Occurrence of disseminated Intravascular coagulation (DIC) in active systemic anaphylaxis: role of platelet-activating factor

Choi, Inhak; Ha, Tai-You; Lee, D. G.; Park, J. S.; Lee, J. H.; Park, Y. M.; Lee, H. K.

doi:10.1111/j.1365-2249.1995.tb03711.x

Cited by 35 publications

(24 citation statements)

References 25 publications

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“…Interestingly, platelet degranulation was reported to occur even before that of mast cells or basophils and might therefore contribute to the very early-phase of anaphylaxis [33]. It is known that fibrinogen levels are significantly reduced during DIC in an active systemic anaphylaxis mouse model [12]. Taking this parameter into consideration, we observed reduction of serum fibrinogen levels at time point 60 min in an independent, but similar mouse model of anaphylaxis using peanut allergen Ara h 2 [data not shown], pointing indeed towards DIC occurrence.…”

Section: Discussionmentioning

confidence: 99%

Monitoring neutrophils and platelets during casein‐induced anaphylaxis in an experimental BALB/c mouse model

Krishnamurthy¹,

Starkl²,

Szalai

et al. 2012

Clin Experimental Allergy

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On the basis of our data we suggest that in addition to mast cells and basophils, neutrophils and platelets participate in the anaphylactic response in this BALB/c mouse model. Platelet and neutrophils expressing relevant immunoglobulin receptors may therefore have a synergistic effect with allergen specific IgE as well as IgG antibodies in food-induced anaphylaxis. We suggest that management of these cells could be of clinical importance to handle anaphylaxis.

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Section: Discussionmentioning

confidence: 99%

Monitoring neutrophils and platelets during casein‐induced anaphylaxis in an experimental BALB/c mouse model

Krishnamurthy¹,

Starkl²,

Szalai

et al. 2012

Clin Experimental Allergy

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“…Prolonged episodes with hypotension can trigger disseminated intravascular coagulation characterized by massive activation of coagulation and fibrinolytic enzymes that may result in depletion of platelets and coagulation factors (consumption coagulopathy). Platelet‐activating factor (PAF) released from mast cells may play an important role in this process (34).…”

Section: Clinical Presentationmentioning

confidence: 99%

Anaphylaxis: past, present and future

Ben‐Shoshan

Clarke

2010

Allergy

157

143

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To cite this article: Ben‐Shoshan M, Clarke AE. Anaphylaxis: past, present and future. Allergy 2011; 66: 1–14. Abstract Anaphylaxis is a clinical emergency, and recent reports suggest increased prevalence. A diverse set of primary genetic and environmental influences may confer susceptibility to anaphylactic reactions. Anaphylaxis presents diagnostic and therapeutic challenges. It often manifests with a broad array of symptoms and signs that might be similar to other diseases. The management of anaphylaxis consists of emergency treatment of acute episodes as well as preventive strategies to avoid recurrences. Treatment is complicated by its rapid onset and progression, presence of concurrent diseases or medications, and need for long‐term allergen avoidance. Health care professionals must be able to recognize the signs of anaphylaxis, treat an episode promptly and appropriately, and provide preventive recommendations. Recognizing the gaps in our understanding and management of anaphylaxis may help identify promising targets for future treatment and prevention and areas that require further study.

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“…PAF released within systemic circulation induces peripheral vasodilation with relative hypovolaemia and severe hypotension [36]. In addition, PAF-induced platelet activation is a major cause of disseminated intravascular coagulation (DIC), associated frequently with fatal anaphylaxis [38]. Taken together, these observations suggest that PAF is a mediator capable of reproducing most, if not all, haemodynamic dysfunctions of severe anaphylaxis.…”

Section: Cardiovascular Effects Of Pafmentioning

confidence: 99%

Allergy and the cardiovascular system

Triggiani

Patella²,

Staiano

et al. 2008

Clinical and Experimental Immunology

154

147

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SummaryThe most dangerous and life-threatening manifestation of allergic diseases is anaphylaxis, a condition in which the cardiovascular system is responsible for the majority of clinical symptoms and for potentially fatal outcome. The heart is both a source and a target of chemical mediators released during allergic reactions. Mast cells are abundant in the human heart, where they are located predominantly around the adventitia of large coronary arteries and in close contact with the small intramural vessels. Cardiac mast cells can be activated by a variety of stimuli including allergens, complement factors, general anesthetics and muscle relaxants. Mediators released from immunologically activated human heart mast cells strongly influence ventricular function, cardiac rhythm and coronary artery tone. Histamine, cysteinyl leukotrienes and platelet-activating factor (PAF) exert negative inotropic effects and induce myocardial depression that contribute significantly to the pathogenesis of anaphylactic shock. Moreover, cardiac mast cells release chymase and renin that activates the angiotensin system locally, which further induces arteriolar vasoconstriction. The number and density of cardiac mast cells is increased in patients with ischaemic heart disease and dilated cardiomyopathies. This observation may help explain why these conditions are major risk factors for fatal anaphylaxis. A better understanding of the mechanisms involved in cardiac mast cell activation may lead to an improvement in prevention and treatment of systemic anaphylaxis.

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Occurrence of disseminated Intravascular coagulation (DIC) in active systemic anaphylaxis: role of platelet-activating factor

Cited by 35 publications

References 25 publications

Monitoring neutrophils and platelets during casein‐induced anaphylaxis in an experimental BALB/c mouse model

Monitoring neutrophils and platelets during casein‐induced anaphylaxis in an experimental BALB/c mouse model

Anaphylaxis: past, present and future

Allergy and the cardiovascular system

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