Pathophysiology of anaphylaxis

Khan, Bilal; Kemp, Stephen F.

doi:10.1097/aci.0b013e3283481ab6

Cited by 83 publications

(104 citation statements)

References 63 publications

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“…Examples of sudden death syndrome from the medical literature support our hypothesis, including thrombohemorrhagic phenomena (THP), such as anaphylaxis [229,230,[237][238][239], disseminated intravascular coagulation (DIC) [240,241], HELLP syndrome [242], acute liver necrosis [243], Waterhouse-Friderichsen's syndrome, hemolytic uremic anemia, idiopathic pulmonary hemorrhage [244], acute pancreatitis [245], acute pituitary necrosis [246], pseudomembranous colitis, thrombotic thrombocytopenic purpura (TTP), Sanarelli-Shwartzman phenomenon (SSP), Henoch-Schonlein purpura (HSP), eclampsia [238], serum sickness, hemolytic anemia, preeclampsia, and stillbirths [247].…”

Section: Zeta Potential and Cardiovascular Diseasementioning

confidence: 92%

“…For this reaction, Richet used a Latin term ana-phylaxis or anti-protection, because the outcome was the opposite from the protection that the vaccine was supposed to provide. In further experiments with numerous other species, including cats, rabbits and horses, Richet showed that anaphylaxis is a universal immune system response [237][238][239]289]. In 1907, Richet demonstrated what is known as passive anaphylaxis.…”

Section: Discussionmentioning

confidence: 99%

“…In most instances, introduction of polycationic surfactants into our bloodstream causes acute interfacial water stress, lowering of ZP, lowering of pH, elevation of viscosity, and electrohemorheologic-hemodynamic derangement. This triggers a cascade of immunologic and hemostatic events, leading inexorably to tissue hypoperfusion, cellular anoxia, seizures, arrhythmias, infarctions, cardiovascular collapse, and death [97][98][99][100]209,229,230,[237][238][239].…”

Section: Discussionmentioning

confidence: 99%

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The Initial Common Pathway of Inflammation, Disease, and Sudden Death

Davidson¹,

Seneff²

2012

Entropy

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Abstract:In reviewing the literature pertaining to interfacial water, colloidal stability, and cell membrane function, we are led to propose that a cascade of events that begins with acute exogenous surfactant-induced interfacial water stress can explain the etiology of sudden death syndrome (SDS), as well as many other diseases associated with modern times. A systemic lowering of serum zeta potential mediated by exogenous cationic surfactant administration is the common underlying pathophysiology. The cascade leads to subsequent inflammation, serum sickness, thrombohemorrhagic phenomena, colloidal instability, and ultimately even death. We propose that a sufficient precondition for sudden death is lowered bioavailability of certain endogenous sterol sulfates, sulfated glycolipids, and sulfated glycosaminoglycans, which are essential in maintaining biological equipose, energy metabolism, membrane function, and thermodynamic stability in living organisms. Our literature review provides the basis for the presentation of a novel hypothesis as to the origin of endogenous bio-sulfates which involves energy transduction from sunlight. Our hypothesis is amply supported by a growing body of data showing that parenteral administration of substances that lower serum zeta potential results in kosmotropic cationic and/or chaotropic anionic interfacial water stress, and the resulting cascade.Keywords: inflammation; serum sickness; colloidal instability; interfacial water stress; bio-sulfates; Shwartzman phenomena; sudden death syndrome Glossary of TermsAnaphylaxis a severe, rapidly progressing, life-threatening, generalized allergic reaction. Biological equipoise a stable, non-equilibrium, dissipative system synonymous with life. Cholesterol sulfate (Ch-S)quantitatively the most important known sterol sulfate in human plasma where it regulates the activity of the serine proteases, in cell membranes where it has a stabilizing role, and in platelet membranes where it supports platelet adhesion. Coherence domain (CD)a water CD is a collection of liquid water molecules which oscillate in unison in tune with a self-trapped electromagnetic field at a well-defined frequency. The coherent oscillations produce an ensemble of quasi-free electrons, able to collect noise energy from the environment and transform it into high-grade coherent energy in the form of electron vortices. This high-grade energy may then activate biomolecules resonating with the water CD. Colloidal instabilitya property attributed to a colloidal suspension that develops when stabilizing repulsive steric and electrostatic forces between colliding particles are insufficient to prevent their natural tendency to aggregate into masses large enough to precipitate.Colloidal suspension a colloid that has a continuous liquid phase in which a solid is suspended in a liquid, e.g., our flowing blood. Exclusion zone (EZ)a glass-like, gel phase consisting of water CDs resonating in-phase, adjacent to hydrophilic surfaces, several hundred micrometers wide which excludes colloi...

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Section: Zeta Potential and Cardiovascular Diseasementioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

The Initial Common Pathway of Inflammation, Disease, and Sudden Death

Davidson¹,

Seneff²

2012

Entropy

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“…1 Most recognized is the powerful mast cell activation caused by allergen cross-linking of immunoglobulin E-loaded high-affinity immunoglobulin E receptors (FceRIs), which leads to the release of an array of different mediators. 2 In allergic asthmatics, mast cell mediators such as histamine and prostaglandin D 2 are secreted rapidly after allergen provocation.…”

Section: Introductionmentioning

confidence: 99%

Lin− CD34hi CD117int/hi FcεRI+ cells in human blood constitute a rare population of mast cell progenitors

Dahlin¹,

Malinovschi²,

Öhrvik³

et al. 2016

Blood

105

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“…41,42 The trigger is either (1) immunologic (IgE or IgG dependent) or (2) non-immunologic (direct stimulation of mast cells by certain drugs, cold air, exercise, etc.). [43][44][45][46] The immunologic pathway involves an allergen-induced crosslinking of IgE antibodies (formed during a clinically silent initial exposure) coupled to mast cells and basophils, which induces a transduction cascade activating mast cells. Note that a very small amount of allergen is needed to trigger the cascade.…”

Section: Pathophysiologymentioning

confidence: 99%

Kounis syndrome: a narrative review

Fourie

2016

Southern African Journal of Anaesthesia and Analgesia

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Inflammatory mediators released from activated mast cells and basophils during hypersensitivity reactions have direct pathological effects on the myocardium and coronary vasculature. It was traditionally thought that cardiovascular signs and symptoms in anaphylaxis are largely due to peripheral vasodilation and increased vascular permeability. However, there is extensive evidence of primary cardiac involvement during hypersensitivity reactions, most notably coronary vasoconstriction as well as atherosclerotic plaque erosion and rupture, leading to angina pectoris and acute coronary syndromes. Furthermore, mast cells are well established as effector cells in atherosclerosis, through their effects on atherosclerotic plaque progression and destabilisation. It was noted over 30 years ago that cardiac patients have a markedly higher concentration of biologic amines (especially histamine) in their coronary vasculature, and, additionally, are hyper-reactive to the effects thereof. This is borne out by the disproportionate mortality rate of those with cardiac disease that suffer a hypersensitivity reaction. Kounis syndrome refers to angina pectoris or an acute coronary syndrome secondary to a hypersensitivity reaction, with the subtypes dependent on the underlying state of the coronaries and presence of a drug-eluting stent or not. This review will focus mainly on the aetiology, pathophysiology, diagnoses and treatment of this important syndrome.

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Pathophysiology of anaphylaxis

Abstract: Recent advances will enhance understanding of the pathophysiology of anaphylaxis and might have future implications for diagnosis and management.

Cited by 83 publications

References 63 publications

The Initial Common Pathway of Inflammation, Disease, and Sudden Death

The Initial Common Pathway of Inflammation, Disease, and Sudden Death

Lin− CD34hi CD117int/hi FcεRI+ cells in human blood constitute a rare population of mast cell progenitors

Kounis syndrome: a narrative review

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