Bladder outlet obstruction accelerates bladder carcinogenesis

Abstract

OBJECTIVE To examine the correlation between partial bladder outlet obstruction (PBOO) and bladder carcinogenesis. MATERIALS AND METHODS Female Wistar rats (6 weeks old) were divided into three groups of 10 each: group 1 was exposed to n‐butyl‐n‐butanol nitrosamine (BBN, a carcinogen) in drinking water for 8 weeks; group 2 had PBOO induced surgically after exposure to BBN for 8 weeks; group 3 had a sham operation and the rats drank normal water (control group). After 20 weeks, all of the rats were killed humanely and their bladders analysed. RESULTS There were no significant differences in body weight among the groups. The bladder weight of group 2 was significantly greater than either group 1 or group 3. Histopathologically, bladder smooth muscle hypertrophy was the major cause of the increased bladder weight for group 2. In group 2 there were increases in bladder wall thickness and many nipple‐shaped urothelial tumours. Basic fibroblast growth factor and hypoxia‐inducible factor‐1α expression were significantly greater in group 2 than in groups 1 and 3. CONCLUSIONS Exposure of the bladder to carcinogens during bladder hyperplasia and hypertrophy induced by PBOO results in a greater incidence of superficial bladder carcinoma.

Impact of post‐void residual urine volume on intravesical recurrence after nephroureterectomy for upper urinary tract urothelial carcinoma

“…Third, obstruction also mediates mucosal and detrusor ischemia, which in turn generates potentially carcinogenic free radicals. 4,[15][16][17][18] As mentioned above, the present study results can be explained by the presence of a residual urine volume causing carcinogen exposure of the inflamed mucosal membrane. Additionally, no significant difference was found between a residual urine volume of 30-59 and ≥60 mL.…”

“…1,2 Sazuka et al investigated the association between post-void residual urinary volume and IVR after RNU, and concluded that the presence of residual urine (defined as ≥30 mL) might be a hotbed of IVR. 4 Although the definition of "presence" of a post-void residual volume of 30 mL requires further investigation, their findings showed that non-severe residual volumes are associated with a higher risk of IVR after RNU. Also, their observation raises the new question of whether this observation can apply to a patient with non-muscle invasive bladder cancer who underwent transurethral resection of the bladder tumor.…”

“…3 In a rat model, exposure of the bladder to carcinogens after induction of bladder hyperplasia and hypertrophy by partial bladder outlet obstruction resulted in a greater incidence of superficial bladder carcinoma. 4 Thus, LUTS might have an association with bladder cancer. One of the reasons for the high incidence of a subsequent tumor is the implantation of tumor cells on the altered urothelial surface after surgery.…”

Benign prostatic hyperplasia is a significant risk factor for bladder cancer in diabetic patients: a population-based cohort study using the National Health Insurance in Taiwan

“…Such a hypothesis is strongly supported by the animal study by Matsumoto et al because bladder cancer induced by the carcinogen n-butyl-n-butanol nitrosamine may also be aggravated by surgically induced bladder outlet obstruction in female Wistar rats [4]. Another circumstantial evidence supporting the hypothesis in humans came from prospective [31] and case–control [32] studies showing that high fluid intake, indicating less concentrated urine or more frequent micturition, was associated with a lower risk of bladder cancer.…”

“…An animal study conducted in female Wistar rats supported such a hypothesis. Matsumoto et al found that surgically induced partial bladder outlet obstruction resulted in a greater incidence of bladder cancer induced by the carcinogen n-butyl-n-butanol nitrosamine [4]. …”