Biochemical Markers of Anaphylactoid Reactions to Drugs Comparison of Plasma Histamine and Tryptase

Laroche, D.; Vergnaud, M; Sillard, B.; Soufarapis, H.; Bricard, H.

doi:10.1097/00000542-199112000-00004

Cited by 180 publications

(87 citation statements)

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“…8), and previous studies showed that increases in plasma mMCP-1 levels may be induced by either IgG or IgE-mediated allergies (Strait et al, 2002). Unlike histamine and PAF, tryptase reaches peak concentrations ∼30-60 minutes after allergy onset, has a serum half-life of 90 minutes, and exhibits low serum concentrations in normal, nonallergic individuals (Laroche et al, 1991). Although other studies have suggested that histamine levels may be a more useful immediate (e.g., 10 minutes) indicator of the onset of allergies compared with the release of mast cell proteases in mice (Nabe et al, 2013), a biomarker of allergy that is elevated and stable for several hours after an allergic reaction may be more useful as an eventual clinical biomarker of asparaginase-induced allergies.…”

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confidence: 89%

Effect of Premedications in a Murine Model of Asparaginase Hypersensitivity

Fernandez

Smith

Karol

et al. 2015

J Pharmacol Exp Ther

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A murine model was developed that recapitulates key features of clinical hypersensitivity to Escherichia coli asparaginase. Sensitized mice developed high levels of anti-asparaginase IgG antibodies and had immediate hypersensitivity reactions to asparaginase upon challenge. Sensitized mice had complete inhibition of plasma asparaginase activity (P 5 4.2 Â 10 213) and elevated levels of mouse mast cell protease 1 (P 5 6.1 Â 10 23) compared with nonsensitized mice. We investigated the influence of pretreatment with triprolidine, cimetidine, the platelet activating factor (PAF) receptor antagonist CV-6209 [2-(2-acetyl-6-methoxy-3,9-dioxo-4,8-dioxa-2,10-diazaoctacos-1-yl)-1-ethyl-pyridinium chloride], or dexamethasone on the severity of asparaginase-induced allergies. Combining triprolidine and CV-6209 was best for mitigating asparaginase-induced hypersensitivity compared with nonpretreated, sensitized mice (P 5 1.2 Â 10 25 ). However, pretreatment with oral dexamethasone was the only agent capable of mitigating the severity of the hypersensitivity (P 5 0.03) and partially restoring asparaginase activity (P 5 8.3 Â 10 24 ). To rescue asparaginase activity in sensitized mice without requiring dexamethasone, a 5-fold greater dose of asparaginase was needed to restore enzyme activity to a similar concentration as in nonsensitized mice. Our results suggest a role of histamine and PAF in asparaginase-induced allergies and indicate that mast cell-derived proteases released during asparaginase allergy may be a useful marker of clinical hypersensitivity.

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mentioning

confidence: 89%

Effect of Premedications in a Murine Model of Asparaginase Hypersensitivity

Fernandez

Smith

Karol

et al. 2015

J Pharmacol Exp Ther

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“…An elevated total serum tryptase level (pro-b and pro-a and mature-btryptase) is therefore highly indicative for mast cell degranulation, as seen in systemic anaphylaxis [for review: (21)]. A rise in total tryptase can be quantified in serum (or plasma) as soon as 30 min after onset of symptoms, but sampling is recommended 60-120 min after onset-ofsymptoms (22). Tryptase's half-life is about 120 min, and levels gradually decrease over time.…”

Section: Tryptasementioning

confidence: 99%

“…ÔFalse-negativeÕ results have been attributed to a mechanism where the reaction involves basophils rather than mast cells (22), whereas false positive results have been reported in cases of extreme stress such as hypoxemia and major trauma (27,28).…”

Section: Tryptasementioning

confidence: 99%

Anaphylaxis during anaesthesia: diagnostic approach

Ebo¹,

Fisher²,

Hagendorens³

et al. 2007

Allergy

195

197

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Anaesthesiologists administer several drugs while providing general anaesthesia. Many of these drugs can elicit adverse drug reactions that fall apart into two major types. First, reactions that are usually dose-dependent and related to the pharmacological properties of the drug and/or its metabolites. Second, reactions that are unrelated to the drug's pharmacological characteristics and that are less dose-dependent. These reactions comprise drug intolerance, idiosyncratic reactions and drug-induced immune-mediated allergic and nonimmune-mediated so-called pseudo-allergic or anaphylactoid reactions. The terms anaphylactic and anaphylactoid, however, have been used inconsistently in the literature. Therefore, the nomenclature task force set up by the European Academy of Allergy and Immunology (EAACI) has proposed that anaphylactic-type reactions should be reclassified into allergic anaphylaxis and nonallergic anaphylaxis. Allergic anaphylaxis being further subdivided in IgE-mediated and non-IgE-mediated reactions (1).The exact prevalence of anaphylaxis during anaesthesia is difficult to ascertain. The estimated overall frequency has been reported to vary between 1 in 3500 and 1 in 13 000 procedures in French series (2, 3) and between 1 in 10 000 and 1 in 20 000 in an Australian study (4). The clinical manifestation of these reactions is not infrequently an almost immediate generalized response with bronchospasm and hypotension. The degree of severity varies and does not allow differentiation between an IgE-mediated or non-IgE mediated reaction resulting from nonspecific mediator release (5). The mortality from these reactions is in the range from 3 to 6%, and an additional 2% of patients experience significant residual brain damage (4).Diagnosis of anaphylaxis during anaesthesia is not always straightforward. It can be hampered as a broad spectrum of different drugs can elicit heterogeneous allergic and nonallergic reactions with distinct and sometimes unclear pathological mechanisms. Problems are certainly compounded as multiple drugs need to be administered during general anaesthesia. In addition, nonanaesthesia related drugs or procedures (e.g. disinfection) are sometimes administered/performed in the perioperative period and can also be the cause of an allergic reaction.In addition, none of the available diagnostic tests demonstrates absolute accuracy. False-positive test Correct management of anaphylaxis during anaesthesia requires a multidisciplinary approach with prompt recognition and treatment of the acute event by the attending anaesthesiologist, and subsequent determination of the responsible agent(s) with strict avoidance of subsequent administration of all incriminated and/or cross-reacting compounds.However, correct identification of the causative compound(s) and safe alternatives is not always straightforward and, too often, not done.This review is not intended to discuss acute management of anaesthesia-related anaphylaxis but summarizes the major causes of anaphylaxis during anaesthesia and the di...

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“…Evidence is emerging that tryptase may be a key mediator of allergic inflammation and a promising target for therapeutic intervention [9] as it has been found to be able to induce microvascular leakage in the skin of guinea pig [10] , bronchoconstriction [11] in allergic sheep airways, inflammatory cell accumulation in peritoneum of mouse [12] and release of IL-8 from epithelial cells [13] . Moreover, tryptase has long been recognised as a marker of mast cells [14,15] , and an indicator of mast cell degranulation in vivo [16,17] . However, the application of tryptase as a unique marker of mast cell degranulation in mast cell challenge study in vitro was only started recently [18] .…”

Section: Introductionmentioning

confidence: 99%

Modulation of tryptase secretion from human colon mast cells by histamine

Xie²

2004

WJG

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AIM:To investigate the ability of histamine to modulate tryptase release from human colon mast cells and the potential mechanisms. METHODS:Enzymatically dispersed cells from human colons were challenged with histamine, anti-IgE or calcium ionophore A23187 (CI), and the cell supernatants after challenge were collected. Tryptase release was determined with a sandwich ELISA procedure. RESULTS:Histamine at concentrations from 1 ng/mL was able to induce a "bell" shape dose related release of tryptase from colon mast cells. The maximum release of tryptase was approximately 3.5 fold more than spontaneous release. As little as 10 ng/mL histamine showed a similar potency to 10 µg/mL anti-IgE in induction of tryptase release. Histamine induced release of tryptase initiated at 10 s when histamine (100 ng/mL) was added to cells, gradually increased thereafter, and completed at 5 min. Both pertussis toxin or metabolic inhibitors were able to inhibit histamine induced tryptase release. When histamine and anti-IgE were added to colon mast cells at the same time, the quantity of tryptase released was similar to that induced by anti-IgE alone. The similar results were observed with CI. However, when various concentrations of histamine were incubated with cells for 20 min before adding anti-IgE or CI, the quantity of tryptase released was similar to that was induced by histamine alone. CONCLUSION:Histamine is a potent activator of human colon mast cells, which represents a novel and pivotal selfamplification mechanism of mast cell degranulation.

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Biochemical Markers of Anaphylactoid Reactions to Drugs Comparison of Plasma Histamine and Tryptase

Cited by 180 publications

References 0 publications

Effect of Premedications in a Murine Model of Asparaginase Hypersensitivity

Effect of Premedications in a Murine Model of Asparaginase Hypersensitivity

Anaphylaxis during anaesthesia: diagnostic approach

Modulation of tryptase secretion from human colon mast cells by histamine

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