Physiologic manifestations of human anaphylaxis.

Abstract

A B S T R A C T In the course of a controlled study to evaluate different forms of immunotherapy for subjects with insect-sting hypersensitivity, we observed 11 subjects who had systemic cutaneous urticarial reactions and 3 subjects who experienced systemic anaphylaxis. With the exception of tachyeardia, there were no cardiopulmonary changes in the subjects with urticaria, whereas the major manifestation of anaphylactic shock in the other three subjects was severe hypotension that was probably secondary to peripheral vasodilation. Significant abnormalities in gas exchange developed in two subjects. In one, bronchospasm precipitated a respiratory arrest followed by endotracheal intubation with mechanical ventilation. Although plasma histamine levels were not related to the development of cutaneous reactions, the plasma histamine levels correlated with the severity and duration of the cardiopulmonary changes observed during anaphylactic shock. The two subjects with the most severe shock showed evidence of intravascular coagulation characterized by a diminution of Factor V, Factor VIII, fibrinogen, and high molecular weight kininogen, as well as changes in components of the complement system. Standard therapy with epinephrine and fluids, usually recommended for the treatment of systemic anaphylaxis, did not immediately reverse either the hemodynamic or the respiratory abnormalities in the two subjects with the most severe

Clinical Profile of Patients With Severe Anaphylaxis Hospitalized in the Spanish Hospital System: 1997-2011

“…In their study based on 2 databases covering a population with employer-sponsored health insurance and individuals aged ≥65 years, Clark et al [6] found that patients with more severe anaphylaxis (leading to admission) had a higher Charlson-Deyo score (modified Charlson comorbidity index) [30,31], a higher number of laboratory/radiology tests performed during the year before admission, or a visit to the emergency department or admission (any cause) during the previous year. Both these findings and ours suggest that more severe anaphylaxis episodes were associated with more severe previous comorbidity.…”

The Human Heart As a Shock Organ in Anaphylaxis

“…ere is increasing evidence of cardiac involvement in human anaphylaxis too [8,9,12,13]. Initially this has been attributed to mediators originating from the lung and reaching the heart.…”

“…HHMC possess FcεRI, C3a receptor (C3aR), and C5a receptor (C5aR) bound to their membrane surface. erefore, it is likely that IgE-, C5a-, and C3a-mediated activation of these cells could play a role in systemic and cardiac anaphylaxis in humans [9,12,13].…”

“…Anaphylaxis is characterized by laryngeal edema, bronchoconstriction, hypotension, and vascular leakage. It is well known that the heart is directly and/or indirectly involved in severe human anaphylaxis [3,4,5,6,7,8,9]. Cardiac anaphylaxis in humans is characterized by coronary spasm, decreased le ventricular contractility, and/or arrhythmias [10,11,12,13].…”

High Molecular Weight Kininogen Activates B2 Receptor Signaling Pathway in Human Vascular Endothelial Cells

“…Therefore, the plasma KKS can be considered to have a spectrum of physiological effects, ranging at one extreme from a hemostatic state of vasodilation and promotion of smooth blood flow, all the way to a prothrombotic state. It is conceivable to suggest that other mechanisms proposed about respiratory, retinal, and renal systems can fit into this spectrum of physiological effects (1)(2)(3). There is accumulating evidence suggesting that when the plasma KKS is activated, the results are a sequential release of proteolytic enzymes and vasoactive peptides, generation of both angiogenic and anti-angiogenic molecules, stabilization of thrombus, and an increase in protease inhibitor activity in blood (4 -7).…”