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Overactive Bladder Disease

Overactive bladder (OAB) disease is a common urban illness. A telephone survey (respondents aged between 40 and 79) conducted by Hong Kong Urological Association in 2009 found that about one in every seven respondents was suffering from this disease, and about 50% of the patients did not have the knowledge of OAB disease. It is thus clear that the public still don’t have adequate understanding of its symptoms and treatment.1


Moreover, there is a widespread fallacy that overactive bladder disease targets only females and the aged. On the contrary, it can happen to people of any age and gender, even a child. In general, the risk for females is slightly higher than that for males at the relatively young age of around 40. However, the risk for males aged 70 or above is higher than that for females because aged males are believed to be particularly vulnerable to other urological conditions such as benign prostatic hyperplasia (BPH) and thus are more prone to secondary overactive bladder disease. “Secondary OAB disease” refers to the occurrence of symptoms similar to the symptoms of overactive bladder disease but due to other causes, e.g. bladder outlet obstruction, neurogenic damage and benign prostatic hyperplasia (in men only).


Overactive bladder disease relates to the improper storage function of the bladder with unknown cause. A normal healthy bladder is able to store approximately 300-500ml but there will be a desire to void when the bladder is filled up with about 250-300ml. However, for the bladder of overactive bladder disease, abrupt involuntary muscle contraction may occur from only small volume of urine, increasing bladder pressure and provoking a strong and sudden urge to void. In this case, the patient feels strong urinary urgency or a non-stoppable need for an instant restroom visit. If the condition is severe, the patient may not be able to hold the flow and result in incontinence.


The pharmacological oral treatment for OAB disease is mainly anti-cholinergic drugs which inhibit abnormal detrusor muscle contraction of the urinary bladder in order to relieve the OAB symptoms; side effects include dry mouth and blurry vision, etc. Unlike the traditional types of drugs, the new version of anti-cholinergic agents such as solifenacin, however, relatively target on influencing the detrusor muscle with less side effects whereby they inhibit abnormal contraction of the detrusor muscle and effectively reduce the daily episodes of sudden urinary urgency, frequency and involuntary leakage to alleviate the symptoms and improve the storage function of the bladder. With relatively lesser side effects, the new agents are more tolerable to patients and can reduce discontinuing medication due to side effects. Thus, the progress of treatment will not be tampered.


In addition, a new class of drug, β3-adrenoceptor agonist (such as mirabegron), is also a recent alternative treatment for OAB disease. It effectively relaxes detrusor muscle and enhances the storage function of the bladder. Due to the difference in drug mechanism and its receptor selectivity of β3-adrenoceptor agonist from anticholinergics, side effects such as dry mouth are drastically minimized. It is a new breakthrough in this field in the past three decades.2


Oral medication continues to be the priority treatment for overactive bladder disease by reason of its safety and efficacy. If the condition worsens or a patient does not respond to the drug prescribed, an alternative therapy such as botulinum A toxin injection into the bladder, may be considered. Assisted by endoscopy, physicians perform botulinum A toxin injection instead of surgery, with outstanding results. However, no comprehensive data on the effects of this new treatment are available, but in any event, it appears to be effective for only six months after which a second dose is required. It may therefore be applied only to persons with severe symptoms or those who do not respond to oral medication.



1. Report of overactive bladder survey conducted by Hong Kong Urological Association in 2009.
2.Chapple CR, et al. Neurourol Urodyn. 2014 ;33(1):17–30.


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