-old man with SMCD (confirmed by bone marrow biopsy) who was incapacitated by severe flushing episodes and hypotension. His baseline mediator levels of plasma calcitonin, urinary histamine, and urinary N-methyl-imidazoleacetic acid were abnormal. Pentagastrin stimulation increased the plasma level of calcitonin from 47 pg/mL to 130 pg/mL (normal, less than or equal to 110) at 5 minutes. Oral aspirin desensitization was begun; however, after a cumulative dose of 620 mg, an anaphylactoid reaction ensued in conjunction with hypotension, abdominal cramping, and flushing. Coincidentally, 1 hour after the episode, the plasma calcitonin level increased from 37 pg/mL to 540 pg/mL, and the serum tryptase level increased from 1 ng/mL to 3.9 ng/mL. Six hours after the episode, the urine level of histamine increased from 90 micrograms/g creatinine to 337 micrograms/g creatinine, and the urinary N-methylimidazoleacetic acid increased from 32 mg/24 h to 81 mg/24 h. Hence, the patient had increased basal levels of plasma calcitonin that increased substantially during aspirin desensitization and increased to above the upper limit of normal during pentagastrin stimulation. Human mast cells may be capable of producing calcitonin or causing secretion of calcitonin in response to skeletal changes.

Background: Only a few groups have reported on idiopathic anaphylaxis. We analyzed our experience with idiopathic anaphylaxis, especially in regards to prognosis., Methods: Thirty-seven patients with the diagnosis of idiopathic anaphylaxis were retrospectively identified by a medical records search from 1989-1992. Thirty-five patients were evaluable and a telephone questionnaire was conducted to determine the current treatment and course of their idiopathic anaphylaxis since their initial evaluation., Results: Patient ages ranged from 26 to 71 years (mean 48), 72% were women, and 43% were atopic. Frequent episodes of idiopathic anaphylaxis (> 5/year) occurred in 31%. At follow-up (mean 2.5 years), 21 patients (60%) had resolution of idiopathic anaphylaxis, and the frequency of anaphylaxis was decreased in nine, increased in two, and the same in three patients. Only three patients were still having frequent episodes and two required chronic glucocorticoids. Patients with frequent idiopathic anaphylaxis treated with only antihistamines and adrenergics underwent remission or improvement as frequently as those treated with chronic glucocorticoids., Conclusions: These results are similar to other reports of idiopathic anaphylaxis and indicate a generally favorable prognosis. Some patients with frequent idiopathic anaphylaxis improved without the need for glucocorticoids. Well controlled studies may be required to analyze the role of glucocorticoids in this disease.

Design: A quality-control retrospective review of medical records was conducted for cases of anaphylaxis encountered at Mayo Clinic Rochester during a 3 1/2-year period., Patients: For inclusion in the study, all patients had to manifest general symptoms of mediator release such as generalized pruritus, urticaria, angioedema, and flushing. Of the 179 patients with anaphylaxis (mean age, 36 years), 66% were female, 49% had atopy, and 37% had a previous history of immediate reactions to allergens. Of these study patients, 11 were receiving medications capable of exacerbating anaphylaxis (beta-blockers in 7 of them)., Results: Consultation with an allergist was obtained in 142 cases, and a probable diagnosis was made after review of the medical records. Causes of anaphylaxis included foods in 59 patients, idiopathic in 34, Hymenoptera in 25, medications in 23, and exercise in 12; false-positive diagnoses were recorded in 18. Allergy prick tests were done in 104 patients, 71 of whom had positive results; allergen-specific IgE tests were done in 44 patients, 23 of whom had positive results. In 19 patients, only allergen-specific IgE testing was done, and results were positive in 12. Normal test results included C1 esterase inhibitor in 33 patients, metabisulfite challenge in 15, and dye or preservative challenge in 10. Food skin tests were graded on a relative value scale and revealed 15 highly allergic, 24 moderately allergic, and 39 weakly allergic food groups., Conclusion: A standard protocol should be used for assessment of patients with anaphylaxis, and fresh food extracts should be used for prick skin testing. A national incidence study of anaphylaxis is needed. The public and school personnel should be educated about food anaphylaxis, and emergency treatment for anaphylaxis should be readily available for patients.

A case of common variable immunodeficiency, a relatively rare disorder, is presented. This case was complicated by the presence of an anti-IgA antibody in the patient's serum and a history of a possible anaphylactic reaction to a prior intravenous infusion of gamma-globulin. Common variable immunodeficiency is actually a heterogeneous group of demonstrable immunoglobulin deficiencies that have in common low levels of most immunoglobulin isotypes, the inability to form antibodies to antigen, an absence of gross defects in cell-mediated immunity, and the presence of recurrent bacterial infections. The history of immunoglobulin deficiency and its treatment is reviewed. Although the primary therapy for common variable immunodeficiency is gamma-globulin replacement, ancillary measures such as early treatment of infections with antibiotics are also important. Intravenous gamma-globulin replacement therapy is preferred to intramuscular replacement therapy in these patients because intramuscular doses must be limited in volume to minimize local pain and take 2 to 14 days to achieve maximal blood levels, during which time in situ degradation of up to 50% of the administered dose can occur. Five intravenous gamma-globulin preparations are currently available in the United States. The potential adverse effects of intravenous gamma-globulin infusion and the precautions currently taken to ensure safety during administration of this product are discussed.

Anaphylactoid reactions to protamine sulfate have been attributed to its capacity for nonimmunologic mast cell degranulation and/or complement consumption. In the current study, evidence is presented for the occurrence of an immunologic anaphylactic reaction mediated by a complement-dependent IgG skin-sensitizing antibody. A retrospective study of blood component donors given protamine for heparin neutralization revealed that prior exposure to protamine is associated with increased risk of adverse reaction to the drug.

A pair of monozygotic twins discordant for systemic lupus erythematosus(SLE) were studied and no differences noted in their immune respose to tetanus toxoid, keyhole lympet hemocyanin, DNCB, delayed sensitivity, or antibody titers to viruses. Both were noted to have biologically false positive serology at an early age, but only one twon developed SLE. The clinically unaffected twin underwent castration at an early age, suggesting that ovarian hormones may play an important role in the development of SLE.

Three weeks after a massive inhalation of mold present on infected oats, a farmer's wife had extrinsic allergic alveolitis. Aspergillus fumigatus was cultured from the moldy oats and from deep bronchial washings obtained at fiberoptic bronchoscopy. Spores and hyphae characteristic of Aspergillus species were demonstrated within granulomas in the pulmonary tissue obtained by transbrochial biopsy. Serum precipitins, delayed (48 hour) cutaneous hypersensitivity and in vitro lymphocyte transformation to A. fumigatus were demonstrated. The findings in this case suggest that a type IV immunologic response and subsequent (lymphocyte-mediated) tissue inflammation may underlie the pathogenesis of this and other forms of hypersensitivity pneumonitis.

Parameters of cell-mediated immunity (CMI) were studied in 17 allergic rhinitis patients selected for markedly elevated total serum IgE levels (greater than 300 IU/ml) and 14 normal controls. Mean serum IgE levels were 1,421 IU/ml and 101 IU/ml in the allergic and control groups, respectively (p less than 0.001). There were no significant differences between the allergic patients and the normal controls in delayed cutaneous hypersensitivity, in mitogen and antigen lymphocyte transformation in heterologous or autologous plasma, or in percentage of sheep erythrocyte rosettes. The allergic patient group had a significantly higher percentage of sheep erythrocyte-antibody-complement rosettes (p less than 0.05). Markedly elevated total serum IgE levels in allergic rhinitis patients were not associated with any detectable impairment of CMI.

Intravenous pretesting with radiocontrast media (RCM) was performed in 204 RCM-sensitive patients considered for repeat contrast radiography. Group 1 had vague histories of prior anaphylactoid reaction and negative pretests, and 2 of 41 (4.9%) had reactions upon contrast radiography. Groups 2 to 5 had definite histories of prior anaphylactoid reaction. Group 2 had the radiographic study cancelled: 18 of 21 (85.7%) had positive pretests. Group 3 had positive pretests and underwent contrast radiography, and 9 of 15 (60%) had reactions despite premedication. Group 4 (no premedication) and group 5 (diphenhydramine premedication) had negative pretests, but 11 of 53 (20.7%) and 3 of 71 (4.2%), respectively, developed reactions (p less than 0.001). The reaction frequency in group 3 (posivie pretest) of 12 of 18 (66.7%) was greater than that in groups 4 and 5 (negative pretest) combined (14 of 124 (11.3%), p less than 0.001). Intravenous pretesting identified a high-risk group and diphenhydramine premedication decreased the frequency of reaction in patients sensitive to radiocontrast media.

Two adult men with recurrent pyoderma due to Staphylococcus aureus and a selective deficiency of immunoglobulin M (IgM) antibody synthesis are described. An analysis of each patient's polymorphonuclear leukocyte chemotaxis, phagocytosis and killing of Staph. aureus, serum opsonizaiton of Staph. aureus, and serum and lymphocyte-mediated responses to antigenic stimulation was performed. Family studies revealed a possible autosomal dominant inheritance pattern with heterogenetic expression of various dysgammaglobulinemic states in each patient's first degree relatives. In vivo studies of delayed hypersensitivity and in vitro studies of polymorphonuclear leukocyte and lymphocyte function were normal. A defect in IgM, but not in IgG (immunoglobulin G), antibody synthesis to a number of antigens, and a mild decrease in serum opsonic activity to Staph. aureus correctable by heat inactivated normal human serum were found in each patient. In these patients, the recurrent staphulococcal pyoderma prompted an investigation of host defense mechanisms and revealed low to absent IgM levels and a defect in IgM antibody synthesis.