Anaphylaxis

Clinically related documents

Print Print icon Tell a friend Tell a friend icon
Jan Hed, Clin Immunologist, MD, PhD
Karolinska Institutet, IMPI, Div of Clin Immunology
Huddinge University Hospital, Sweden
 
The statements below are based on conclusions from selected publications. Their intention is to highlight recent research and information that could be beneficial in allergy in vitro testing. They can include seemingly contradictory statements due to differences in selecting patient populations as well as in the study design.
  • Anaphylaxis is defined as a severe IgE-mediated systemic allergic reaction. No universal definition exists. The reaction involves episodes of urticaria, angioedema, bronchospasm, and hypotension that are life threatening in nature. Confusion arises because the allergic reaction can be mild, moderate, or severe (for review, see 1-6).
     
  • Urticaria and pruritus are the most common early manifestations and in most cases begin within 30 to 60 minutes after exposure (3).
     
  • There is a dose-response mechanism operative in anaphylaxis and the severity of the reaction is directly proportional to the rapidity of onset (for review see 3).
     
  • Most studies suggest that atopic persons are at greater risk of developing anaphylaxis to foods (7), whereas no such correlation exists for developing IgE-mediated anaphylaxis in response to drugs or to insect stings (7-10, for review, see 5).
     
  • However, the immunologic sensitization to Hymenoptera venoms is associated with atopy-related humoral IgE hyper-responsiveness (11).
     
  • Anaphylactoid reaction is a second form of systemic reaction to foreign substances with a similar clinical expression to anaphylaxis but it does not involve IgE (for review, see 2).
     
  • Idiopathic anaphylaxis is a recently described third form of systemic reaction and is characterized by all of the features of anaphylaxis but is without an identifiable exogenous antigen or cause (12, for review, see 6).
     
  • Unlike antigen induced anaphylaxis, idiopathic anaphylaxis is treatable with a tapering course of oral glucocorticoids (13).
     
  • Roughly 20% to 40% of anaphylactic reactions are idiopathic (5, 14, 15).
     
  • The incidence of anaphylaxis has been described as being 3 to 30 cases in 100,000 individuals per year  (15, 16).
     
  • Tryptase is released from mast cells in anaphylactic and, to a lesser extent, in anaphylactoid reactions (17, 18).
     
  • Serum level of tryptase peaks 60-120 minutes after the onset of anaphylaxis and provides useful evidence for mast cell activation as a cause of the acute reaction (19).
     
  • Tryptase level, a reliable measure of mast cell degranulation, suggests that anaphylaxis was probably responsible for a number of previously unexplained sudden deaths (20, 21). 
     
  • Using ROC-analysis based on 30 patients with anaphylaxis, the best cut-off of tryptase levels at 8.23 ng/ml showed a sensitivity of 94.12% and a specificity of 92.31% (22).
     
  • Baseline levels of tryptase may predict the severity of response to allergen in sensitive subjects since patients that have severe, hypotensive response to a sting challenge to bee venom had higher baseline levels of tryptase than mild, non-reactors and controls (23).
     
  • Tryptase is generally markedly elevated in cases of bee sting-induced (19, 23, 24, 25) or drug-induced severe anaphylaxis (17, 19, 24).
     
  • In food-induced anaphylaxis, no elevated tryptase was seen in one study (24) but was noted in six of eight fatalities in another study (25).
     
  • Common causes of anaphylaxis are foods, insect stings, drugs, latex and exercise (5, 14, 15 for review, see 3,4).
     
  • Severe anaphylaxis in children treated in emergency departments was due to foods in 57% of cases (8)
     
  • Asthma is a risk factor for the severity of symptoms in food-dependent anaphylaxis (26).
     
  • Foods commonly causing anaphylaxis are peanuts, tree nuts, fish, shellfish, cows milk and eggs (5, 7, 8, 14).
     
  • Numerous foods have been implicated in food-dependent, exercise-induced anaphylaxis (27, 28), but IgE sensitization to wheat seems to be the most common cause (27, 29).
     
  • Drugs causing anaphylaxis or anaphylactic reactions are antibiotics (penicillin,sulfamethoxazole and trimethoprim), intravenous anaesthetic drugs, aspirin, non-steroidal anti-inflammatory drugs (NSAID), intravenous contrast media and opoid analgesics (30).

References:

    1. Ewan PW. Anaphylaxis. BMJ 1998;316:1442-5.
    2. Weiler JM. Anaphylaxis in the general population: A frequent and occasionally fatal  disorder that is underrecognized. J Allergy Clin Immunol 1999;104:271-3.
    3. Yunginger J. Anaphylaxis. Ann Allergy 1992;69:87-96.
    4. Kagy L, Blaiss MS. Anaphylaxis in children. Pediatric annals 1998;27:727-34.
    5. Kemp SF, Lockey RF, Wolf BL, Lieberman P. Anaphylaxis - a review of 266 cases. Arch Intern Med 1995;155;1749-54.
    6. Hogan MB, Kelly MA, Wilson NW. Idiopathic anaphylaxis in children. Ann Allergy Asthma Immunol 1998;81:140-2.
    7. Pumphrey RSH, Stanworth SJ. The clinical spectrum of anaphylaxis in north-west England. Clin Exp Allergy 1996;26:1364-70.
    8. Novembre E, Cianferoni A, Bernardini R, Mugnaini L, Caffarelli C, Cavagni G et al. Anaphylaxis in children: clinical and allergologic features. Pediatrics 1998;101:E8.
    9. Kalyoncu AF, Demir AU, Ozcan U, Ozkuyumcu C, Sahin AA, Baris YI. Bee and wasp venom allergy in Turkey. Ann Allergy Asthma Immunol 1997;78:408-12.
    10. Birnbaum J, Vervloet D, Charpin D. Atopy and systemic reactions to hymenoptera stings. Allergy Proc 1994;15;49-52.
    11. Schafer T, Przybilla B. IgE antibodies to Hymenoptera venoms in the serum are common in the general population and are related to indications of atopy. Allergy 1996;51:372-7.
    12. Bacal E, Patterson R, Zeiss CR. Evaluation of severe (anaphylactic) reactions. Clin Allergy 1978;8:295-304.
    13. Wong S, Yarnold PR, Yango C, Patterson R, Harris KE. Outcome of prophylactic therapy for idiopathic anaphylaxis. Ann Intern Med 1991;114:133-6.
    14. Yocum MW, Khan DA. Assessment of patients who have experienced anaphylaxis: a 3-year survey. Mayo Clin Proc 1994;69:16-23.
    15. Yocum MW, Butterfield JH, Klein JS, Volcheck GW, Schroeder DR, Silverstein MD. Epidemiology of anaphylaxis in Olmsted County: A population-based study. J Allergy Clin Immunol 1999;104:452-6.
    16. Sorensen HT, Nielsen B, Ostergaard Nielsen J. Anaphylactic shock occurring outside hospitals. Allergy 1989;44:288-90.
    17. Ordoqui E, Zubeldia JM, Aranzabal A, Rubio M, Herrero T, Rodriguez VM et al. Serum tryptase levels in adverse drug reactions. Allergy 1997;52:1102-5.
    18. Fisher MM, Baldo BA. Mast cell tryptase in anaesthetic anaphylactoid reactions. Br J Anaesth 1998;80;26-9.
    19. Schwartz LB, Yunginger JW, Miller J, Bokhari R, Dull D. The time course of appearance and disappearance of human mast cell tryptase in the circulation after anaphylaxis. J Clin Invest 1989;83:1551-5.
    20. Edston E, van Hage-Hamsten M. Beta-tryptase measurements post-mortem in anaphylactic deaths and in controls. Forensic Sci Int 1998;93:135-42.
    21. Schwartz HJ, Yunginger JW, Schwartz LB. Is unrecognized anaphylaxis a cause of sudden unexpected death? Clin Exp Allergy 1995;25:866-70.
    22. Enrique E, Garcia-Ortega P, Sotorra O, Gaig P, Richart C. Usefulness of UniCAP-Tryptase fluoroimmunoassay in the diagnosis of anaphylaxis. Allergy 1999;54:602-6.
    23. Schwartz LB, Bradford TR, Rouse C, Irani AM, Rasp G, Van der Zwan JK et al. Development of a new, more sensitive immunoassay for human tryptase: use in systemic anaphylaxis. J Clin Immunol 1994;14:190-204.
    24. Schwartz LB, Metcalfe DD, Miller JS, Earl H, Sullivan T. Tryptase levels as an indicator of mast cell activation in systemic anaphylaxis and mastocytosis. N Engl J Med 1987;316:1622-6.
    25. Yunginger JW, Nelson DR, Squillace DL, Jones RT, Holley KE, Hyma BA et al. Laboratory investigation of deaths due to anaphylaxis. J Forensic Sci. 1991;36:857-65.
    26. Sampson HA, Mendelson L, Rosen JP. Fatal and near-fatal anaphylactic reactions to food in children and adolescents. N Engl J Med 1992;327:380-4.
    27. Dohi M, Suko M, Sugiyama H, Yamashita N, Tadokoro K, Juji F et al. Food-dependent, exercise-induced anaphylaxis: a study on 11 Japanese cases. J Allergy Clin Immunol 1991;87:34-40.
    28. Romano A, DiFonso M, Giuffreda F, Quaratino D, Papa G, Palmieri V, et al. Diagnostic work-up for food-dependent, exercise-induced anaphylaxis. Allergy 1995;50:817-24.
    29. Kushimoto H, Aoki T. Masked type I wheat allergy. Relation to exercise-induced anaphylaxis. Arch Dermatol 1985;121:355-60.
    30. Van der Klauw MM, Wilson JHP, Stricker BHCh. Drug-associated anaphylaxis: 20 years of reporting in the Netherlands (1974-1994) and review of the literature. Clin Exp Allergy 1996;26:1355-63.