Pakran Jaheersha, George Mamatha, Riyaz Najeeba, Arakkal Riyaz, George Sandhya, Rajan Uma, Khader Anza, Thomas Sumi, Abdurahman Rahima, Sasidharanpillai Saritha, Thumbayil Lekha
Department of Dermatology, Calicut Medical College, Calicut, Kerala, India.
Int J Dermatol. 2011 Jan;50(1):61-9. doi: 10.1111/j.1365-4632.2010.04644.x.
Chikungunya (CHIK) is an emerging viral disease with a myriad of cutaneous manifestations.
The aim of our study was to document the morphology and evolution of skin lesions in cases presenting with fever, purpuric macules and vesiculobullous lesions, to confirm its causative relationship with CHIK, and to investigate further in order to delineate possible mechanisms of bulla formation in these cases.
A prospective, descriptive hospital-based study was carried out at a tertiary health care centre in Kerala. A total of 10 patients were enrolled in the study and investigated.
All cases had morbilliform eruption prior to onset of purpuric macules. Eight cases developed vesiculobullous lesions that arose either de novo or over a part or whole of the purpuric macules. Skin lesions resolved within an average of 7.6 days leaving post-inflammatory hypopigmentation. IgM CHIK enzyme-linked immunosorbent assay (ELISA) was positive in all 10 patients. Tzanck smear from the bullae showed lymphocytes in most cases along with acantholytic cells, necrotic keratinocytes or occasional neutrophils. Skin biopsy showed intraepidermal or subepidermal bullae. Immunohistochemistry revealed predominantly CD8 positive T lymphocytes in the infiltrate. The prognosis was good with supportive management alone.
The clinical features in our cases are comparable to the 3 previous reports of vesiculobullous lesions in CHIK affected infants. Based on the current evidence, we hypothesize that at least 2 mechanisms are at play for these skin lesions; CHIK virus induced keratinocyte necrosis followed by a cytotoxic immune response, and possible modulation of rash by drugs.
With severe epidemics of CHIK spreading from Asia and Africa to the Western hemisphere, we must consider bullous CHIK as a differential diagnosis in cases with fever and purpuric and vesiculobullous lesions.
基孔肯雅热（CHIK）是一种新出现的病毒性疾病，有多种皮肤表现。
我们研究的目的是记录出现发热、紫癜性斑疹和水疱大疱性皮损病例的皮肤损害形态及演变过程，确认其与基孔肯雅热的因果关系，并进一步研究以阐明这些病例中水疱形成的可能机制。
在喀拉拉邦的一家三级医疗保健中心开展了一项前瞻性、基于医院的描述性研究。共有10例患者纳入研究并接受调查。
所有病例在紫癜性斑疹出现之前均有麻疹样皮疹。8例出现水疱大疱性皮损，这些皮损要么是新发的，要么出现在部分或全部紫癜性斑疹上。皮肤损害平均在7.6天内消退，留有炎症后色素减退。10例患者的基孔肯雅热IgM酶联免疫吸附试验（ELISA）均为阳性。水疱的Tzanck涂片在大多数病例中显示淋巴细胞，同时伴有棘层松解细胞、坏死角质形成细胞或偶尔的中性粒细胞。皮肤活检显示表皮内或表皮下水疱。免疫组织化学显示浸润中主要为CD8阳性T淋巴细胞。仅通过支持治疗，预后良好。
我们病例中的临床特征与之前关于基孔肯雅热感染婴儿水疱大疱性皮损的3份报告相似。基于目前的证据，我们推测这些皮肤损害至少有2种机制在起作用；基孔肯雅热病毒诱导角质形成细胞坏死，随后引发细胞毒性免疫反应，以及药物可能对皮疹产生的调节作用。
随着基孔肯雅热的严重疫情从亚洲和非洲蔓延到西半球，对于出现发热、紫癜性和水疱大疱性皮损的病例，我们必须将大疱性基孔肯雅热作为鉴别诊断考虑。
