Hypothesis for Synergistic Toxicity of Organophosphorus Poisoning-induced Cholinergic Crisis and Anaphylactoid Reactions

Cowan, Fred M.; Shih, Tsung‐Ming; Lenz, David E.; Madsen, James M.; Broomfield, Clarence A.

doi:10.1002/(sici)1099-1263(199601)16:1<25::aid-jat303>3.0.co;2-5

Cited by 29 publications

(13 citation statements)

References 4 publications

(5 reference statements)

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“…Animal studies have also suggested that chronic OP exposure may cause oxidative damage of the vascular endothelium (27). One study has suggested that mast cell-mediated effects (anaphylaxis) may occur after OP poisoning (28), potentially leading to histamine-induced hypotension.…”

Section: Discussionmentioning

confidence: 99%

Hypotension in severe dimethoate self-poisoning

Davies

Roberts

Eyer³

et al. 2008

Clinical Toxicology

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Introduction. Acute self-poisoning with the organophosphorus (OP) pesticide dimethoate has a human case fatality three-fold higher than poisoning with chlorpyrifos despite similar animal toxicity. The typical clinical presentation of severe dimethoate poisoning is quite distinct from that of chlorpyrifos and other OP pesticides: many patients present with hypotension that progresses to shock and death within 12-48 h post-ingestion. The pathophysiology of this syndrome is not clear. Case reports. We present here three patients with proven severe dimethoate poisoning. Clinically, all had inappropriate peripheral vasodilatation and profound hypotension on presentation, which progressed despite treatment with atropine, i.v. fluids, pralidoxime chloride, and inotropes. All died 2.5-32 h post-admission. Continuous cardiac monitoring and quantification of troponin T provided little evidence for a primary cardiotoxic effect of dimethoate. Conclusion. Severe dimethoate self-poisoning causes a syndrome characterized by marked hypotension with progression to distributive shock and death despite standard treatments. A lack of cardiotoxicity until just before death suggests that the mechanism is of OP-induced low systemic vascular resistance (SVR). Further invasive studies of cardiac function and SVR, and post-mortem histology, are required to better describe this syndrome and to establish the role of vasopressors and high-dose atropine in therapy.

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Section: Discussionmentioning

confidence: 99%

Hypotension in severe dimethoate self-poisoning

Davies

Roberts

Eyer³

et al. 2008

Clinical Toxicology

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“…Cowan et al [43] have recently highlighted that despite variable clinical outcomes following exposure to the chemical warfare agents organophosphorous, soman, or sulfur mustard (2,2 0 -dichlorodiethyl sulfide), there may be common inflammatory and proteolytic pathways induced. In particular, serine proteases are activated and contribute to the dermal-epidermal separation that underlies blistering.…”

Section: Proteolysis During Cytotoxicitymentioning

confidence: 86%

Can Peptidomics Provide a Useful Approach for the Identification of Biomarkers of Toxicological Exposure or Effect?

Griffiths

2007

Peptidomics

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“…The ability of SPA to aggregate host Ig probably explain s this toxicity [14]. SP A (M W 40,000) and the Russian organophosphorus nerve agent som an (MW 180) can cause anaphylactoid reactio ns at about the sam e m olar dose [30], so SP A toxicity should not be taken ligh tly . However, it is the toxicological versus the therapeu tic index that ultim ately determ ines whether a drug can be safely used.…”

mentioning

confidence: 89%

Staphylococcus Aureus Protein A Immunoadsorption: The Rationale for Systemic Protein A Immunotherapy

Cowan

1997

Toxicology Methods

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Sum m ary:Staphylo coccus aureus protein A (SPA) bound to af® nity colum n m atrixes has been used for extracorp oreal imm unoadsorp tion for the treatm ent of hum an autoim m une and neoplastic diseases. SPA is a bacterial im munoglobu lin binding factor (IBF) that binds to the Fc region of antibody. T he mechanism (s) of action of protein A im munoadsor ption is not know n. However, protein A im munoadsorpt ion and system ic injection of SPA have dem onstrated sim ilar anti-neo6 -plastic and anti-retro viral responses in anim als. Cellular Fc receptor (FcR) im munity and hum oral IBF status are often abnorm al in autoim munity, cancer, and AIDS. T he im munothera peutic activity of protein A im munoadsor ption m ay be produced by SPA leaching off colum ns and acting as a soluble FcR-like IBF, capable of in¯uencing FcR dependent im munity. If this is the case then system ic SPA therapy may provide a sim pler, safer, and more predicabl e mode of immunotherapy than imm unoadsorp tion. K ey W ord s: extracorp oreal, Fc receptor, imm unoglobuli n binding factor, Staphyloc occus aureus protein A.Extraco rporeal im m unotherapy with protein A containin g bacteria was ® rst used by Bansal et al. in 1978 [1] to treat canin e and human breast adenocarcinom a. Since that tim e S ynder et al. [2], Term an et al. [3], M esserschm idt et al. [4], Kinet [5], and others [6] have continu ed investigati on of the anti-neo plastic activ ity of protein A im m unoadsorption . Despite the prelim inary clinica l success for treatin g som e autoimm une and neoplastic diseases [6] such as breast adenocarcin om a, Kaposi' s sarco m a, and refractory rheumatoid arth ritis [7], S PA colum n treatm ent of autoim m une thrombocytopenic purpura (IT PP) is the only use approved by United States Food and Drug Adm inistrat ion [6,8]. Num erous clin ical param eters such as circulating im m une

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Hypothesis for Synergistic Toxicity of Organophosphorus Poisoning-induced Cholinergic Crisis and Anaphylactoid Reactions

Cited by 29 publications

References 4 publications

Hypotension in severe dimethoate self-poisoning

Hypotension in severe dimethoate self-poisoning

Can Peptidomics Provide a Useful Approach for the Identification of Biomarkers of Toxicological Exposure or Effect?

Staphylococcus Aureus Protein A Immunoadsorption: The Rationale for Systemic Protein A Immunotherapy

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