Intravesical Bacillus Calmette-Guerin Cystitis

Abstract

Intravesical BCG is known to significantly reduce superficial bladder cancer recurrence and progression rates, and as such has become a standard adjuvant treatment in medium and high-risk disease. It is however known that only 16% of patients are able to tolerate the full 36-month schedule, and the reasons for cessation are often due to local and systemic side effects. This review aims to look at ways to reduce local toxicity (and increase compliance) and the evidence base behind various strategies. The magnitude and level of evidence for all methods employed to try to reduce toxicity is scant. Reducing the amount of BCG in contact with the urothelium has been tried both by reducing dwell time and using lower (1/3) dose regimes. There is no oncological data to support or refute the use of a shorter dwell time, and furthermore, there is no evidence that reducing the dose has any effect on local side effect profiles. Good practice guidelines have been written to ensure BCG is administered in a way that reduces local side effects as much as possible; however, local toxicity is still common. Other approaches used to decrease BCG toxicity include oral anticholinergic use, anti-tuberculous chemotherapy, quinolone antibiotics, oral pentosan polysulphate as well as intravesical instillations. The oncological outcomes of using these adjuncts are largely unreported. Although it is usually self-limiting, BCG cystitis has important implications for patients, as it is the most common reason for cessation of BCG therapy. Despite the frequency with which it occurs, the treatment options for BCG cystitis are very limited and not backed up by high level evidence. More research is needed into the oncological outcomes of adjuvant therapies that appear to have good symptomatic benefit.