Berry A, Iriart X, Fillaux J, Magnaval J-F
Service de parasitologie-mycologie, CHU Toulouse, France.
Centre de physiopathologie de Toulouse Purpan, INSERM UMR 1043 / CNRS UMR 5282 Université Toulouse 3, Toulouse, France.
Bull Soc Pathol Exot. 2017 Feb;110(1):68-75. doi: 10.1007/s13149-017-0547-4. Epub 2017 Feb 10.
The existence of a link between urinary schistosomiasis (US) and bladder carcinoma was first suspected by C. Goebel in 1905. In 1911, A.R Ferguson, who was a professor of Pathology and Microbiology at the Faculty of Medicine in Cairo, published a more detailed survey from 40 autopsies, and reported a likely association of bladder carcinoma with granulomas caused by US. Subsequently, published results from several studies reinforced Ferguson's hypothesis. Moreover, in most countries where US was endemic, association of high prevalence of bladder carcinoma with US had been pointed out. A further circumstantial evidence was a higher prevalence of bladder squamous cell carcinoma in areas endemic for SU, whereas urothelial carcinomas were more prevalent in areas which were free of SU. However, evidence of a positive correlation between SU and bladder carcinoma was delivered only many decades later, following the results from case-control studies which were adjusted on age, sex, type of dwelling and tobacco consumption. During SU, the mechanisms underlying the onset of bladder carcinoma are still poorly understood due to the lack of any convenient animal model. Classically, two processes are thought to be involved. Chronic inflammation inside bladder would be caused by granulomas centered by eggs, and would result in a neoplasmic evolution, after years. Moreover, alteration of the bladder dynamics would elicit urine stasis which in turn would cause repeated infection of bacterial or viral origin. Beside the high prevalence of squamous cell type, the natural history of bladder carcinomas caused by SU is similar to that of other malignant tumors of the bladder. Also the treatment and prognosis are identical. Albeit genital involvement is very frequent during SU, Schistosoma haematobium does not appear to be a cause of cancers of genital organs. Schistosoma mansoni and S. japonicum have been suspected to be associated with liver or colic carcinomas, but epidemiological studies have not yielded any firm evidence so far. The entire sequencing of S. haematobium genome, along with the recent availability of a more efficient mouse model, must provide a better understanding of the genesis of bladder carcinomas during SU. However, the key for a sharp decrease in both morbidity and mortality due to SU-linked carcinomas lies in a better control of haematobium schistosomiasis, such as observed in Egypt since 1970.
1905年,C. 戈贝尔首次怀疑尿路血吸虫病(US)与膀胱癌之间存在联系。1911年,开罗医学院病理学和微生物学教授A.R. 弗格森发表了一份基于40例尸检的更详细调查报告,报告指出膀胱癌可能与US引起的肉芽肿有关。随后,多项研究发表的结果强化了弗格森的假设。此外,在大多数US流行的国家,都指出了膀胱癌高发病率与US之间的关联。另一个间接证据是,在SU流行地区,膀胱鳞状细胞癌的发病率较高,而在无SU的地区,尿路上皮癌更为普遍。然而,在对年龄、性别、居住类型和烟草消费进行调整的病例对照研究得出结果之后,又过了几十年才找到了SU与膀胱癌之间存在正相关的证据。在SU期间,由于缺乏合适的动物模型,膀胱癌发病的潜在机制仍知之甚少。传统上认为涉及两个过程。膀胱内的慢性炎症由以虫卵为中心的肉芽肿引起,经过数年,会导致肿瘤演变。此外,膀胱动力学改变会引发尿液淤积,进而导致细菌或病毒源性的反复感染。除了鳞状细胞类型的高发病率外,SU引起的膀胱癌的自然史与膀胱其他恶性肿瘤相似。治疗和预后也相同。尽管在SU期间生殖器受累非常常见,但埃及血吸虫似乎不是生殖器器官癌症的病因。曼氏血吸虫和日本血吸虫曾被怀疑与肝癌或结肠癌有关,但迄今为止,流行病学研究尚未得出任何确凿证据。埃及血吸虫基因组的全序列测定,以及最近更有效的小鼠模型的出现,必将有助于更好地了解SU期间膀胱癌的发生机制。然而,要大幅降低SU相关癌症的发病率和死亡率,关键在于更好地控制血吸虫病,就像自1970年以来在埃及所观察到的那样。