Augmentation Cystoplasty: Risks for Malignancy and Suggestions for Follow-Up Evaluations

The realization that neoplasia could develop as a consequence of urologic reconstructive procedures first became evident with ureterosigmoidostomy in the 1970s [1, 2]. Specifically, long-term follow-up of patients following ureterosigmoidostomy revealed that approximately 3 % of the patients per decade developed adenocarcinoma of the colon, with another 5 % per decade developing benign adenomatous colonic polyps [1–3]. Interestingly, the site of the malignant lesions and/or adenomatous polyps almost inevitably occurred either at or adjacent to the ureteroenteric anastomosis [1–4]. At that time, it was hypothesized that the development of the neoplastic lesions were dependent on the enteric epithelium employed (colon > ileum), and resulted from chronic inflammation incited by the production of nitrosamines, a known carcinogen, produced from the bacterial breakdown of the fecal, urinary slurry [1–4]. Due to the association of the ureterosigmoidostomy with malignant transformation, the procedure was largely abandoned by the early 1980s. In its place surgeons turned to the alternatives of enteric bladder augmentation or continent urinary reservoirs, surgical procedures that were believed to be free of the risk of carcinogenesis. The reduced risk for carcinogenesis was based on two important assumptions; the absence of the fecal, urinary slurry would prevent the production of nitrosamines and the reliance on ileum as the first choice for use as the enteric component for urologic reconstructive procedures [4–6]. Concern, that this hypothesis was in error arose with the reported development of adenocarcinoma in patients augmented for the contracted bladders arising from tuberculosis and schistosomiasis [5–9]. These random case reports prompted an alternative hypothesis that it was not the chronic inflammatory response arising from the fecal, urinary slurry, but rather, the inflammatory response that is inevitably associated with all forms of urologic reconstructive procedures that would lead to malignant transformation. In particular, it was hypothesized that either the presence of chronic bacteriuria, urine infiltrating into the enteric wall, and or mixed cellular interactions from the juxtaposition of tissues from two disparate origins (intestinal and urothelial) would lead to mutagenic sequence. In essence, the presence of chronic inflammation resulted in the production of toxic oxygen radicals, DNA mutagenesis, and cancer [2, 5–7, 10–14]. This hypothesis appeared to be substantiated when several case reports of malignancy following augmentation for congenital etiologies were published [5, 6, 13, 15–18]. The compilation of the case reports revealed that malignancies in the augmented bladder began to develop about a decade after augmentation, presented at a high stage and were associated with poor cancer-specific survival [5, 6, 13, 15–18]. These findings prompted the recommendation that all individuals who had undergone a bladder augmentation, continent urinary reservoir, or enteric neobladder formation for benign urologic conditions, should undergo annual endoscopic and cytologic evaluation beginning 10 years after their surgery. Indeed, concern by some authorities in the field reached high enough levels; they recommended intermittent biopsy of the reconstructed bladder at the time of surveillance [5, 7, 15, 19–22].