Uncovering Histologic Criteria With Prognostic Significance in Toxic Epidermal Necrolysis

Quinn, Adam M.; Brown, Kimberly M.; Bonish, Brian K.; Curry, Jonathan L.; Gordon, Kenneth B.; Sinacore, James; Gamelli, Richard L.; Nickoloff, Brian J.

doi:10.1001/archderm.141.6.683

Cited by 82 publications

(45 citation statements)

References 26 publications

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“…In addition, fullthickness epidermal necrosis is not unique to TEN and occurs in the centers of human EM major lesions. 20,23 Our results are consistent with TEN in humans, 19 in whom histopathologic examination confirms but lacks specificity to differentiate EM and SJS/TEN. Furthermore, this reinforces the findings of Hinn et al, 12 which emphasized the need for clinical information to differentiate these conditions in dogs.…”

Section: Discussionsupporting

confidence: 81%

Clinical and Microscopic Characteristics of Canine Toxic Epidermal Necrolysis

et al. 2014

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Canine toxic epidermal necrosis (TEN), a rare and life-threatening cutaneous drug reaction, traditionally has been described as full-thickness devitalization of the epidermis with minimal dermal inflammation; however, few reports detail the histologic findings. We characterize the clinical features and histologic variations of 3 canine TEN patients. Clinically, irregular erythematous and purpuric macules evolved into widespread and severely painful erosions. The number of eroded mucosae varied; however, periocular and perilabial mucocutaneous junctions frequently were affected. Thirteen of 17 biopsies were evaluated. Apoptosis at multiple epidermal levels was the most common pattern of epidermal necrosis (12/13 biopsies, 92%). In contrast, full-thickness coagulation necrosis was present less often (7/13 biopsies, 52%). Lymphocytic interface dermatitis was the predominant inflammatory pattern, and intraepidermal lymphocytes, along with fewer histiocytes, were present to some degree in all samples along with lymphocytic satellitosis of apoptotic keratinocytes. The sequence of changes points to lymphocyte-mediated keratinocyte apoptosis as an early step in lesion development with subsequent variation in progression to coagulation necrosis among patients. Histopathologic changes overlapped with those reported for erythema multiforme, in contrast to traditional histologic descriptions of canine TEN. A specific algorithm for assessment of drug causality in epidermal necrolysis (ALDEN) was applied for each patient; carprofen was associated with a probable score for causality in 1 dog. Clinicians should be encouraged to take multiple biopsies in TEN suspect cases as nearly 25% of all biopsies lacked epithelium and were not diagnostic.

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Section: Discussionsupporting

confidence: 81%

Clinical and Microscopic Characteristics of Canine Toxic Epidermal Necrolysis

et al. 2014

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“…7 Dense dermal inflammation was observed in the biopsy specimen from the patient who experienced ocular sequelae (ie, cicatrizing conjunctivitis) that required therapy with mycophenolate mofetil and dapsone, but only moderate dermal inflammation was found in the patient who died of SJS-related complications. The limited histologic data in our study prevent any firm conclusions about clinical and etiologic correlates based on histologic patterns.…”

Section: Dermal Infiltrate Epidermal Infiltratementioning

confidence: 97%

“…Other studies have described histopathologic correlates in patients with EM, SJS, and toxic epidermal necrolysis (TEN). [6][7][8][9] The aim of the current study was to retrospectively examine clinical, etiologic, and histopathologic data from patients with SJS to identify possible correlates of clinical disease severity related to specific etiologic and histopathologic findings.…”

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confidence: 99%

Clinical, Etiologic, and Histopathologic Features of Stevens-Johnson Syndrome During an 8-Year Period at Mayo Clinic

Wetter

Camilleri

2010

Mayo Clinic Proceedings

125

104

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“…First, keratinocytes exhibit large metabolic capabilities through their various transport-associated and detoxifying enzymes [5,7] . Second, most TEN lesions show a minimal inflammatory infiltrate [14] . In addition, immunohistochemical and functional studies have shown the overexpression of different proapoptotic systems by TEN keratinocytes, including tumor necrosis factor ␣ and Fas receptor/Fas ligand (CD95R/ …”

Section: Discussionmentioning

confidence: 99%

Glutathione-S-Transferase Pi Expression in Toxic Epidermal Necrolysis: A Marker of Putative Oxidative Stress in Keratinocytes

Paquet

Pierard

2006

Skin Pharmacol Physiol

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Background: Toxic epidermal necrolysis (TEN) is a dramatic drug-induced emergency related to extensive destruction of the epidermis. There is evidence that its pathomechanism involves impaired detoxication of xenobiotics. Glutathione-S-transferase π (GST-π) is a phase II detoxifying enzyme involved in drug metabolization by human keratinocytes. Method: Immunohistochemistry was performed in order to assess the expression of GST-π in keratinocytes of TEN, other cutaneous adverse drug reactions and bullous pemphigoid. Results: GST-π was disclosed in the involved epidermis of 16/16 TEN patients. It was present in the cytoplasm of suprabasal keratinocytes. GST-π was also expressed in the clinically uninvolved skin in a majority (8/12) of TEN patients. By contrast, it was rarely and poorly expressed in the other tested dermatoses. Conclusion: The pathomechanism of TEN is not related to an impaired quantitative expression of GST-π. GST-π expression is an early event in TEN. As oxidative stress is a major inducer of GST-π, this mechanism might be involved in TEN. Its GST-π expression mainly restricted to the suprabasal keratinocytes suggests that the pathomechanisms leading to keratinocyte death in TEN are distinct at different levels of the epidermis.

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Uncovering Histologic Criteria With Prognostic Significance in Toxic Epidermal Necrolysis

Cited by 82 publications

References 26 publications

Clinical and Microscopic Characteristics of Canine Toxic Epidermal Necrolysis

Clinical and Microscopic Characteristics of Canine Toxic Epidermal Necrolysis

Clinical, Etiologic, and Histopathologic Features of Stevens-Johnson Syndrome During an 8-Year Period at Mayo Clinic

Glutathione-S-Transferase Pi Expression in Toxic Epidermal Necrolysis: A Marker of Putative Oxidative Stress in Keratinocytes

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