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  • Beck, F. Bodog (1935) (USA) –  Bee Venom Therapy. Bee Venom, Its Nature, and its effect on Arthritic and Rheumatoid Conditions.
    Appleton-Century Co., Incorporated.
    New York. London. 238 pp. (***).



  • Bernard, A. A.; Kersley, J. B. (1986)  –  Sensitivity to insect stings in patients taking anti-inflammatory drugs,
    in British Medical Journal 292,  378-379.



  • Boutin, Y.; Jobin, M.; Bedard, P. M.;  Hebert, M.;  Hebert, J. (1994) (Canada)  –  Possible dual role of anti-idiotypic antibodies in combined passive and active immunotherapy in honeybee sting allergy,
    in J Allergy Clin Immunol, Jun;93(6),  1039-46 (***-abstract). [i]



  • Brooks R., Viky J.A.,  Shipman W.,  Mraz C.,  Warren G.B. (1989) (USA)  –  Studies of the venom of the honeybee,
    in the XXXII-Nd. Apimondia Congress, Rio de Janeiro, Brazil,  506-516 (French, German and Spanish abstracts included) (***).



  • Bousquet, J. (1981) (France) –  Allergie chez les apiculteurs,
    in the XXVIII-Th. Apimondia Congress, Acapulco, Mexico,  443-445 (***).



  • Cherbuliez, Theodore (1997) (USA) –  Bee Venom Therapy and Safety,
    in Bee Informed # 3, volume 4, Autumn,  10-11.



  • Croft, L. R. (1988) (UK) –  Allergy to bee stings and its prevention.
    Elmwood Medical Monographs. ISBN 0 946019 03 7. British Library Cataloguing in Publication Data, 103 pp.   (***).



  • Donald Mac Sue (1983) (USA) –  A new hope for the people allergic to bee venom,
    in American Bee Journal, August,  578.



  • Egner, W.; Ward, C.;  Brown, D. L.;  Ewan, P. W. [ii](1998) (UK)  –  The frequency and clinical significance of specific IgE to both wasp (Vespula) and honey-bee (Apis) venoms in the same patient,
    in Clin Exp Allergy, Jan;28(1),  26-34 (***-abstract). [iii]



  • Faux, J. A.; Moffatt, M. F.;  Lalvani, A.;  Dekker, J.;  Warrell, D. A.;  Cookson, W. O. (1997) (U.K.)  – Sensitivity to bee and wasp venoms: association with specific IgE responses to the bee and wasp venom and HLA DRB1 and DPB1,
    in Clin Exp Allergy, May;27(5),  578-83 (***-abstract). [iv]



  • Fierro Morales, Walter (1991) (Uruguay) –  Accidentes provocados por picaduras de abejas,
    in XII congreso de la Asociacion  Latinoamericana de Farmacologia Montevideo, Diciembre.



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    in X Congreso Argentino de Alergia e Inmunologia, Buenos Aires,



  • Fierro Morales, Walter (1993) (Uruguay) –  Reacciones alergicas a las picaduras de abejas. 25 Encuentro de pediatras alergistas Argentinos  y 2 Encuentro pediatras alergista uruguayos
    Solis, Diciembre.



  • Fierro Morales, Walter (1995) (Uruguay) –  Alergia a picadura de insectos,
    in VI Congreso de Alergia e Imunologia del cono Sur. Punta del Este, Marzo.



  • Fierro Morales, Walter (1996) (Uruguay) –  Prevalence of Systemic Adverse Reaction to Hymenoptera Sting in a General Population in Uruguay,
    in the 52-nd Annual Meeting of the American Academy of Allergy, Asthma & Immunology. New Orleans, LA, Marzo.



  • Fierro Morales, Walter (1996) (Uruguay) –  Anafilaxia por picadura de insectos,
    in I Jornada de Actualizacion en Alergia e Imunologia Infantil, Junio.



  • Ford, R. M. (1980) –  Honeybee venom immunotherapy. Letter,
    in Med J Aust, 1(10),  500.



  • Ford, R. M. (1984) –  Bee venom immunotherapy and bee-sting mortality. Letter,
    in Med J Aust, 140(9),  563-64.



  • Forster, K. A.(1969) (Germany) –  Chemistry, pharmacology and therapeutically effectiveness of bee venom,
    in the XXII-Nd. Apimondia Congress, München, Germany (***).



  • Frankland, A. W. (1976) –  Bee sting allergy.
    in Bee World 57(4),  145-50;
    IBRA Reprint M88, 6 pp. (***).



  • Gallesio Maria Teresa (1986) (Italy) –  Diagnosis and therapy of allergy to hymenoptera venom,
    in Apiacta, # 3.



  • Gencheva G.; Shkenderov, S. V.  (1986)   Inhibition of complement activity by certain bee venom components,
    in Doklady Bolgarskoi Akad. Nauk 39,  137-139.



  • Golden, D. B. K.; Schwartz, J. (1986)  –  Guidelines for venom immunotherapy,
    in Journal of Allergy and Clinical Immunology 77,  727-728.



  • Hoffman,D.R., Shipman,W.H.,  Babin,D. (1977)  –  Allergens in bee venom. Two new high molecular weight allergenic specifities,
    in Journal of Allergology and Clinical Immunology 59,  p.147.



  • Hunt,K.J., Sobotka,A.K.,  Valentine,M.D.,  Amodio,F.J.,  Benton,A.W.,  Lichtenstein,L.M. (1978)  –  A controlled trial of immunotherapy in insect hypersensitivity,
    in New England Journal of Medicine 4,  257-261.



  • Ingold Labs, Christopher; Buku A.;  Blandina P.;  Birr C.;  Gazis D. (1989)  –  Solid-phase synthesis and biological activity of Mast Cell Degranulating (MCD) peptide, a component of bee venom,
    in J. Peptide Protein Res. 33(2),  p86-93, 58
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  • Knulst, A.C.; de Maat-Bleeker, F.;  Bruijnzeel-Koomen, C. A.[v]  (1998) (Netherlands)  – Wasp and bee venom allergy (original article in Dutch),
    in Ned Tijdschr Geneeskd, Apr 18;142(16),  889-92 (***-abstract). [vi]



  • Krylov,N. Vasily. (1995) (Russia) –  Bee venom: properties, production, usage (Russian).
    Nizhny Novgorod. Lobachevsky University. 224 pp., illustrations;
    ISBN -5-85746-076-X.



  • Lessof, M. H.; Sobotka, A. K.;  Lichtenstein, L. M. (1978)  –  Effects of passive antibody in bee venom anaphylaxis,
    in Johns Hopkins Med J, Jan;142(1),  1-7 (*** – abstract). [vii]



  • Maly, F. E.; Marti-Wyss, S.;  Blumer, S.;  Cuhat-Stark, I.;  Wuthrich, B.[viii] (1997) (Switzerland)  –  Mononuclear blood cell sulfidoleukotriene generation in the presence of interleukin-3 and whole blood histamine release in honey bee and yellow jacket venom allergy,
    in J Investig Allergol Clin Immunol, Jul;7(4),  217-224 (***-abstract). [ix]



  • Mezrina, O. V. (1975) –  Oral administration of novocaine solution for treatment of allergic complications of apitherapy,
    in Vrach Delo(7),  125-7.



  • Mueller, Ulrich; Fricker, M.;  Wymann, D.;  Blaser, K.;  Crameri, R.[x] (1997) (Switzerland)  –  Increased specificity of diagnostic tests with recombinant major bee venom allergen phospholipase A2,
    in Clin Exp Allergy, Aug;27(8),  915-920 (***-abstract). [xi]



  • Muresan, Dumitru (1981) (Romania) –  Etude des modifications immunologiques dans l’allergie aux piqures d’abeilles,
    in the XXVIII-Th. Apimondia Congress, Acapulco, Mexico,  464-466 (***).



  • Mueller, Ulrich, R.[1] (1990) (Switzerland)Insektenstichallergie.
    Gustav Fischer Verlag, Stuttgart-Germany ISBN 3-437-30621-9;
    Insect Sting Allergy, New York-USA, ISBN 0-89574-313-2, 183 pp.



  • Neumann, W.; Stracke, A. (1951)  –  Untersuchungen mit Bienengift und Histamin an der Formaldehydarthritis der Ratte,
    in Exper. Path. Pharmakol. 213,  pp.8-17.



  • Orlov, N. B.; Khomutov, A. E. (1981) (USSR)  –  L’heparine, substance antagonique du venin d’abeille,
    in the XXVIII-Th. Apimondia Congress, Acapulco, Mexico,  473 (***-abstract).



  • Patrizzi, R.; Muller, U.;  Yman, L.;  Hoigne, R. (1979)  – Comparison of skin tests and RAST for the diagnosis of bee sting allergy,
    in Allergy, Aug;34(4),  249-56 (***-abstract). [xii]



  • Riches, Harry (1982) (UK) –  Hypersensitivity to bee venom,
    in Bee World 63,  7-22.



  • Riches, Harry (1989) (UK) –  Bee venom hypersensitivity update,
    in Bee World 70(1),  12-18;
    IBRA’s reprint. ISBN 0 86098 195 9. 7 pp. (***).



  • Roy, Leo (1978) (Canada) –  Sclerolysis,
    in the Second Symposium (January 16, 1978) of the North American Apiotherapy Society. University of Maryland, College Park, Maryland, USA (***).



  • Sabbah, A.; Plassais, R.;  Grenapin, S.;  Drouet, M.;  Lauret, M. G.;  Loiry, M.;   Sainte-Laudy, J.[xiii] (1998) (France)  –  Testing basophil activation by flow cytometry in the diagnosis of allergy to hymenopteran venom,
    in Allerg Immunol (Paris), Feb;30(2),  44-48. [xiv]



  • Schmidt, J. (1992 ) (USA) –  Allergy to venemous insects,
    in The Hive and the Honey Bee, Ch 27. Published by Dadant and Sons, Hamilton, Illinois (***).



  • Simics, Mihály (1994) (Canada) –  Bee Venom: Exploring the Healing Power. Age-Old Remedies for Arthritis, Rheumatism and other Ailments. Plus: First Aid for Accidental Bee Stings. (Allergy related pages: 59-65.
    Apitronic Publishing. 77 pp. ISBN 0-9697654-0-1. (***).



  • Simics, Mihály (1995) (Canada) –  First Aid for Bee and Wasp Stings.
    Apitronic Publishing. Alberta, Canada. 31 pp. (***).



  • Urbanek,R., Karitzky,D.,  Forster,J. (1978)  –  Hyposensitization therapy with pure bee venom,
    in Deutsche Medizinische Wochenschrift 103,  1656-1660.



  • Thurnheer, U.; Muller, U.;  Stoller, R.;  Lanner, A.;  Hoigne, R. (1983)  – Venom immunotherapy in hymenoptera sting allergy. Comparison of rush and conventional hyposensitization and observations during long-term treatment,
    in Allergy, Oct;38(7),  465-75 (***-abstract). [xv]



  • van der Brempt, X.; Ledent, C.;  Mairesse, M.[xvi] (1997) (Belgium)  –   Accelerated desensitization for hymenoptera venom allergy in 30 hours: efficacy and safety in 150 cases (original article in French),
    in Rev Med Brux Jun;18(3),  120-124. [xvii]



  • Warren,D., Harman,A.,  Garber,T. (1981) (USA)  –  Le venin d’abeille dans la recherche medicale,
    in the XXVIII-Th. Apimondia Congress, Acapulco, Mexico,  504 (***-abstract).




  • Yee, C. J.; Morato-Castro, F. F.;  Palma, M. S.;  Malaspina, O.;   Azevedo Neto, R. S.;  Costa-Manso, E.;  Croce, J. [xviii](1997) (Brazil)  –  Acquired immunity to Africanized honeybee (Apis mellifera) venom in Brazilian beekeepers,
    in J Investig Allergol Clin Immunol., Nov;7(6),  583-587 (***-abstract). [xix]



  • Youlten, L. J.; Atkinson, B. A.; Lee, T. H. (1995) (UK) – The incidence and nature of adverse reactions to injection immunotherapy in bee and wasp venom allergy,
    in Clin Exp Allergy, Feb;25(2),  159-65 (***-abstract). [xx]



  • Zhang Shifen; Yang Xiao;  Yan Hong (1997) (China)    Bee sting acupuncture used to prevent and cure the hypersensitivity reaction caused by mellisotherapy,
    in the XXXV-Th. Apimondia Congress, Antwerp, Belgium (***). [2]



[1] Dr. Mueller is a professor in Bern, Switzerland.




413                                                                         ZHANG Shi-fen, YANG Xiao, YAN Hong



Hypersensitivity reactions are very popular in clinic treatment in China, being a result of mellissotherapy.  After the first 2-3 weeks of treatment, when the patients are administered mellissotherapy again, some of them develop a hypersensitivity reaction.  To be able to successfully continue the application of mellissotherapy and to prevent hypersensitivity reactions, in the third week of treatment, we used bee sting to perform acupuncture in the “Chihshin” point (Urinary Bladder 52 = ZHISHI point), which is the projection of the adrenal gland on the skin. 264 patients were observed and we noticed that none of them developed any hypersensitivity reaction to mellissotherapy any more.  By this method, we cured many kinds of hypersensitivity reactions, thus contributing to the development of apitherapy.


[i] Boutin, Y.;  Jobin, M.; Bedard, P. M.;  Hebert, M.;  Hebert, J. (1994) (Canada)  –  Possible dual role of anti-idiotypic antibodies in combined passive and active immunotherapy in honeybee sting allergy,
in J Allergy Clin Immunol, Jun;93(6),  pp.1039-46 (abstract).

Address: Centre de Recherche en Inflammation et Rhumatologie-Immunologie, Centre de Recherche du Centre Hospitalier de l’Universite Laval, Laurier, Ste-Foy, Canada.

BACKGROUND: Passive infusion of beekeepers’ plasma was shown to protect patients against systemic reactions occurring during active immunotherapy by mechanisms still to be clarified. It is tempting to speculate that anti-idiotypic antibodies could play a role because they are found in beekeepers’ plasma and are involved in the regulation of IgE synthesis. METHODS: In this report we studied the effects of passive infusion of a beekeeper’s plasma rich in anti-idiotypic antibodies to a patient who experienced systemic reactions to honeybee venom. RESULTS: We reported, during the days after the infusion, a decrease of clinical sensitivity to the honeybee venom. Indeed, the patient tolerated a cumulative dose of 280 micrograms of venom without adverse reactions. We also observed decreases in skin mast cell and in basophil sensitivity. After the plasma infusion, a modified rush immunotherapy with honeybee venom was initiated in our patient. In the following 76 weeks, increased levels of anti-idiotypic antibodies in the serum of the patient were associated with a diminution of specific antibodies (IgG and IgE) to honeybee venom. CONCLUSION: These results suggest a dual role of anti-id in our combined protocol of passive and active immunotherapy: an immediate action on clinical sensitivity along with a decrease of skin mast cell and basophil sensitivity and an immunoregulatory role on specific antibody production.
PMID: 7516355, UI: 94275034.


[ii] Address:  Department of Clinical Immunology, Addenbrooke’s NHS Trust, Cambridge, UK.

[iii] BACKGROUND: Changeover from Phadebas RAST to Pharmacia AutoCAP increased double-positivity to both honey-bee and common wasp (vespula) venom in our patients. OBJECTIVE: We examined the frequency of IgE double-positivity, its clinical relevance and utility in investigating potentially allergic patients.
METHODS: One hundred and eighty-two patients with hymenoptera allergy were tested using RAST (n = 51) and AutoCAP (n = 131) assays over 4 years. Patients had a history of reactions to vespulae (22), honey-bee (10) and unidentified hymenoptera (vespinae) (7). RESULTS: After changing from RAST to AutoCAP double-positivity increased from 10 (5/ 51) to 30% (39/131) (P < 0.01). RAST and CAP assays gave similar median class results (vespula = 3, honey-bee = 2). Thirty-six CAP patients had systemic reactions of Mueller grade II and above.
In vespula-allergic double-positive subjects, high CAP classes (> or = class 3) to honey-bee were common (30%). In 25% the CAP classes were equal. In honey-bee-allergic subjects, all vespula venom CAP IgE was low titre (class 1 or 2) and 20% were equal for both venoms. In 43% of vespinae-allergic patients the CAP class was equal to both (class 2 and 3). In contrast, intradermal skin test double-positivity was uncommon. Double-negative skin test results were common in the CAP double-positive population (22% of honey-bee-allergic, 13% of vespula-allergic and 43% of vespinae-allergic patients). Vespula allergic patients have higher bee-venom IgE than vice versa. Twenty-seven per cent of CAP double-positive patients (representing 8% of all venom allergic patients tested over this period) had equal class IgE to both venoms which was not helpful in diagnosis. Combination of skin testing and CAP is unhelpful in only 5/37 (14%) of patients with double-positive serology. CONCLUSION: If used in isolation CAP may be misleading, especially if only one venom is tested. Identification of the causative venom must utilize both clinical history and skin testing in these double-positive patients, and challenge testing if indicated.
Comments:  Comment in: Clin Exp Allergy 1998 Jan;28(1):4-6.


[iv] Faux JA, Moffatt MF, Lalvani A, Dekker J, Warrell DA, Cookson WO (1997) (U.K.)  – Sensitivity to bee and wasp venoms: association with specific IgE responses to the bee and wasp venom and HLA DRB1 and DPB1,
in Clin Exp Allergy, May;27(5),  pp.578-83 (abstract).

Faux et al. address: Nuffield Department of Clinical Medicine, University of Oxford, John Radcliffe Hospital, UK.

BACKGROUND: Stings from bees and wasps can cause systemic reactions which can be fatal in some individuals. In these venom-sensitive patients, specific IgE to the venom is produced and is considered to participate in the adverse reactions. This immune response requires antigen presentation by human leucocyte antigens (HLA) class II molecules, which includes DR and DP, which are present on antigen presenting cells. OBJECTIVE: To test for associations between HLA class II DRB1 and DPB1 alleles and life-threatening sensitivity to both bee and wasp venoms. To establish further whether any associations are independent of the atopy phenotype. METHODS: A total of 33 bee- and 44 wasp-venom-sensitive patients was studied. DRB1 genotypes were determined by single stranded oligonucleotide (SSO) probing of PCR products, and DPB1 genotypes by amplified fragment length polymorphism (AFLP) analysis. Total and specific IgE were measured using the Pharmacia Immunocap, FEIA. Patients with specific IgE to the venom antigens only were termed monosensitive and those with additional specific IgE to HDM and/or GP were termed polysensitive. RESULTS: Allele frequencies were compared to an unrelated control population. The 33 bee-sensitive patients had a greater prevalence of DRB1*07 alleles than the control subjects, 26% vs 14%, with an odds ratio (OR) of 2.1 (95% CI, 1.2-3.7, P = 0.015, corrected for multiple comparisons, Pc = ns). This association was confined to the 15 monosensitive bee patients, who had a 43% DRB1*07 allele frequency when compared with 11% in the 18 polysensitive bee patients, OR 6.1 (95% CI, 1.73-22, P = 0.004, Pc = 0.05), and when compared with a control group of non-venom subjects, 43% vs 16%, OR 3.9 (95% CI, 1.72-9.0, P = 0.002, Pc = 0.02). The 44 wasp-sensitive patients had an increase in the DRB1*11 allele when compared with the control subjects, 13% vs 6%, with an OR 2.2 (95% CI, 1.0-4.6, P = 0.04, Pc = NS), and a decreased prevalence of DRB1*04 alleles, 10% vs 19%, with an OR 0.33 (95% CI, 0.24-0.99, P = 0.04, Pc = NS), but these were not significant when multiple comparisons were taken into account. The DPB1 alleles were not significantly different between the venom sensitive patients and the controls. CONCLUSION: Patients monosensitive to bee venom had a significantly greater prevalence of DRB1*07 alleles than the non-venom, control population suggesting that IgE responses in these patients may, in part be controlled by immune response HLA class II genes. These results are also suggestive of wasp-sensitive patients having a higher prevalence of DRB1*11 and a lower prevalence of DRB1*04 than the control population.
PMID: 9179434, UI: 97322944.


[v] Knulst’s et al. address:  Academisch Ziekenhuis, afd. Dermatologie-Allergologie, Utrecht.

[vi] Knulst, A.C.;  de Maat-Bleeker, F.;  Bruijnzeel-Koomen, C. A. (1998) (Netherlands)  – Wasp and bee venom allergy (original article in Dutch),
in Ned Tijdschr Geneeskd, Apr 18;142(16),  pp.889-92 (***-abstract).

To diagnose insect venom allergy a good patient history is important. Allergological tests (skin test, specific IgE titre) confirm the diagnosis. Patients are advised on preventive measures (e.g. with respect to clothing and use of perfume). They are also instructed on medical treatment (antihistaminics, epinephrine) in case they are stung again. In patients having had a serious systemic reaction immunotherapy should be considered. Immunotherapy leads to complete protection in more than 98% of patients with wasp (yellow jacket) venom allergy and in 75-80% of patients with bee venom allergy. Serious adverse reactions to immunotherapy are rare. Immunotherapy lasts at least 3 to 5 years. After cessation of immunotherapy the frequency of systemic reactions to the sting of a wasp or bee is in the range of 5-15%. There are insufficient data on the long-term effect of immunotherapy.
PMID: 9623183, UI: 98286386.


[vii] Lessof, M. H.;  Sobotka, A. K.;  Lichtenstein, L. M. (1978)  –  Effects of passive antibody in bee venom anaphylaxis,
in Johns Hopkins Med J, Jan;142(1),  pp.1-7 (abstract).

Twelve patients allergic to honeybees were challenged by injections of bee venom; five responded systemically to the venom, with symptoms ranging from angioedema to respiratory distress. These patients were given intramuscular or intravenous infusions of gamma-globulin obtained from the plasma of hyperimmune beekeepers who had high levels of antibody to an allergen (phospholipase A) in the venom. Post-infusion, all five patients tolerated 1.5 to 5 times the venom dose that previously elicited adverse reactions. The quantity of passive IgG antibody infused did not impair the patient’s own immune response to venom. These results represent the best available evidence for a direct role for IgG blocking antibodies in clinical protection against anaphylaxis occurring as a result of parenteral antigenic challenge as may be observed in penicillin and insect hypersensitivity.
PMID: 75280, UI: 78112042


[viii] Address: Institute of Clinical Chemistry, University Hospital Zurich, Switzerland.

[ix] Cross-linking IgE on basophils is known to cause both sulfidoleukotriene (sLT) generation and histamine release. We recently developed an ELISA to determine sulfidoleukotriene generation by blood mononuclear cells which employs pretreatment with IL-3 to enhance leukotriene generation (cellular antigen stimulation test, CAST). Here, we compared the CAST and whole blood histamine release in response to honey bee/yellow jacket venom (BV/YJV) in 23 patients clinically suspected of type-I allergy to these venoms. Of these, 17 were diagnosed as “definitive venom allergics,” defined by a positive skin test at 100 ng/ml of venom or less. The six in whom such skin reactivity was absent were labelled “suspected venom allergics.” Both venoms stimulated sulfidoleukotriene generation and histamine release also from control individuals (n = 10). In patients, insect venoms generally stimulated histamine release and sulfidoleukotriene generation in excess of the mean + 3 SD of values obtained with control individuals. However, about half of the patients reacted predominantly with either histamine release or sulfidoleukotriene generation. No overall correlation was found between threshold doses necessary to stimulate sulfidoleukotriene generation (ThsLT) and histamine release (ThHist). (Linear correlation coefficients between ThsLT and ThHist were -0.02 for honey bee venom and 0.13 for yellow jacket, n = 23). Both findings are in contrast to the concept that these responses occur in parallel. From results with “definitive venom allergics,” CAST sensitivity was calculated as 100% for honey bee venom and 83% for yellow jacket, and that of the histamine release assay as 62.5% for honey bee venom and 50% for yellow jacket. Specificity of the CAST was calculated as 77% for honey bee venom and 100% for yellow jacket, and that of the histamine release assay as 44% for honey bee venom and 60% for yellow jacket. Thus, CAST results are closer to skin test results than to those of the whole blood histamine release assay.
PMID: 9330184, UI: 97471243.


[x] Address: Medical Division, Zieglerspital Bern, Switzerland.

[xi] BACKGROUND: In diagnosis of type I allergy recombinant allergens have potential advantages over conventional allergenic extracts, both regarding specificity and reproducibility. OBJECTIVES: We therefore decided to study honey bee venom (BV) and its major allergen phospholipase A2 (PLA) in native and recombinant form for diagnosis of bee sting allergy. METHOD: We investigated 85 patients with a history of a recent systemic allergic bee sting reaction and positive intracutaneous skin test to BV, and 21 controls with no history of allergic bee sting reaction and negative skin test to BV. Intracutaneous skin tests and determination of specific IgE by ImmunoCAP(R) to BV, native PLA (nPLA) and recombinant PLA (rPLA) were done in all patients and controls. RESULTS: In skin testing 84 (99%) of the 85 patients reacted to nPLA and 81 (95%) to rPLA, while none of the 21 controls was positive with nPLA or rPLA. Specific serum IgE to BV could be detected in 82 of the patients (96%), to nPLA in 73 (86%) and to rPLA in 66 (78%). Four (19%) of the controls had a positive CAP to BV, one (4.8%) to nPLA and none to rPLA. Analysis of discordant results in CAP showed, that most patients with specific IgE to BV, but not to nPLA and rPLA, had positive skin tests to both PLA preparations and low levels of BV specific IgE. Patients with specific IgE to nPLA but not to rPLA were usually sensitized to minor allergens of BV which contaminated the commercial nPLA. CONCLUSIONS: PLA is the major allergen in BV. While diagnostic tests with BV are more sensitive, the specificity of tests with PLA, especially rPLA is clearly increased as compared with BV.
Publication Types:
Clinical trial
Controlled clinical trial
PMID: 9291289, UI: 97435066


[xii] Patrizzi, R.;  Muller, U.;  Yman, L.;  Hoigne, R. (1979)  – Comparison of skin tests and RAST for the diagnosis of bee sting allergy,
in Allergy, Aug;34(4),  pp.249-56.

Skin tests and estimation of specific IgE-antibodies by the RAST are evaluated as diagnostic procedures in bee sting hypersensitivity with the following extracts. (2) With bee venom results of skin tests and RAST correspond in 82%, with bee wholebody extracts in 68%. (3) Both with skin tests and the RAST with bee venom a good discrimination between patients with bee sting hypersensitivity and non-allergic controls is observed. Skin tests with bee venom are somewhat more sensitive than bee venom-RAST. (4) With the careful skin test procedure chosen, no adverse reactions were observed.
PMID: 517710, UI: 80085818


[xiii] Laboratoire d’Immuno-Allergologie-CHU, Angers France.

[xiv] Diagnosis of allergy to hymenoptera venom must be precise and depends onindisputable bio-clinical criteria, because of specific immunotherapy for indications such as systemic and/or anaphylactic reactions. Until nowadays, diagnosis was by specific IgE, histamine release and skin tests, most often done for the venoms of wasp, honey bee and hornet at the same time since, in 7-8 cases in 10 the patients had not identified the responsible insect. Basophil activation test (TAB) by Flux cytometry and measurement of leukotriene C4 (LTC4) are new techniques of great reliability. The work shows the correlations between the different immunobiological parameters by reference to TAB by CAF and measurement of LTC4. When the overall results for mixed venoms or those for single venoms are considered, the correlation between TAB, LTC4 and the other parameters are highly significant. It can now be considered objectively that TAB by CTF and measurement of LCT4 are the two highest-performing techniques for diagnosis of hymenoptera venom allergy and so validates them.


[xv] 42 patients with confirmed hypersensitivity to honey bee (HBV) and/or yellow jacket (YJV) were treated with the respective venoms (7 with HBV, 5 with YJV and 30 with both venoms). Treatment tolerance, skin tests (ST), specific IgE- and specific IgG-antibodies were monitored before, after 3, 6, 12, 24 and 36 months. 21 patients had a rush and 21 a conventional treatment schedule. Maintenance dose was 100 micrograms. Adverse effects occurred as large local (8 patients), slight systemic (12 patients) and moderate to severe systemic reactions (4 patients). Of 24 re-exposed patients 17 had no reaction at all, six a markedly decreased and one an unchanged reaction. After 3 years of treatment ST became negative in nine of 31 patients on HBV and in seven of 26 patients on YJV. RAST became negative in three of 30 patients on HBV and 17 of 29 patients on YJV treatment. Both ST and RAST became negative in five HBV- and 10 YJV-treated patients. Loss of venom hypersensitivity according to diagnostic tests may correspond to actual desensitization and enable discontinuation of immunotherapy.
PMID: 6638413, UI: 84050107


[xvi] Departement de Pneumo-allergologie, Clinique Saint-Luc, Bouge, Belgium.

[xvii] In this study, we performed 150 desensitizations in 139 Hymenoptera venom allergic patients (109 Yellow jacket allergic patients, 19 Honey bee allergic patients and 11 patients sensitized to both insects, who received a dual desensitization). We used a rush protocol, allowing injection of a total cumulated dose of 125,1 (Honey bee) to 175,1 (Yellow jacket) microgram of venom in 30 hours. Patients were hospitalized, with all emergency precautions for treating systemic reactions. The protocol was well tolerated in 147/150 cases; 3 patients had a benign systemic reaction. Patients received monthly maintenance doses of 100 micrograms venom. 39 patients experienced a field sting during immunotherapy; 2 of them (5%) had a benign systemic reaction.
Thus, our rush desensitization protocol seems to be safe and effective.
PMID: 9273600, UI: 97391533.

[xviii] Allergy Department, School of Medicine, Sao Paulo University, Brazil.

[xix] Seventy-eight Brazilian beekeepers who had been stung on average six times per month were studied. Sixty-eight beekeepers (87.1%) showed restricted local clinical reactions; nine individuals (11.5%) had extensive local reactions, and only one (1.2%) suffered anaphylactic shock. The humoral immunologic pattern of these individuals were studied by using immunoenzymatic methods to determine the serum titres of specific IgE and specific IgG4. Three groups of beekeepers presenting different humoral immunologic patterns were identified, in which the predominant pattern was the absence of specific IgE and high levels of specific IgG4 (38.4%). There was a positive correlation between the high levels of specific IgG4 and the number of bee stings. This correlation was not found in either specific or total IgE. The results of the present study suggest: i) the immunologic response to the number of exposures to Africanized honey-bee venom is not related to the number of exposures; and, ii) other nonhumoral and/or nonimmunologic factors may be involved in the reaction to the insect sting, which are responsible for both the clinical symptoms and protection.


[xx] Youlten, L. J.; Atkinson, B. A.; Lee, T. H. (1995) (UK)  – The incidence and nature of adverse reactions to injection immunotherapy in bee and wasp venom allergy,
in Clin Exp Allergy, Feb;25(2),  pp.159-65 (abstract).

Department of Allergy & Respiratory Medicine, UMDS, Guy’s Hospital, London, U. K.

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.
PMID: 7750008, UI: 95269160.