Delabie J, De Wolf-Peeters C, Mooren M, Karien K, Roskams T, Desmet V
Department of Pathology, University Hospital, Leuven, Belgium.
Br J Dermatol. 1991 Apr;124(4):348-53. doi: 10.1111/j.1365-2133.1991.tb00595.x.
The histological features of biopsies from 18 previously unreported cases of Sweet's syndrome are reported. The dermal infiltrate in the majority of the cases contained numerous histiocytes that at first sight appeared to mimic neutrophils. The immunophenotype of these histiocytes was consistent with monocytes that have freshly infiltrated into the lesions. Only two of the cases in this series, associated with leukaemia, displayed the histological features of Sweet's syndrome with a predominant neutrophilic infiltration. We suggest that the initiating mechanisms in Sweet's syndrome are that monocyte/histiocyte-derived cytokines such as the interleukins IL-1 and IL-8, secreted either by infiltrating histiocytes in the non-leukaemia-associated cases of Sweet's syndrome or by tumoural myelomonocytic cells in those associated with leukaemia, are responsible for the systemic manifestations and the infiltration with neutrophils in the skin lesions.
报告了18例此前未报道的Sweet综合征活检组织的组织学特征。大多数病例的真皮浸润中有大量组织细胞，乍一看似乎类似中性粒细胞。这些组织细胞的免疫表型与刚浸润到病变中的单核细胞一致。该系列中只有两例与白血病相关，表现出Sweet综合征以嗜中性粒细胞为主的浸润的组织学特征。我们认为，Sweet综合征的起始机制是单核细胞/组织细胞衍生的细胞因子，如白细胞介素IL-1和IL-8，在Sweet综合征非白血病相关病例中由浸润的组织细胞分泌，或在白血病相关病例中由肿瘤性骨髓单核细胞分泌，它们导致了全身表现以及皮肤病变中的中性粒细胞浸润。
