Distinct delayed T‐cell response to <i>β</i>‐methasone and penicillin‐G in the same patient

Scala, Enrico; Giani, Mauro; Pastore, Saveria; Pallotta, Sabatino; Guerra, Emanuele; Pirrotta, L.; Locanto, Maria; Frezzolini, Alessandra; Pità, Ornella De; Puddu, Pietro

doi:10.1034/j.1398-9995.2003.00117.x

Cited by 8 publications

(6 citation statements)

References 40 publications

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“…In contrast a heterogeneous cytokine pattern was found by other authors [31, 33]. We demonstrated the coexistence in the same patient of a delayed hypersensitivity to both penicillin G and betamethasone, driven by penicillin G-specific Th2-skewed CD8+ and betamethasone Th0 CD4+ T cells, respectively [24]. …”

Section: Discussionmentioning

confidence: 37%

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Delayed Allergic Reaction to Suxamethonium Driven by Oligoclonal Th1-Skewed CD4+CCR4+IFN-γ+ Memory T Cells

Scala

Guerra

Giani

et al. 2006

Int Arch Allergy Immunol

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Background: Muscle relaxants represent the drugs most frequently involved in intraoperative anaphylaxis during surgical procedures. Our aim was to report the case of a delayed reaction to suxamethonium and analyze specific T cell lines with regard to their specificity, phenotype and cytokine profile. Methods: We generated a drug-specific T cell line from a biopsy at the site of positive intradermal reactions and analyzed the immunophenotype, T cell receptor Vβ domain expression and cytokine profile. Results: T cells isolated from positive intradermal test reactions to suxamethonium showed a strict dose-dependent proliferation in response to drug-pulsed autologous antigen-presenting cells. The drug-specific CD4+ T cells were oligoclonal memory CD3+CD4+ T cells and expressed the skin homing receptors cutaneous lymphocyte antigen (CLA) and CCR4. Furthermore CD4+ suxamethonium-reactive T cell lines were IFN-γ-positive and synthesized high levels of IFN-γ and TNF-α. Conclusion: The study describes a delayed hypersensitivity to suxamethonium, driven by an oligoclonal T helper cell 1-skewed CD4+ memory T cell population, expressing the skin homing receptors CLA and CCR4.

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Section: Discussionmentioning

confidence: 37%

“…Different stimulation procedures were chosen, as previously described [24]. Briefly, both a direct stimulation of peripheral blood mononuclear cells (PBMC) and TCL with different doses of suxamethonium (from 0.01 to 1 m M /l) and PBMC and TCL stimulation with drug-modified autologous PBMC, named Ag-pulsed APC, were performed.…”

Section: Methodsmentioning

confidence: 99%

Delayed Allergic Reaction to Suxamethonium Driven by Oligoclonal Th1-Skewed CD4+CCR4+IFN-γ+ Memory T Cells

Scala

Guerra

Giani

et al. 2006

Int Arch Allergy Immunol

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“…-Clobetasol propionate I% in alcoholic solution " " 389 rather than a cell-mediated one. Few reports have been made in literature of allergic type reactions immediately after the administration of Betamethasone (7-9), and no specific IgE have yet been identified in vitro either to Betamethasone or to other fluorinated CSs, while lymphocytes T CD4+ for Betamethasone were isolated in the blood of a patient who manifested a generalized urticarioid eruption 24 hours after the administration of the steroid (10).…”

Section: Discussionmentioning

confidence: 99%

Anaphylaxis Induced by Intramuscular Betamethasone Disodium Phosphate: Reflections on a Clinical Case

Ventura

Sanapo

GF³

et al. 2007

Int J Immunopathol Pharmacol

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Glucocorticoids could be responsible for allergic symptoms correlated to an Ig-E mediated hypersensitivity mechanism. We describe the case of an anaphylactic reaction in a professional nurse, occurring after an intramuscular administration of Betamethasone. After performing skin prick tests, intramuscular tests and patch tests we concluded that the patient had Ig-E mediated sensitization. She was prescribed oral Prednisone and Deflazacort and shows good tolerance of these drugs. This demonstrates that in these patients it is possible to administrate glucocorticoids without the changes in the sites indicated by Wilkinson. Nevertheless, our patient showed a negative allergy test for Dexamethasone disodium phosphate, and in those patients sensitized to fluorinated glucocorticoids, tolerance to other glucocorticoids is not so easily predictable as in patients with hypersensitivity to first generation steroids or in corticosteroid contact dermatitis, according to the four patterns of cross-reactivity proposed by Coopman and Dooms-Goossens.

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“…It is generally accepted, however, that the same cross-reactivity patterns observed for topical preparations occur when they are used systemically. Such patterns should be taken into account for choosing an alternative GC molecule in sensitive patients [89][90][91]. As with their topical counterparts, there will be exceptions to systemic steroid cross-reactivity patterns.…”

Section: Preservatives In Gc Topical Preparations Responsible For Amentioning

confidence: 93%

Cross-Reactivity in Cell-Mediated and IgE-Mediated Hypersensitivity to Glucocorticoids

Ventura

Calogiuri²,

Muratore³

et al. 2006

CPD

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In the last few decades, glucocorticoids have received increasing attention for their capability of provoking systemic hypersensitivity reactions, when administered orally, parenterally, or intralesionally, as well as allergic skin and mucosal symptoms, when applied locally to the skin in patients with contact dermatitis or to the mucosa in patients with asthma and/or rhinitis. However, because of their anti-inflammatory and immunosuppressive properties, glucocorticoids are often not suspected of such hypersensitivity reactions. In addition, because glucocorticoids retain their anti-inflammatory potential, even if they act as sensitizers, the signs and symptoms of allergic reactions are not always obvious, particularly when they overlap with those caused by the very diseases glucocorticoids are used to treat. Moreover, interpretation of diagnostic tests, specifically that of patch-test reactions, can be difficult. In this review, particular attention is addressed to the problem of allergenic cross-reactivity among topical and systemic glucocorticoids. We also look at the clinical and practical aspects of both cell-mediated and IgE-mediated hypersensitivity reactions to glucocorticoids and their consequences on anti-inflammatory therapeutic choices.

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Distinct delayed T‐cell response to β‐methasone and penicillin‐G in the same patient

Cited by 8 publications

References 40 publications

Delayed Allergic Reaction to Suxamethonium Driven by Oligoclonal Th1-Skewed CD4+CCR4+IFN-γ+ Memory T Cells

Delayed Allergic Reaction to Suxamethonium Driven by Oligoclonal Th1-Skewed CD4+CCR4+IFN-γ+ Memory T Cells

Anaphylaxis Induced by Intramuscular Betamethasone Disodium Phosphate: Reflections on a Clinical Case

Cross-Reactivity in Cell-Mediated and IgE-Mediated Hypersensitivity to Glucocorticoids

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