Carbamazepine‐induced fixed drug eruption

Argila, D. de; Gonzalo, Montserrat; Rovira, I.

doi:10.1111/j.1398-9995.1997.tb02430.x

Cited by 5 publications

(3 citation statements)

References 4 publications

(13 reference statements)

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“…Finally, we observed two cases of FDE induced by anticonvulsants (ie, carbamazepine and phenobarbital). Some sporadic case reports described FDE induced by these two drugs …”

Section: Discussionmentioning

confidence: 97%

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Clinical features, culprit drugs, and allergology workup in 41 cases of fixed drug eruption

et al. 2019

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Background: Fixed drug eruption (FDE) represents a drug-related cutaneous reaction.Many drugs been associated with this clinical entity, with continually evolving documentation of implicated agents and clinical presentations. A bullous form can occur although it is rare.Objectives: To assess the epidemiological and clinical characteristics of FDE. Methods: We retrospectively analysed all FDE cases who presented to the ClinicalPharmacology Department at the University Hospital, Monastir, Tunisia, for allergy workup.Results: The mean age of the 41 confirmed FDE cases was 43.8 ± 15.5 years. The time between first lesion onset and FDE diagnosis was less than 1 month for 13 patients (31.7%). Fifteen patients had bullous lesions. The upper limbs were the most common location (65.9% of cases). The patch tests were positive in 27 cases; a provocation test yielded a positive response in the four cases tested. Nonsteroidal anti-inflammatory drugs (NSAIDs) were involved in 51.2%, antibiotics in 24.4%, and other analgesics in 19.5%. The most common offending drug was mefenamic acid in 24.4% of cases. Bullous lesions were significantly associated with paracetamol intake (P = .014; odds ratio 16.7; 95% confidence interval: 1.76-158).Conclusions: NSAIDs and antibiotics were the most implicated in inducing FDE; paracetamol was associated with bullous lesions. K E Y W O R D Sepidemiology, fixed drug eruption, oral rechallenge, patch test

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“…Finally, we observed two cases of FDE induced by anticonvulsants (ie, carbamazepine and phenobarbital). Some sporadic case reports described FDE induced by these two drugs …”

Section: Discussionmentioning

confidence: 97%

“…Some sporadic case reports described FDE induced by these two drugs. [17][18][19] In conclusion, FDE diagnosis is often initially missed, leading to multiple episodes. This drug side effect seems to be a cutaneous adverse reaction mainly induced by NSAIDs and antibiotics.…”

Section: Discussionmentioning

confidence: 99%

Clinical features, culprit drugs, and allergology workup in 41 cases of fixed drug eruption

et al. 2019

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“…For GBFDE, there are numerous case reports in the literature providing information on possible drug triggers ( 47 – 50 ); however, no analyses have been conducted on large patient numbers. The range of triggers include antimicrobial sulphonamides (especially cotrimoxazole), analgesics (especially metamizole, but also paracetamol), and, less frequently, antibiotics, allopurinol, and antiepileptic drugs (especially carbamazepine) ( 47 – 50 ). The latency between the start of drug use and reaction onset ranges from a few hours to a few days.…”

Section: Aetiology and Medication Riskmentioning

confidence: 99%

Bullous Drug Reactions

Mockenhaupt¹

2020

Acta Derm Venerol

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This is an open access article under the CC BY-NC license. www.medicaljournals.se/acta Acta Derm Venereol 2020; 100: adv00057 Centenary theme section: BLISTERING SKIN DISORDERS SIGNIFICANCE Drug reactions with blisters (known as bullous drug reactions) are challenging for patients and physicians. Often there are early signs and symptoms that may lead to the suspicion of a bullous drug reaction before blisters and erosions of the skin and mucosa appear. Once the diagnosis is suspected, appropriate diagnostic and therapeutic procedures must be initiated. A detailed history, including clinical symptoms, drug use and infections, is crucial. In cases with drug causality, the potentially culprit agent must be withdrawn, while in cases with other aetiology, the underlying condition, e.g. infection, must be treated. In addition to best supportive care, immunomodulating therapy may be considered. Bullous drug eruptions are infrequent, but because they pose a challenge both to affected patients and to treating physicians they are considered to be the most severe cutaneous adverse reactions (SCAR). It is important to recognize these conditions and to differentiate them from other clinical entities involving blister formation. There may be early signs and symptoms that indicate a severe bullous drug eruption even before blisters and erosions of the skin and mucous membranes become obvious. Once the diagnosis is suspected, appropriate diagnostic procedures and adequate management must be initiated. The latter includes identification of the potentially inducing drug, although it should be taken into account that not all cases of bullous eruptions are drug-induced. In cases with drug causality the potentially culprit agent must be withdrawn, while in cases with other aetiology the underlying condition, e.g. an infection, must be treated appropriately. In addition to best supportive care, immunomodulating therapy may be considered.

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Schwere Hautreaktionen: klinisches Bild, Epidemiologie, Ätiologie, Pathogenese und Therapie

Paulmann

Mockenhaupt

2019

Allergo J

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Background: Stevens Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are serious, life threatening severe immune-mediated cutaneous reactions with mortality ranging from 10 to 30 %. The commonest causes are drugs. SJS/TEN is characterised by widespread epidermal detachment due to keratinocyte cell death. Increased concentrations of cytotoxic molecules may act as potential serum biomarkers of SJS/TEN. However, to date no mechanism based biomarker has been validated for diagnostic utility in this field. HMGB1 is a well-validated biomarker of cell death and inflammation. This study investigated whether HMGB1 represents a valid, utilisable biomarkers for drug-induced SJS/TEN. Materials and methods: Serum samples from nevirapine-treated Malawian HIV patients (27 MPE, 12 DRESS, 12 SJS/TEN cases and matched tolerant controls) were analysed for total HMGB1 by ELISA. Novel mass-spectrometric protocols were also used to analyse posttranslationally modified forms of HMGB1. In addition serum from 20 Taiwanese SJS patients (five carbamazepine, eight allopurinol, five phenytoin, two sulfamethoxazole) both during and post-reaction were analysed for HMGB1 isoforms. Results: There was a significant elevation of mean total serum HMGB1 at time of reaction in patients with nevirapine-induced MPE (6.0 ng/ ml), HSS (6.3 ng/ml) and SJS/TEN (15.9 ng/ml) compared to tolerant controls at weeks (1.3 ng/ml) (p < 0.001). Analysis of post-translationally modified isoforms of the HMGB1 in the different phenotypes (Fig. 1) showed patients with MPE and DRESS had elevation the acetylated form of HMGB1 which is a marker of innate immunity. By contrast, SJS/ TEN patient sera contained comparable levels of acetylated HMGB1, but also had very high levels of the non-acetylated form, which is associated with cell death/tissue injury. The tolerant control patients had low levels of the unacetylated form. This pattern of HMGB1 isoform elevation was replicated in the Taiwanese SJS cohort. As patients recovered, the total HMGB1 concentrations went down, although there was still significant elevation of the sulphonyl (partially reduced) HMGB1 isoform which has no known immune function and may represent a marker of innate immunity returning to "steady state". Conclusions: In conclusion, our data suggest that post-translationally modified HMGB1 may represent mechanism-based diagnostic and prognostic markers for drug-induced SJS/TEN. This needs to be studied in more patients.

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Carbamazepine‐induced fixed drug eruption

Cited by 5 publications

References 4 publications

Clinical features, culprit drugs, and allergology workup in 41 cases of fixed drug eruption

Clinical features, culprit drugs, and allergology workup in 41 cases of fixed drug eruption

Bullous Drug Reactions

Schwere Hautreaktionen: klinisches Bild, Epidemiologie, Ätiologie, Pathogenese und Therapie

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