Advances in allergic skin disease, anaphylaxis, and hypersensitivity reactions to foods, drugs, and insects
2007; Elsevier BV; Volume: 119; Issue: 6 Linguagem: Inglês
10.1016/j.jaci.2007.02.013
ISSN1097-6825
AutoresScott H. Sicherer, Donald Y.M. Leung,
Tópico(s)Asthma and respiratory diseases
ResumoThis review highlights some of the research advances in anaphylaxis and hypersensitivity reactions to foods, drugs, and insects and in allergic skin disease that were reported primarily in the Journal in 2006. Advances in diagnosis include identification of food proteins to which IgE binding is associated with severe reactions; elucidation of diagnostic relationships of skin prick test wheal size with outcomes of egg, tree nut, and sesame allergy; evaluation of the diagnostic utility of atopy patch testing for food; and the observation that yellow jacket sting outcomes are influenced by species. Mechanistic observations include the following: heating of birch pollen–related foods disrupts IgE binding but not T-cell epitopes; a simple imbalance of TH1/TH2 response does not explain variations in clinical expression of peanut allergy; and elucidation of the role of dendritic cells in drug hypersensitivity. With regard to treatment, a rapidly disintegrating epinephrine tablet showed promise for sublingual treatment of anaphylaxis, RNA interference techniques showed promise in creating lower-allergenic foods, and anti–IL-5 showed promise for treatment of eosinophilic esophagitis. Progress in our understanding of the immunology and the etiology of skin barrier dysfunction in atopic dermatitis has also been made. These observations will likely contribute toward optimizing management of these common allergic disorders. This review highlights some of the research advances in anaphylaxis and hypersensitivity reactions to foods, drugs, and insects and in allergic skin disease that were reported primarily in the Journal in 2006. Advances in diagnosis include identification of food proteins to which IgE binding is associated with severe reactions; elucidation of diagnostic relationships of skin prick test wheal size with outcomes of egg, tree nut, and sesame allergy; evaluation of the diagnostic utility of atopy patch testing for food; and the observation that yellow jacket sting outcomes are influenced by species. Mechanistic observations include the following: heating of birch pollen–related foods disrupts IgE binding but not T-cell epitopes; a simple imbalance of TH1/TH2 response does not explain variations in clinical expression of peanut allergy; and elucidation of the role of dendritic cells in drug hypersensitivity. With regard to treatment, a rapidly disintegrating epinephrine tablet showed promise for sublingual treatment of anaphylaxis, RNA interference techniques showed promise in creating lower-allergenic foods, and anti–IL-5 showed promise for treatment of eosinophilic esophagitis. Progress in our understanding of the immunology and the etiology of skin barrier dysfunction in atopic dermatitis has also been made. These observations will likely contribute toward optimizing management of these common allergic disorders. This review highlights key advances in allergic skin diseases, anaphylaxis, and hypersensitivity to foods, drugs, and insect venom from among over 90 articles on these topics published in the Journal in 2006. Some of the key advances are summarized in Table I.Table ISummary of selected key advances reported in the JournalTopicClinical or basic research concernsAdvances and observationsAnaphylaxisDiagnosis and management• A National Institute of Allergy and Infectious Diseases-Food Allergy & Anaphylaxis Network cosponsored panel defines anaphylaxis and suggests diagnostic criteria.• A rapidly disintegrating epinephrine tablet shows promise for sublingual rather than intramuscular administration.Food allergyEpidemiology• Infants supplemented with vitamins A and D in peanut oil were less prone to allergy by age 4 y than those receiving the vitamins in water-soluble form.Molecular aspects of food allergy• Heating disrupts IgE but not T-cell epitopes in birch-related foods.• Identification of IgE binding to lipid transfer proteins in chestnut, apple, and grape may allow more specific diagnosis (severity).• A simple imbalance of TH1/TH2 does not explain differences in clinical expression of peanut allergy.Diagnostic testing• The clinical utility of considering skin test wheal size in addition to serum IgE level was reported for egg allergy.• Diagnostic relationships of skin test wheal size to outcomes of tree nut allergy were reported.• The atopy patch test shows modest additional predictive value (used with tests for specific IgE).Treatment/management• Anti–IL-5 shows promise for therapy of eosinophilic esophagitis.• RNA interference techniques show that several tomato allergens can be suppressed.• A study evaluated the persistence of peanut allergen in saliva, allowing for evidence-based patient advice.Drug allergyMechanisms• Elucidation of the role of dendritic cells in drug hypersensitivity to amoxicillin.Insect allergyDiagnosis and treatment• Patient satisfaction is higher with venom immunotherapy compared with providing epinephrine self-injectors.• There is significant species-specific variation in outcome of yellow jacket stings.UrticariaDiagnosis• Chronic urticaria sera increases basophil CD203c.Mechanisms• Possible role for thrombin in chronic urticaria.Treatment• Reduction of urticaria with anti-IgE treatment.ADMechanisms• Genetic association with filaggrin null mutations.• Increased IL-31 in AD skin as potential cause of T cell–mediated pruritus.• Propensity for viral skin infections associated with reduced innate immunity. Open table in a new tab There are very few population-based studies describing the incidence of food allergy in infancy. A whole population birth cohort of 969 infants was established on the Isle of Wight, United Kingdom (September 2001 to August 2002) and followed periodically to age 1 year.1Venter C. Pereira B. Grundy J. Clayton C.B. Roberts G. Higgins B. et al.Incidence of parentally reported and clinically diagnosed food hypersensitivity in the first year of life.J Allergy Clin Immunol. 2006; 117: 1118-1124Abstract Full Text Full Text PDF PubMed Scopus (196) Google Scholar The cumulative incidence of parentally reported food hypersensitivity was 25.8%, and 2.2% of those tested (n = 763) were sensitized to at least 1 food. Open or double-blind, placebo-controlled food challenges were offered to confirm most of the suspected reactions. About 1/8 were confirmed, indicating the need to evaluate suspected allergy to avoid a high rate of needless dietary exclusions. Depending on the stringency of criteria applied, the authors estimated that 2.2% to 5.5% of infants have food hypersensitivity during the first year of life. Little is known about the influence of ethnicity on food allergy outcomes. In a population-based cohort of South Asian and white children both in Leicestershire, United Kingdom, South Asian ethnicity was independently associated with food-related wheezing at age 1 to 4 years (odds ratio, 3.8) and 6 to 9 years (odds ratio, 9.1).2Kuehni C.E. Strippoli M.P. Silverman M. Food intolerance and wheezing in young South Asian and white children: prevalence and clinical significance.J Allergy Clin Immunol. 2006; 118: 528-530Abstract Full Text Full Text PDF Scopus (18) Google Scholar Although genetic predisposition is an apparent risk factor, several studies have added insights for the apparent environmental influence on a high and increasing rate of food allergy and atopic disease in Westernized countries. For example, the hygiene hypothesis was supported by observations that atopic disease was less common in schoolchildren following an anthroposophic lifestyle, which includes restrictive use of antibiotics3Floistrup H. Swartz J. Bergstrom A. Alm J.S. Scheynius A. van Hage M. et al.Allergic disease and sensitization in Steiner school children.J Allergy Clin Immunol. 2006; 117: 59-66Abstract Full Text Full Text PDF Scopus (149) Google Scholar and in children living with poor sanitation and increased helminth infection.4Flohr C. Tuyen L.N. Lewis S. Quinnell R. Minh T.T. Liem H.T. et al.Poor sanitation and helminth infection protect against skin sensitization in Vietnamese children: a cross-sectional study.J Allergy Clin Immunol. 2006; 118: 1305-1311Abstract Full Text Full Text PDF PubMed Scopus (86) Google Scholar Although there has been some suspicion that breast-feeding may contribute to atopic disease, data from a prospective birth cohort of 620 infants from Melbourne, Australia, indicated that early symptoms of atopic disease might prolong the duration of exclusive breast-feeding, underscoring the need to consider reverse causation in studies evaluating risk factors for atopy.5Lowe A.J. Carlin J.B. Bennett C.M. Abramson M.J. Hosking C.S. Hill D.J. et al.Atopic disease and breast-feeding: cause or consequence?.J Allergy Clin Immunol. 2006; 117: 682-687Abstract Full Text Full Text PDF PubMed Scopus (94) Google Scholar Another concern regarding risk for atopy has been the use of vitamin supplements. Kull et al6Kull I. Bergstrom A. Melen E. Lilja G. van Hage M. Pershagen G. et al.Early-life supplementation of vitamins A and D, in water-soluble form or in peanut oil, and allergic diseases during childhood.J Allergy Clin Immunol. 2006; 118: 1299-1304Abstract Full Text Full Text PDF PubMed Scopus (82) Google Scholar followed a birth cohort of 4089 infants to age 4 years and found that subjects supplemented with vitamins A and D in a water-soluble form were roughly twice as likely to have food allergy, allergen sensitization, and asthma compared with those who received the vitamins in peanut oil; the reason for this difference remains unclear, because potentially beneficial fats in the oil as a contribution to the total diet seems unlikely. Studies that evaluate IgE binding to food allergens and related pollen allergens in well characterized patient populations (eg, relating characteristics of sensitization to outcomes on oral challenge), and studies evaluating IgE binding to food proteins before and after heating or digestion, provide insights that are relevant to diagnosis, prediction of cross-reactivity, reaction severity, and treatment.7Tawde P. Venkatesh Y.P. Wang F. Teuber S.S. Sathe S.K. Roux K.H. Cloning and characterization of profilin (Pru du 4), a cross-reactive almond (Prunus dulcis) allergen.J Allergy Clin Immunol. 2006; 118: 915-922Abstract Full Text Full Text PDF PubMed Scopus (58) Google Scholar, 8Palacin A. Cumplido J. Figueroa J. Ahrazem O. Sanchez-Monge R. Carrillo T. et al.Cabbage lipid transfer protein Bra o 3 is a major allergen responsible for cross-reactivity between plant foods and pollens.J Allergy Clin Immunol. 2006; 117: 1423-1429Abstract Full Text Full Text PDF PubMed Scopus (63) Google Scholar, 9Puumalainen T.J. Poikonen S. Kotovuori A. Vaali K. Kalkkinen N. Reunala T. et al.Napins, 2S albumins, are major allergens in oilseed rape and turnip rape.J Allergy Clin Immunol. 2006; 117: 426-432Abstract Full Text Full Text PDF PubMed Scopus (43) Google Scholar, 10Flinterman A.E. Hoekstra M.O. Meijer Y. van Ree R. Akkerdaas J.H. Bruijnzeel-Koomen C.A. et al.Clinical reactivity to hazelnut in children: association with sensitization to birch pollen or nuts?.J Allergy Clin Immunol. 2006; 118: 1186-1189Abstract Full Text Full Text PDF PubMed Scopus (41) Google Scholar For example, Vassilopoulou et al11Vassilopoulou E. Rigby N. Moreno F.J. Zuidmeer L. Akkerdaas J. Tassios I. et al.Effect of in vitro gastric and duodenal digestion on the allergenicity of grape lipid transfer protein.J Allergy Clin Immunol. 2006; 118: 473-480Abstract Full Text Full Text PDF Scopus (85) Google Scholar showed that lipid transfer protein in grape maintained its biological activity after exposure to simulated gastric and duodenal digestion. IgE responses to these stable proteins may be associated with a higher risk for severe reactions and may indicate that sensitization may be prone to occur from the oral route. Similarly, Fernandez-Rivas et al12Fernandez-Rivas M. Bolhaar S. Gonzalez-Mancebo E. Asero R. van Leeuwen A. Bohle B. et al.Apple allergy across Europe: how allergen sensitization profiles determine the clinical expression of allergies to plant foods.J Allergy Clin Immunol. 2006; 118: 481-488Abstract Full Text Full Text PDF PubMed Scopus (304) Google Scholar evaluated allergen sensitization in regard to apple allergy in 389 patients in the Netherlands, Austria, Italy, and Spain. In 3 countries whose patients' apple allergy was typically mild, they found a relationship to birch pollenosis and sensitization to Bet v 1 and its apple homologue, Mal d 1, with an odds ratio of having local oral reactions of 2.8. In Spain, in contrast with the other 3 countries, patients more commonly had severe apple allergy (>35% systemic reactions), and sensitization was related to peach allergy and sensitization to Mal d 3, a nonspecific lipid transfer protein, with an odds ratio of systemic reactions of 7.76. Another complex food allergen is chestnut, which is often considered an allergic risk for persons with latex allergy. Sanchez-Monge et al13Sanchez-Monge R. Blanco C. Lopez-Torrejon G. Cumplido J. Recas M. Figueroa J. et al.Differential allergen sensitization patterns in chestnut allergy with or without associated latex-fruit syndrome.J Allergy Clin Immunol. 2006; 118: 705-710Abstract Full Text Full Text PDF Scopus (42) Google Scholar evaluated 12 patients sensitized to chestnut but not to latex and found IgE binding to a 9-kd lipid transfer protein in 91%; allergenic lipid transfer proteins from peach were also reactive, but latex related proteins (avocado class I chitinase and latex hevein) were not. The clinical and diagnostic importance of evaluating binding to specific proteins was further demonstrated by Kondo et al,14Kondo Y. Komatsubara R. Nakajima Y. Yasuda T. Kakami M. Tsuge I. et al.Parvalbumin is not responsible for cross-reactivity between tuna and marlin: a case report.J Allergy Clin Immunol. 2006; 118: 1382-1383Abstract Full Text Full Text PDF Scopus (32) Google Scholar who described a child who tolerated many types of fish but had anaphylaxis to tuna and marlin; they identified a unique cross-reactive allergen for this child whose serum did not bind the major fish allergen, parvalbumin. Together, these studies show promise for diagnostic tests that could more clearly predict reaction severity and likelihood of cross-reactivity with related foods or other related substances, such as latex. Dissection of cellular immune responses will likely provide further insights of diagnostic and therapeutic potential. Thottingal et al15Thottingal T.B. Stefura B.P. Simons F.E. Bannon G.A. Burks W. HayGlass K.T. Human subjects without peanut allergy demonstrate T cell-dependent, TH2-biased, peanut-specific cytokine and chemokine responses independent of TH1 expression.J Allergy Clin Immunol. 2006; 118: 905-914Abstract Full Text Full Text PDF Scopus (27) Google Scholar measured peanut allergen–driven cytokine and chemokine responses in short-term primary culture of PBMCs, paired with ELISAs, in adults with peanut allergy and adults sensitized or not sensitized to peanut who tolerated ingestion of peanut. Individuals with positive skin tests had more frequent or intense IL-5, IL-13 and CCL22 responses than those without, whether or not they had clinical peanut allergy. Surprisingly, the 3 groups were not distinguishable by IFN-γ or CXCL10 responses, which were absent, indicating that a protective TH1 bias does not explain the distinction in clinical outcomes, whereas a spectrum of TH2 responses may. In regard to elucidating a direct pathogenic role of T cells in food hypersensitivity, Bohle et al16Bohle B. Zwolfer B. Heratizadeh A. Jahn-Schmid B. Antonia Y.D. Alter M. et al.Cooking birch pollen-related food: divergent consequences for IgE- and T cell-mediated reactivity in vitro and in vivo.J Allergy Clin Immunol. 2006; 118: 242-249Abstract Full Text Full Text PDF PubMed Scopus (138) Google Scholar showed, using both in vitro systems and clinical oral food challenge studies, that heating birch pollen related food proteins can disrupt IgE binding—for example, extinguish symptoms of oral allergy or pollen-food related syndrome—but that T-cell–binding epitopes remain. These heated birch-related food proteins were capable of stimulating Bet v 1–specific T cells in vitro, and the heated foods induced exacerbations of atopic dermatitis (AD). Although the studies described reveal a potential diagnostic utility of evaluating IgE binding to particular food allergen components, additional clinical studies correlating oral food challenge outcomes to results of currently available diagnostic tests provide immediate insight for improved diagnosis. Knight et al17Knight A.K. Shreffler W.G. Sampson H.A. Sicherer S.H. Noone S. Mofidi S. et al.Skin prick test to egg white provides additional diagnostic utility to serum egg white-specific IgE antibody concentration in children.J Allergy Clin Immunol. 2006; 117: 842-847Abstract Full Text Full Text PDF PubMed Scopus (90) Google Scholar showed that among a group of children with low egg white–specific serum IgE (<2.5 kIU/L), where chances of tolerating egg was reasonable, skin test wheal size provided additional diagnostic utility. For example, children who tolerated egg had a median wheal of 3 mm, whereas those who did not had a median wheal of 5 mm. Increasing wheal sizes correlated with failing to tolerate egg, from 14% with a negative skin test failing a challenge to 80% failing when the skin test wheal was 8 mm or larger. Ho et al18Ho M.H. Heine R.G. Wong W. Hill D.J. Diagnostic accuracy of skin prick testing in children with tree nut allergy.J Allergy Clin Immunol. 2006; 117: 1506-1508Abstract Full Text Full Text PDF PubMed Scopus (57) Google Scholar presented data on sensitivity, specificity, and predictive value of various tree nut, sesame, and peanut skin test wheal sizes derived from 906 food challenges in 680 children. Several of the nuts (cashew, hazel, walnut) showed a positive predictive value of 1.0 at skin test wheal sizes of 8 mm or higher. Scibilia et al19Scibilia J. Pastorello E.A. Zisa G. Ottolenghi A. Bindslev-Jensen C. Pravettoni V. et al.Wheat allergy: a double-blind, placebo-controlled study in adults.J Allergy Clin Immunol. 2006; 117: 433-439Abstract Full Text Full Text PDF PubMed Scopus (77) Google Scholar performed double-blind, placebo-controlled food challenges to wheat in adults with suspected wheat allergy and confirmed reactions in 48% of 27 subjects. In addition to showing some variation in reactivity to raw or cooked wheat, they found a very poor correlation of challenge outcome to skin test or serum IgE results, partly attributable to cross-reactivity in subjects with grass pollen allergy, although persons with negative IgE tests also reacted. Another modality to improve predictions about food allergic reactions that may also identify individuals with food allergy without positive food-specific IgE tests is the atopy patch test. In this test, the food is placed in a Finn chamber on the skin for 48 hours and the results read in the subsequent days. Mehl et al20Mehl A. Rolinck-Werninghaus C. Staden U. Verstege A. Wahn U. Beyer K. et al.The atopy patch test in the diagnostic workup of suspected food-related symptoms in children.J Allergy Clin Immunol. 2006; 118: 923-929Abstract Full Text Full Text PDF PubMed Scopus (178) Google Scholar presented the results of 1700 such tests in regard to the outcomes of 873 oral food challenges to milk, egg, wheat, or soy in children with suspected food allergy. Although the test showed the best specificity from among serum food-specific IgE and skin prick tests and improved overall sensitivity and specificity of outcome predictions when combined with results from the IgE tests, it added only modest diagnostic information in the context of avoiding an oral food challenge. For example, with combined testing including the atopy patch test, and considering a positive predictive value of 95% to 99% reaction rates to warrant deferring a food challenge, only 0.5% to 14% of study patients would have avoided the food challenge because of the positive patch test. No routine tests have done well in predicting severity of a food-allergic reaction,21Flinterman A.E. Pasmans S.G. Hoekstra M.O. Meijer Y. Van Hoffen E. Knol E.F. et al.Determination of no-observed-adverse-effect levels and eliciting doses in a representative group of peanut-sensitized children.J Allergy Clin Immunol. 2006; 117: 448-454Abstract Full Text Full Text PDF PubMed Scopus (94) Google Scholar although a study by Astier et al22Astier C. Morisset M. Roitel O. Codreanu F. Jacquenet S. Franck P. et al.Predictive value of skin prick tests using recombinant allergens for diagnosis of peanut allergy.J Allergy Clin Immunol. 2006; 118: 250-256Abstract Full Text Full Text PDF PubMed Scopus (192) Google Scholar using recombinant peanut proteins showed that persons polysensitized to recombinant (r) Ara h 2 and either rAra h 1 or rAra h 3 were more likely to have severe reactions than persons monosensitized to rAra h 2. Although there are numerous modalities under investigation to treat food allergy,23Sicherer S.H. Sampson H.A. Food allergy.J Allergy Clin Immunol. 2006; 117: S470-S475Abstract Full Text Full Text PDF PubMed Scopus (600) Google Scholar management currently requires a large dose of education about food avoidance and emergency management.24Sicherer S.H. Bock S.A. An expanding evidence base provides food for thought to avoid indigestion in managing difficult dilemmas in food allergy.J Allergy Clin Immunol. 2006; 117: 1419-1422Abstract Full Text Full Text PDF Scopus (29) Google Scholar A review of reported accidental exposures to peanut from 252 patients at Montreal Children's Hospital indicated that accidental exposures occurred at an annual incidence rate of 14%, lower than most previous reports.25Yu J.W. Kagan R. Verreault N. Nicolas N. Joseph L. St Pierre Y. et al.Accidental ingestions in children with peanut allergy.J Allergy Clin Immunol. 2006; 118: 466-472Abstract Full Text Full Text PDF PubMed Scopus (146) Google Scholar This good news is likely the result of increased education and awareness. In a study of adolescents with food allergy, a group at special risk for fatal food-induced anaphylaxis, risk-taking behaviors were associated with social circumstances and feelings of isolation.26Sampson M.A. Munoz-Furlong A. Sicherer S.H. Risk-taking and coping strategies of adolescents and young adults with food allergy.J Allergy Clin Immunol. 2006; 117: 1440-1445Abstract Full Text Full Text PDF PubMed Scopus (240) Google Scholar The major need identified by the teenagers was third-party education of their peers, which would presumably increase understanding, reduce peer pressure, and present an additional layer of safety. An identified concern of the teens, and a worry for intimate partners of persons with food allergy, is the transfer of food protein in saliva during kissing or sharing utensils or straws. Maloney et al27Maloney J.M. Chapman M.D. Sicherer S.H. Peanut allergen exposure through saliva: assessment and interventions to reduce exposure.J Allergy Clin Immunol. 2006; 118: 719-724Abstract Full Text Full Text PDF PubMed Scopus (61) Google Scholar evaluated the time course of the peanut protein Ara h 1 in saliva and determined with 95% confidence that 90% of persons who ingested peanut butter would have no detectable Ara h 1 in their saliva after a peanut-free meal along with a waiting period of several hours. If engineering of less allergenic foods were possible, many of the concerns of food allergy could be allayed. This may someday be a plausible approach, because RNA interference techniques were successfully used to create less allergenic forms of tomato by silencing expression of profilin28Le L.Q. Mahler V. Lorenz Y. Scheurer S. Biemelt S. Vieths S. et al.Reduced allergenicity of tomato fruits harvested from Lyc e 1-silenced transgenic tomato plants.J Allergy Clin Immunol. 2006; 118: 1176-1183Abstract Full Text Full Text PDF Scopus (79) Google Scholar or lipid transfer protein.29Lorenz Y. Enrique E. Lequynh L. Fotisch K. Retzek M. Biemelt S. et al.Skin prick tests reveal stable and heritable reduction of allergenic potency of gene-silenced tomato fruits.J Allergy Clin Immunol. 2006; 118: 711-718Abstract Full Text Full Text PDF Scopus (43) Google Scholar Eosinophilic esophagitis is typically a food-responsive gastrointestinal disease, but food elimination is often an unsatisfactory treatment because numerous foods are commonly implicated, resulting in frustrating dietary trials and socially and nutritionally restrictive treatment diets.30Blanchard C. Wang N. Rothenberg M.E. Eosinophilic esophagitis: pathogenesis, genetics, and therapy.J Allergy Clin Immunol. 2006; 118: 1054-1059Abstract Full Text Full Text PDF PubMed Scopus (166) Google Scholar Stein et al31Stein M.L. Collins M.H. Villanueva J.M. Kushner J.P. Putnam P.E. Buckmeier B.K. et al.Anti-IL-5 (mepolizumab) therapy for eosinophilic esophagitis.J Allergy Clin Immunol. 2006; 118: 1312-1319Abstract Full Text Full Text PDF PubMed Scopus (354) Google Scholar undertook an open-label phase I/II study of a humanized monoclonal IgG1 antibody against IL-5 in 4 adults with eosinophilic esophagitis. After 3 monthly infusions, mean esophageal eosinophil counts fell from 46 to 6 per high power field (P < .001) and clinical symptoms and quality of life improved, indicating promise for this novel treatment. There has been a lack of an accepted definition of anaphylaxis, or criteria for diagnosis, 2 deficits that likely hinder research and treatment. A significant advance for the field was a report summarizing a second symposium that was cosponsored by the National Institute of Allergy and Infectious Diseases and the Food Allergy & Anaphylaxis Network in which various stake holders convened and recommended the following definition: "Anaphylaxis is a serious allergic reaction that is rapid in onset and may cause death."32Sampson H.A. Muñoz-Furlong A. Campbell R.L. Adkinson Jr., N.F. Bock S.A. Branum A. et al.Second symposium on the definition and management of anaphylaxis: summary report: Second National Institute of Allergy and Infectious Disease/Food Allergy and Anaphylaxis Network symposium.J Allergy Clin Immunol. 2006; 117: 391-397Abstract Full Text Full Text PDF PubMed Scopus (1587) Google Scholar The group also offered clinical criteria for diagnosing anaphylaxis that can be validated through future study and identified various research needs. In addition, the Journal offered a review of community management of anaphylaxis authored by F. Estelle R. Simons, MD,33Simons F.E. Anaphylaxis, killer allergy: long-term management in the community.J Allergy Clin Immunol. 2006; 117: 367-377Abstract Full Text Full Text PDF PubMed Scopus (183) Google Scholar and a review of genetic and diagnostic aspects of tryptase in anaphylaxis by George H. Caughey, MD.34Caughey G.H. Tryptase genetics and anaphylaxis.J Allergy Clin Immunol. 2006; 117: 1411-1414Abstract Full Text Full Text PDF PubMed Scopus (111) Google Scholar Practical observations about anaphylaxis included a reminder that accidental injection of a digit with epinephrine from an autoinjector may require therapy with warm soaks, topical nitroglycerin, or localized phentolamine injection;35Skorpinski E.W. McGeady S.J. Yousef E. Two cases of accidental epinephrine injection into a finger.J Allergy Clin Immunol. 2006; 117: 463-464Abstract Full Text Full Text PDF PubMed Scopus (18) Google Scholar that in an office-based allergy practice, 0.67% of injection immunotherapy treatments required treatment with epinephrine and 16% of these required more than 1 dose;36Kelso J.M. A second dose of epinephrine for anaphylaxis: how often needed and how to carry.J Allergy Clin Immunol. 2006; 117: 464-465Abstract Full Text Full Text PDF PubMed Scopus (62) Google Scholar and that serum tryptase could sometimes be elevated for a prolonged period in idiopathic anaphylaxis.37Shanmugam G. Schwartz L.B. Khan D.A. Prolonged elevation of serum tryptase in idiopathic anaphylaxis.J Allergy Clin Immunol. 2006; 117: 950-951Abstract Full Text Full Text PDF Scopus (31) Google Scholar Unique or rare causes of anaphylaxis were reported, including topical benzocaine,38Vu A.T. Lockey R.F. Benzocaine anaphylaxis.J Allergy Clin Immunol. 2006; 118: 534-535Abstract Full Text Full Text PDF PubMed Scopus (12) Google Scholar the disinfectant solution ortho-phthalaldehyde,39Suzukawa M. Yamaguchi M. Komiya A. Kimura M. Nito T. Yamamoto K. Ortho-phthalaldehyde-induced anaphylaxis after laryngoscopy.J Allergy Clin Immunol. 2006; 117: 1500-1501Abstract Full Text Full Text PDF Scopus (19) Google Scholar and prostate-specific antigen in seminal plasma.40Weidinger S. Mayerhofer A. Raemsch R. Ring J. Kohn F.M. Prostate-specific antigen as allergen in human seminal plasma allergy.J Allergy Clin Immunol. 2006; 117: 213-215Abstract Full Text Full Text PDF PubMed Scopus (38) Google Scholar In regard to future therapy, a fast-disintegrating tablet to provide sublingual epinephrine was tested in a rabbit model and showed favorable pharmacokinetics compared with intramuscular injection.41Rawas-Qalaji M.M. Simons F.E. Simons K.J. Sublingual epinephrine tablets versus intramuscular injection of epinephrine: dose equivalence for potential treatment of anaphylaxis.J Allergy Clin Immunol. 2006; 117: 398-403Abstract Full Text Full Text PDF Scopus (67) Google Scholar Considering that fear of needles is a likely reason for underuse of epinephrine in the community, this novel delivery system may be a promising alternative. In regard to elucidating the mechanisms underlying drug hypersensitivity, Rodrigez-Pena et al42Rodriguez-Pena R. Lopez S. Mayorga C. Antunez C. Fernandez T.D. Torres M.J. et al.Potential involvement of dendritic cells in delayed-type hy
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