Banovic F, Olivry T, Bazzle L, Tobias J R, Atlee B, Zabel S, Hensel N, Linder K E
Department of Clinical Sciences, NC State University, College of Veterinary Medicine, Raleigh, NC, USA Center for Comparative Medicine and Translational Research, NC State University, College of Veterinary Medicine, Raleigh, NC, USA.
Department of Clinical Sciences, NC State University, College of Veterinary Medicine, Raleigh, NC, USA.
Vet Pathol. 2015 Mar;52(2):321-30. doi: 10.1177/0300985814537530. Epub 2014 Jun 6.
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.
犬中毒性表皮坏死松解症（TEN）是一种罕见且危及生命的皮肤药物反应，传统上被描述为表皮全层坏死，真皮炎症轻微；然而，很少有报告详细描述其组织学发现。我们对3例犬TEN患者的临床特征和组织学变化进行了描述。临床上，不规则的红斑和紫癜斑演变为广泛且严重疼痛的糜烂。糜烂黏膜的数量各不相同；然而，眼周和唇周黏膜皮肤交界处经常受累。对17例活检标本中的13例进行了评估。多个表皮层面的凋亡是表皮坏死最常见的模式（13例活检中有12例，92%）。相比之下，全层凝固性坏死较少见（13例活检中有7例，52%）。淋巴细胞界面性皮炎是主要的炎症模式，所有样本中均存在一定程度的表皮内淋巴细胞，以及较少的组织细胞，同时伴有凋亡角质形成细胞的淋巴细胞卫星现象。变化顺序表明淋巴细胞介导的角质形成细胞凋亡是病变发展的早期步骤，随后患者进展为凝固性坏死的情况有所不同。组织病理学变化与多形红斑报道的情况重叠，这与犬TEN的传统组织学描述不同。对每位患者应用了一种评估表皮坏死松解症药物因果关系评分的特定算法（ALDEN）；卡洛芬与1只犬的可能因果关系评分相关。应鼓励临床医生在疑似TEN的病例中进行多次活检，因为几乎25%的活检标本缺乏上皮组织，无法诊断。
