1102 Sting challenge (SC) trial III. Variable affecting the outcome of insect sting

2000 ◽  
Vol 105 (1) ◽  
pp. S377
Author(s):  
A KAGEYSOBOTKA
Keyword(s):  
Insect Sting ◽  
Sting Challenge

scholarly journals Activation of the contact system in insect-sting anaphylaxis: association with the development of angioedema and shock

Blood ◽  
1993 ◽  
Vol 82 (6) ◽  
pp. 1732-1739 ◽  
Author(s):  
PW van der Linden ◽  
CE Hack ◽  
AJ Eerenberg ◽  
A Struyvenberg ◽  
JK van der Zwan
Keyword(s):  
Contact System ◽  
Factor Xii ◽  
C1 Inhibitor ◽  
System Parameters ◽  
Insect Sting ◽  
Activation Products ◽  
History Of ◽  
Sting Challenge ◽  
Insect Stings

Abstract A postulated role of the contact system in anaphylactic reactions to insect stings was investigated. During prospective, in-hospital sting challenge, we collected serial blood samples from five normal volunteers and 16 patients with a history of insect-sting anaphylaxis. Activation of the contact system was assessed by measuring plasma levels of factor XIIa-C1-inhibitor and kallikrein-C1-inhibitor complexes as well as those of cleaved high molecular weight kininogen (HK). In addition, antigenic levels of (pre)kallikrein, factor XII, and HK were measured. No significant changes in contact system parameters were observed in any of the five volunteers or the four patients who did not develop an anaphylactic reaction after sting challenge. In contrast, significant changes in contact system parameters occurred in 7 of the 12 patients with anaphylactic symptoms after challenge. Peak levels of either C1-inhibitor complex were found 5 minutes after the onset of anaphylactic symptoms. The increase in C1-inhibitor was most pronounced in the 4 patients with angioedema, 2 of which also developed shock. However, activation of HK was observed in all four patients with angioedema, the two patients with shock but no angioedema, as well as in 1 of the remaining 6 patients with anaphylactic symptoms other than angioedema or shock. Thus, activation products of the contact system may be involved in the pathogenesis of angioedema and shock in insect- sting anaphylaxis.

ANAPHYLACTIC SHOCK AFFER INSECT-STING CHALLENGE IN 138 PERSONS WITH A PREVIOUS INSECT-STING REACTION

PEDIATRICS ◽  
1994 ◽  
Vol 94 (2) ◽  
pp. 249-250
Author(s):  
Peter Cvietusa ◽  
Joseph Spahn ◽  
Allen ADinoff
Keyword(s):  
Blood Pressure ◽  
Anaphylactic Reaction ◽  
Anaphylactic Shock ◽  
Severe Reaction ◽  
Angiotensin I ◽  
Significant Information ◽  
Arterial Blood ◽  
Insect Sting ◽  
History Of ◽  
Sting Challenge

Purpose of the Study. The goal of the study was to establish the frequency with which anaphylactic reactions reoccur after sting challenge in persons with previous insect-sting anaphylactic reactions, as well as the relation between the severity of anaphylaxis and levels of catecholamines and angiotensins. Methods. One hundred thirty-eight patients with a history of an anaphylactic reaction and eight normals (including five patients who had been previously stung) were subjected to provocation test with the relevant insect. Blood samples were collected and assayed for epinephrine, norepinephrine, dopamine, and angiotensin I and II levels. Findings. "Only" 39 of 138 (28%) patients with a previous insect sting anaphylactic reaction developed anaphylactic symptoms after sting challenge. Only those with a history of a severe reaction developed anaphylactic shock. No change in cardiovascular mediators or blood pressure was seen in patients with no or mild reactions, while those patients with anaphylactic shock had a mean arterial blood pressure drop of 33%. Significant increases in epinephrine, norepinephrine, and angiotensin II were observed within 5 minutes after the onset of symptoms and were strongly correlated with a drop in blood pressure. Dopamine and angiotensin I levels did not change significantly in any participants. Reviewers' Comments. The repeat rate of systemic reactions of 28% is substantially lower than the previously reported rate of 60% (Hung KJ, et al. NEJM. 1978;299:157). Unfortunately, the present study does not provide significant information regarding the study population, particularly the time lapsed between the original and rechallenge stings. We are all aware of the associated problems of beta-blockers and anaphylaxis.

Insect-sting challenge in 138 patients: Relation between clinical severity of anaphylaxis and mast cell activation†

1992 ◽  
Vol 90 (1) ◽  
pp. 110-118 ◽  
Author(s):  
P VANDERLINDEN ◽  
C HACK ◽  
J POORTMAN ◽  
Y VIVIEKIPP ◽  
A STRUYVENBERG ◽  
...  
Keyword(s):  
Mast Cell ◽  
Cell Activation ◽  
Clinical Severity ◽  
Mast Cell Activation ◽  
Insect Sting ◽  
Sting Challenge

scholarly journals Controlled insect-sting challenge in 55 patients: correlation between activation of plasminogen and the development of anaphylactic shock

Blood ◽  
1993 ◽  
Vol 82 (6) ◽  
pp. 1740-1748
Author(s):  
PW van der Linden ◽  
CE Hack ◽  
A Struyvenberg ◽  
D Roem ◽  
MC Brouwer ◽  
...  
Keyword(s):  
Mast Cell ◽  
Anaphylactic Shock ◽  
Clinical Symptoms ◽  
Mast Cell Degranulation ◽  
Tissue Type ◽  
Insect Sting ◽  
Type Plasminogen Activator ◽  
Fibrinolytic Parameters ◽  
Sting Challenge ◽  
Von Willebrand

The pathogenesis of anaphylactic shock is not completely understood. Mast cell degranulation products may stimulate endothelial cells, leading to activation of fibrinolytic and coagulation systems. We investigated the activation of these systems in insect-sting anaphylaxis. Fifty-five patients with a previous insect-sting anaphylactic reaction and 8 volunteers were challenged with an in- hospital sting. Plasma levels of von Willebrand factor (vWF), coagulation, and fibrinolytic parameters were assessed. After the sting challenge, 20 patients developed anaphylactic symptoms, 7 of whom developed hypotension. In only these 7 patients, but not in the volunteers or in the other patients with no or mild anaphylactic symptoms, vWF levels increased from 107% +/- 33% (mean +/- SD) before, to 235% +/- 134% 60 minutes after the onset of clinical symptoms. This increase of vWF was accompanied by an increase of circulating tissue- type plasminogen-activator (tPA) levels from 5 +/- 3 micrograms/L to 50 +/- 59 micrograms/L and of plasminogen-alpha 2-antiplasmin complex (PAP- c) levels from 6 +/- 3 nmol/L to 297 +/- 225 nmol/L. Both tPA and PAP-c levels peaked 5 minutes after the onset of clinical symptoms. Such increases of tPA and PAP-c were not observed in the volunteers or in the patients who did not develop shock. The increase of tPA and PAP-c levels in the hypotensive patients correlated positively with the degree of mast cell degranulation and inversely with the mean arterial pressure. We conclude that activation of plasminogen may be involved in the pathogenesis of anaphylactic shock induced by insect venom.

scholarly journals Controlled insect-sting challenge in 55 patients: correlation between activation of plasminogen and the development of anaphylactic shock

Blood ◽  
1993 ◽  
Vol 82 (6) ◽  
pp. 1740-1748 ◽  
Author(s):  
PW van der Linden ◽  
CE Hack ◽  
A Struyvenberg ◽  
D Roem ◽  
MC Brouwer ◽  
...  
Keyword(s):  
Mast Cell ◽  
Anaphylactic Shock ◽  
Clinical Symptoms ◽  
Mast Cell Degranulation ◽  
Tissue Type ◽  
Insect Sting ◽  
Type Plasminogen Activator ◽  
Fibrinolytic Parameters ◽  
Sting Challenge ◽  
Von Willebrand

Abstract The pathogenesis of anaphylactic shock is not completely understood. Mast cell degranulation products may stimulate endothelial cells, leading to activation of fibrinolytic and coagulation systems. We investigated the activation of these systems in insect-sting anaphylaxis. Fifty-five patients with a previous insect-sting anaphylactic reaction and 8 volunteers were challenged with an in- hospital sting. Plasma levels of von Willebrand factor (vWF), coagulation, and fibrinolytic parameters were assessed. After the sting challenge, 20 patients developed anaphylactic symptoms, 7 of whom developed hypotension. In only these 7 patients, but not in the volunteers or in the other patients with no or mild anaphylactic symptoms, vWF levels increased from 107% +/- 33% (mean +/- SD) before, to 235% +/- 134% 60 minutes after the onset of clinical symptoms. This increase of vWF was accompanied by an increase of circulating tissue- type plasminogen-activator (tPA) levels from 5 +/- 3 micrograms/L to 50 +/- 59 micrograms/L and of plasminogen-alpha 2-antiplasmin complex (PAP- c) levels from 6 +/- 3 nmol/L to 297 +/- 225 nmol/L. Both tPA and PAP-c levels peaked 5 minutes after the onset of clinical symptoms. Such increases of tPA and PAP-c were not observed in the volunteers or in the patients who did not develop shock. The increase of tPA and PAP-c levels in the hypotensive patients correlated positively with the degree of mast cell degranulation and inversely with the mean arterial pressure. We conclude that activation of plasminogen may be involved in the pathogenesis of anaphylactic shock induced by insect venom.

scholarly journals Activation of the contact system in insect-sting anaphylaxis: association with the development of angioedema and shock

Blood ◽  
1993 ◽  
Vol 82 (6) ◽  
pp. 1732-1739 ◽  
Author(s):  
PW van der Linden ◽  
CE Hack ◽  
AJ Eerenberg ◽  
A Struyvenberg ◽  
JK van der Zwan
Keyword(s):  
Contact System ◽  
Factor Xii ◽  
C1 Inhibitor ◽  
System Parameters ◽  
Insect Sting ◽  
Activation Products ◽  
History Of ◽  
Sting Challenge ◽  
Insect Stings

A postulated role of the contact system in anaphylactic reactions to insect stings was investigated. During prospective, in-hospital sting challenge, we collected serial blood samples from five normal volunteers and 16 patients with a history of insect-sting anaphylaxis. Activation of the contact system was assessed by measuring plasma levels of factor XIIa-C1-inhibitor and kallikrein-C1-inhibitor complexes as well as those of cleaved high molecular weight kininogen (HK). In addition, antigenic levels of (pre)kallikrein, factor XII, and HK were measured. No significant changes in contact system parameters were observed in any of the five volunteers or the four patients who did not develop an anaphylactic reaction after sting challenge. In contrast, significant changes in contact system parameters occurred in 7 of the 12 patients with anaphylactic symptoms after challenge. Peak levels of either C1-inhibitor complex were found 5 minutes after the onset of anaphylactic symptoms. The increase in C1-inhibitor was most pronounced in the 4 patients with angioedema, 2 of which also developed shock. However, activation of HK was observed in all four patients with angioedema, the two patients with shock but no angioedema, as well as in 1 of the remaining 6 patients with anaphylactic symptoms other than angioedema or shock. Thus, activation products of the contact system may be involved in the pathogenesis of angioedema and shock in insect- sting anaphylaxis.

scholarly journals Hymenoptera Venom Immunotherapy: Immune Mechanisms of Induced Protection and Tolerance

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1575
Author(s):  
Ajda Demšar Luzar ◽  
Peter Korošec ◽  
Mitja Košnik ◽  
Mihaela Zidarn ◽  
Matija Rijavec
Keyword(s):  
Current Knowledge ◽  
Allergic Diseases ◽  
Hymenoptera Venom ◽  
Venom Immunotherapy ◽  
Effector Cells ◽  
Immune Mechanisms ◽  
Protection Mechanisms ◽  
Sting Challenge ◽  
Effectiveness Data

Hymenoptera venom allergy is one of the most severe allergic diseases, with a considerable prevalence of anaphylactic reaction, making it potentially lethal. In this review, we provide an overview of the current knowledge and recent findings in understanding induced immune mechanisms during different phases of venom immunotherapy. We focus on protection mechanisms that occur early, during the build-up phase, and on the immune tolerance, which occurs later, during and after Hymenoptera venom immunotherapy. The short-term protection seems to be established by the early desensitization of mast cells and basophils, which plays a crucial role in preventing anaphylaxis during the build-up phase of treatment. The early generation of blocking IgG antibodies seems to be one of the main reasons for the lower activation of effector cells. Long-term tolerance is reached after at least three years of venom immunotherapy. A decrease in basophil responsiveness correlates with tolerated sting challenge. Furthermore, the persistent decline in IgE levels and, by monitoring the cytokine profiles, a shift from a Th2 to Th1 immune response, can be observed. In addition, the generation of regulatory T and B cells has proven to be essential for inducing allergen tolerance. Most studies on the mechanisms and effectiveness data have been obtained during venom immunotherapy (VIT). Despite the high success rate of VIT, allergen tolerance may not persist for a prolonged time. There is not much known about immune mechanisms that assure long-term tolerance post-therapy.

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