Lebbé Céleste, Legendre Christophe, Francès Camille
Service de Dermatologie, APHP Hôpital Saint Louis, University Paris VII, 1 av Claude Vellefaux 75010 Paris, France.
Transplant Rev (Orlando). 2008 Oct;22(4):252-61. doi: 10.1016/j.trre.2008.05.004. Epub 2008 Jul 24.
Kaposi sarcoma (KS) is a multicentric neoplasm of lymphatic endothelium derived cells infected with Kaposi's human herpesvirus 8 (HHV8). Post-transplant KS can lead to multifocal, progressive (florid) lesions with frequent primary involvement of the oral mucosa and dissemination to the viscera. KS prevalence after organ transplantation varies greatly depending on the prevalence of HHV8 infection in the general population. Most cases of post-transplant KS develop as a result of viral reactivation. Immunohistochemistry using a monoclonal antibody against HHV8 latent nuclear antigen on paraffin embedded sections, although less sensitive than polymerase chain reaction, is useful for pathological diagnosis of difficult angiogenic proliferations. Although HHV8 viral load in peripheral blood mononuclear cells of KS individuals correlates with tumor burden, due to low interval variations this test cannot be used in clinical practice to monitor KS patients nor to predict the occurrence of KS in transplant recipients. The main objectives of KS treatment is to control disease progression and relieve symptoms, as opposed to achieving complete tumor remission. The cornerstone in treatment of post-transplant KS is to taper down immunosuppressive regimens to the lowest possible level, while attempting to keep the allograft functional. Specific local or, less frequently, systemic treatment modalities can be used such as chemotheraphy. Other therapeutic strategies could rely in targeting signaling pathways important for HHV8 de novo infection, reaction, cell persistence or cellular pathways activated by viral pirated genes such as the mitogen-activated protein kinase or the PI3 kinase pathway. Rapamycin, a mammalian target of rapamycin inhibitor located downstream the PI3 kinase, has already proven of benefit and should be discussed in all post-transplant KS.
卡波西肉瘤（KS）是一种由感染卡波西人疱疹病毒8型（HHV8）的淋巴内皮衍生细胞形成的多中心肿瘤。移植后KS可导致多灶性、进行性（ florid）病变，口腔黏膜常为首发受累部位，并可播散至内脏。器官移植后KS的患病率因普通人群中HHV8感染率的不同而有很大差异。大多数移植后KS病例是病毒重新激活所致。在石蜡包埋切片上使用抗HHV8潜伏核抗原的单克隆抗体进行免疫组织化学检测，虽然不如聚合酶链反应敏感，但对诊断困难的血管生成性增殖病变很有用。虽然KS患者外周血单个核细胞中的HHV8病毒载量与肿瘤负荷相关，但由于其变化区间较小，该检测在临床实践中不能用于监测KS患者，也不能预测移植受者KS的发生。KS治疗的主要目标是控制疾病进展和缓解症状，而非实现肿瘤完全缓解。移植后KS治疗的基石是将免疫抑制方案逐渐减至尽可能低的水平，同时努力保持移植物功能。可采用特定的局部治疗或较少见的全身治疗方式，如化疗。其他治疗策略可针对对HHV8初次感染、反应、细胞持续存在或由病毒窃取基因激活的细胞途径（如丝裂原活化蛋白激酶或PI3激酶途径）重要的信号通路。雷帕霉素是一种位于PI3激酶下游的雷帕霉素靶蛋白抑制剂，已被证明有益，应在所有移植后KS病例中进行讨论。
