Cell-Mediated Immunologic Mechanism and Severity of TEN

Faye, Ousmane; Wechsler, Janine; Roujeau, Jean‐Claude

doi:10.1001/archderm.141.6.775

Cited by 14 publications

(7 citation statements)

References 16 publications

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“…4,9,11 Some humans initially exhibit epidermal detachment over less than 10% of their body surface, an extent typical of SJS, but progress to 30% of the body surface area in a few days, which is more typical of TEN. 4,6 Similarly, epidermal detachment progressed to more than 30% of body surface over a period of 2 to 3 days in all 3 of our canine cases. This progression illustrates that the timing of clinical lesions should be taken into account when classifying SJS/TEN in dogs.…”

Section: Discussionmentioning

confidence: 52%

“…15 To the authors' knowledge, this is the first reported association between carprofen and TEN. Carprofen belongs to the propionic acid class of nonsteroidal anti-inflammatory drugs (NSAIDs), including ketoprofen, ibuprofen, naproxen, benoxaprofen, and fenoprofen, 6 with which carprofen shares an ATC code up to the fourth level (WHO). Currently among NSAIDs, oxicam derivatives are associated with a higher risk and acetic acid derivatives with a lower risk for SJS and TEN.…”

Section: Discussionmentioning

confidence: 99%

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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: Discussionmentioning

confidence: 52%

Section: Discussionmentioning

confidence: 99%

Clinical and Microscopic Characteristics of Canine Toxic Epidermal Necrolysis

et al. 2014

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“…5 Internal involvement may be caused by the release of massive amounts of proinflammatory cytokines into the systemic circulation. 6 Involvement of respiratory mucosa is insidious, and serious pulmonary disease can be seen with a normal chest radiograph. Clinical clues include dyspnea, tachypnea, and hypoxemia.…”

Section: Clinical Aspects Of Sjs/tenmentioning

confidence: 99%

“…63 This study also underscores the fact that TEN is a T celle mediated disorder. 6 To expedite diagnosis, two biopsy specimens should be taken from patients with suspected TEN: one for routine, formalin-fixed hematoxylin and eosin processing, and the other for immediate frozen section. Epidermis must be present to make the diagnosis, as epidermal necrosis is the pathognomonic finding in this entity.…”

Section: Histopathology and Differential Diagnosismentioning

confidence: 99%

Toxic epidermal necrolysis

Pereira

Mudgil

Rosmarin

2007

Journal of the American Academy of Dermatology

286

237

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“…It has been proposed that drug or their metabolites act as haptens, and drug‐specific CD 8 cells secrete interferon‐gamma which renders keratinocytes antigenic to produce tumour necrosis factor‐alpha (TNF‐α), Fas ligand (FaSL), interleukin‐6 (IL‐6) and IL‐10. TNF‐alfa up‐regulates expression of MHC‐1 and MHC‐11 molecules, which increase exposure of keratinocytes to cytotoxic T cells (CTLS) 3,4 . Cytotoxic T lymphocytes can induce apoptosis through perforin/granzyme caspase cascade.…”

mentioning

confidence: 99%

Herpes zoster virus associated ‘sparing phenomenon’: is it an innate possess of HZV or keratinocyte cytokine(s) mediated or combination?

Kannangara

Yosipovitch

et al. 2008

Acad Dermatol Venereol

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to 87% and from 30% to 47%, respectively. 1,3 Unlike other sarcomas, the high rate of nodal metastasis (14-60%) is characteristic of ES. 1,3 Whereas the occurrence of lymph node metastasis in sarcoma is recognized as a rare event (2.6%), 4 many types of carcinoma show the frequent lymph node metastasis (20-35%). 5 The frequent nodal metastasis of ES implies that ES could have the biological potential as well as morphological appearance shared by epithelial neoplasms.FGFRs and their ligands, 23 members of FGF family, are involved in developmental processes, angiogenesis, wound healing and tumorigenesis. Four FGFRs (FGFR1-4) have been identified in mammals. Alternative splicing of mRNA in FGFR1-3 generates two receptor isoforms, IIIb and IIIc. The expression of the FGFR transcriptional variant is tightly regulated by cell lineage, and these isoforms show quite different ligand-binding specificities. 2 FGFR2-IIIb is a specific receptor of FGF-7, also designated keratinocyte growth factor, whose expression is restricted to epithelial cells, whereas isotype IIIc of FGF1-3 mainly serves as the receptor for various FGF members in mesenchymal cells. Such specificity gives rise to lineage-specific behaviour compared with other growth factor receptors universally expressed in a wide range of cells. The expression of FGFR2-IIIb in ES implied epithelial differentiation accompanied by a basal mesenchymal nature. The in vitro experiments indeed showed that ES cells were subject to a mitogenic effect of FGF-7, indicating that FGFR2-IIIb could functionally render ES the behaviour shared by cells of epithelial origin. 6 Although it is a future subject to be addressed whether FGFR2-IIIb is commonly expressed in ES, the specific expression of FGFR2-IIIb could partially evidence the carcinomatous behaviour of ES including the frequent nodal metastasis. References1 Assier H, Bastugigarin S, Revel J, Roujeau JC. Clinical classification of cases of Toxic epidermal necrolysis, Stevens-Johnson Syndrome. Arch Dermatol 1993; 129: 92-96. 2 Pereira FA, Mudgil AV, Rosmarin DM. Toxic epidermal necrolysis. J Am Acd Dermatol 2007; 56: 181-200. 3 Mockenhaupl M, Messenheimer J, Tennis P, Schlingmann J. Risk of Stevans-Johnson Syndrome and Toxic Epidermal Necrolysis in new users of antileptics. Neurology 2005; 64: 1134-1138. 4 Eaye O, Wechslor Roujeau JC. Cell-mediated immunologic mechanism and severity of TEN. Arch Dermatol 2005; 141: 775-776. 5 Mackie RM. Cutaneous Lymphomas and lymphocytic infiltrates. In: Rook A, Wilkinson DS, Ebling EJG, eds. Text book of Dermatology, 6th edn. Oxford Blackwell science, 1998: 2374-2382. 6 Miller RA, Coleman CN, Fawcett HD, Hoppe RT, McDougall IR. Sezary Syndrome: a model for migration of T Lymphocytes to the skin. N Eng J Med 1980; 303: 89-92. 7 Nikkels AJ, Sadzot-Delvaux C. Absence of intercellular adhesion molecule 1 expression in varicella zoster virus-infected keratinocytes during herpes zoster. Another immune evasion strategy? Am

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Cell-Mediated Immunologic Mechanism and Severity of TEN

Cited by 14 publications

References 16 publications

Clinical and Microscopic Characteristics of Canine Toxic Epidermal Necrolysis

Clinical and Microscopic Characteristics of Canine Toxic Epidermal Necrolysis

Toxic epidermal necrolysis

Herpes zoster virus associated ‘sparing phenomenon’: is it an innate possess of HZV or keratinocyte cytokine(s) mediated or combination?

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