Wahman A, Melnick S L, Rhame F S, Potter J D
Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis 55454-1015.
Epidemiol Rev. 1991;13:178-99. doi: 10.1093/oxfordjournals.epirev.a036068.
The etiology of Kaposi's sarcoma remains somewhat obscure. While lesions of classic Kaposi's sarcoma, African Kaposi's sarcoma, and immunosuppressed Kaposi's sarcoma have been found to be indistinguishable from one another, the reasons for the variations in type and severity have not been established. The origin of the spindle cell is yet to be agreed on. Geographic variation does not seem as important as ethnic variation. The very young and the very old, perhaps two ages of weakened immunity, tend to have a higher incidence of Kaposi's sarcoma. Children and AIDS patients tend to develop more virulent disease. Males tend to get Kaposi's sarcoma at higher rates than do females. Jewish and Mediterranean males have the highest incidence of classic Kaposi's sarcoma, and African Bantu have the highest incidence of African Kaposi's sarcoma, classifications which do not apply to the Kaposi's sarcoma population in the United States. Male homosexuals have much higher incidence of Kaposi's sarcoma than do male heterosexuals, but since the early 1980s, its incidence as the presenting manifestation of AIDS has decreased dramatically. There is no unequivocal association with HLA haplotype (though DR5 carriers may be at especially high risk) or evidence of family clustering. There is an impressive but not always consistent association between Kaposi's sarcoma development and immunodeficiency. Environmental factors, such as nitrite use, immunosuppression, and repeated cytomegalovirus infection, are associated with Kaposi's sarcoma, but the exact mechanism is unclear and the associations remain inconsistent. Finally, it is still unclear if there is a causative infectious agent for Kaposi's sarcoma. While cytomegalovirus has been linked to Kaposi's sarcoma, there are weaknesses in its hypothetical role as an etiologic agent as is the case for HIV itself.(ABSTRACT TRUNCATED AT 400 WORDS)
卡波西肉瘤的病因仍有些不明。虽然已发现经典型卡波西肉瘤、非洲型卡波西肉瘤和免疫抑制相关型卡波西肉瘤的病变彼此难以区分，但类型和严重程度差异的原因尚未明确。梭形细胞的起源也尚无定论。地理差异似乎不如种族差异重要。非常年轻和非常年老的人群，可能是两个免疫功能较弱的年龄段，卡波西肉瘤的发病率往往较高。儿童和艾滋病患者往往会患上更具侵袭性的疾病。男性患卡波西肉瘤的几率高于女性。犹太男性和地中海地区男性经典型卡波西肉瘤的发病率最高，非洲班图人非洲型卡波西肉瘤的发病率最高，这些分类并不适用于美国的卡波西肉瘤人群。男性同性恋者患卡波西肉瘤的几率比男性异性恋者高得多，但自20世纪80年代初以来，其作为艾滋病首发表现的发病率已大幅下降。与人类白细胞抗原单倍型没有明确关联（尽管携带DR5的人可能风险特别高），也没有家族聚集的证据。卡波西肉瘤的发生与免疫缺陷之间存在显著但并非始终一致的关联。环境因素，如亚硝酸盐的使用、免疫抑制和反复的巨细胞病毒感染，与卡波西肉瘤有关，但确切机制尚不清楚，且这些关联并不一致。最后，卡波西肉瘤是否存在致病感染因子仍不清楚。虽然巨细胞病毒已与卡波西肉瘤相关联，但其作为病因的假设作用存在缺陷，就像HIV本身一样。（摘要截选至400字）
