Delayed hypersensitivity in ampicillin-induced toxic epidermal necrolysis

Tagami, Hachiro

doi:10.1001/archderm.119.11.910

Cited by 22 publications

(11 citation statements)

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“…Tagami et al suggested that in some cases, delayed hypersensitivity is involved. In a patient with an upper respiratory tract infection and TEN thought to be caused by ampicillin, incubation of the patient's lymphocytes with ampicillin produced enhanced transformation (11). Our patient died before mitogen stimulation studies could be performed, and their reliability may have been uncertain since he received several transfusions that may have contained lymphocytes.…”

Section: Commentmentioning

confidence: 89%

“…Toxic epidermal necrolysis (TEN) has tiot been reported in infants younger than 4 months of age (1) and is usually considered to occur secondary to drug adtninistration (2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15), graft-versus-host reaction (1,16), or infection, particularly that caused by gratn-negative bacteria (9,(17)(18)(19). When related to drug administration, it is often preceded by a milder cutaneous reaction to the same medication (7,12,13,20).…”

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confidence: 99%

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Toxic Epidermal Necrolysis in a 6‐week‐old Infant

Hawk

Storer

Daum

1985

Pediatric Dermatology

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Toxic epidermal necrolysis was documented in a 6-week-old infant with Klebsiella pneumoniae sepsis who received many medications. We inoculated infant mice with the K. pneumoniae isolate but were unable to produce histologic changes resembling those seen in our patient. This condition should be included in the differential diagnosis of severe drug reactions in very young infants with clinical scalded-skin syndromes.

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Section: Commentmentioning

confidence: 89%

mentioning

confidence: 99%

Toxic Epidermal Necrolysis in a 6‐week‐old Infant

Hawk

Storer

Daum

1985

Pediatric Dermatology

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“…The utility of PT in IM-ADRs caused by quinolones and trimethoprim-sulfamethoxazole (TMP-SMX) is notoriously poor [112,119,120]. PT has been demonstrated to be effective in a small number of antibiotic-associated SJS/TEN [114,121–123], AGEP [70,112,120,124,125], FDE [126–128], DRESS [112,129], MPE [130] and EM [131] case series. To date, success with PT in cases of suspected antiretroviral hypersensitivity has been limited to abacavir.…”

Section: Historical Approaches To T-cell-mediated Hypersensitivitiesmentioning

confidence: 99%

“…Recommendations for IDT vary regionally and there is a lack of evidence-based volumes and reagents (beta-lactam versus non-beta-lactam) [121,133–135]. IDT has predominately been utilized for beta-lactam antimicrobials, especially penicillins > cephalosporins, in patients with a history of non-SJS/TEN T-cell-mediated ADR [122,123,137]. A positive result involves dermal induration/erythema at injection site, which will significantly exceed 5 mm from baseline, 24–72 hours post-testing.…”

Section: Summary and Recommendationsmentioning

confidence: 99%

Old dog begging for new tricks: current practices and future directions in the diagnosis of delayed antimicrobial hypersensitivity

Konvinse

Phillips

White

et al. 2016

Current Opinion in Infectious Diseases

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Purpose of review Antimicrobials are a leading cause of severe T-cell-mediated adverse drug reactions (ADRs). The purpose of this review is to address the current understanding of antimicrobial cross-reactivity and the ready availability of and evidence for in vitro, in vivo and ex vivo diagnostics for T-cell-mediated ADRs. Recent findings Recent literature has evaluated the efficacy of traditional antibiotic allergy management including patch testing, skin prick testing, intradermal testing and oral challenge. While patch and intradermal testing are specific for the diagnosis of immune-mediated (IM) ADRs, they suffer from drug-specific limitations in sensitivity. The use of ex vivo diagnostics, especially ELISpot has been highlighted as a promising new approach to assigning causality. Knowledge of true rates of antimicrobial cross-reactivity aids empirical antibiotic choice in the setting of previous IM-ADRs. Summary In an era of increasing antimicrobial resistance and use of broad-spectrum antimicrobial therapy, ensuring patients are assigned the correct “allergy label” is essential. Re-exposure to implicated antimicrobials, especially in the setting of severe adverse cutaneous reaction is associated with significant morbidity and mortality. The process through which an antibiotic label gets assigned, acted on and maintained is still imprecise. Predicting T-cell-mediated ADRs via personalised approaches, including HLA-typing may pave future pathways to safer antimicrobial prescribing guidelines.

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“…It is also interesting to compare the reactivity of acetone with that of biacetyl, where the carbonyl groups are mutually activating and also that of methyl vinyl ketone which reacts at the beta-vinyl carbon. Propiolactam was modelled to represent the class of penicillins, some of which express an ACD response [34]. The related propiolactone is a known carcinogen reactive with nucleotide bases.…”

Section: Simple Electrophilic Haptensmentioning

confidence: 99%

Exploring the Potential for Allergic Contact Dermatitisvia Computed Heats of Reaction of Haptens with Protein End-groups Heats of Reaction of Haptens with Protein End-groups by Computation

Magee¹

2000

Quant. Struct.-Act. Relat.

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Unlike human sensitization in allergic contact dermatitis, the primary event in the guinea pig maximization test (GPMT) is not penetration to the viable epidermis as the skin is compromised in both the sensitization and elicitation steps. The primary event is the chemical reaction of a hapten with simple protein end-groups at the recognition site of the major histocompatibility complex, class 2 (MHC II) on the cell surface of the Langerhans cells (LC). This reaction converts a benign LC into an allergen presenting cell that a T(CD4) lymphocyte recognizes as non-self and initiates the sensitizing sequence in the local draining lymph node. The widely used GPMT was selected for the purpose of modelling the sensitizing reaction without the complications of penetration to the viable epidermis.The compounds selected for study represent the class of electrophilic haptens that, along with their metabolic precursors (prohaptens) comprise the majority of known contact allergens. As the whole MHC II structure has no involvement with the sensitizing reaction beyond the ®rst few atoms of the end group, methoxide ion and thiomethoxide ion were used to model activated serine and cysteine. In addition, the GPMT has a relatively broad range of error which allows the use of AM1 as an adequate method for modelling the relative heats of reaction in the rate determining step.The relative reactivity of most of the known electrophilic haptens in the simplest aliphatic and aromatic form are modelled in this study. For many of those that are sensitive to substituent effects, sets of 7±10 substituted analogs were modelled to provide excellent Hammett relations with the heats of reaction. These linear free energy relations allow prediction of ACD potential in new related haptens.As a ®nal validation of the procedure, a set of compounds scoring non (1), weak (2), moderate (3) and strong (4) as measured in the GPMT are computed for comparison with the test results and found to be in good concordance.

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Delayed hypersensitivity in ampicillin-induced toxic epidermal necrolysis

Cited by 22 publications

References 0 publications

Toxic Epidermal Necrolysis in a 6‐week‐old Infant

Toxic Epidermal Necrolysis in a 6‐week‐old Infant

Old dog begging for new tricks: current practices and future directions in the diagnosis of delayed antimicrobial hypersensitivity

Exploring the Potential for Allergic Contact Dermatitisvia Computed Heats of Reaction of Haptens with Protein End-groups Heats of Reaction of Haptens with Protein End-groups by Computation

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