Trospium Chloride in the Treatment of Overactive Bladder

In: Main

5 May 2010

Trospium ChlorideINTRODUCTION

Overactive bladder (OAB) is a symptom syndrome that refers to the layered, smooth muscle that surrounds the bladder, the detrusor muscle. This muscle contracts spastically, sometimes without a known cause, resulting in sustained, high bladder pressure and the urgent need to urinate. People with OAB often experience urgency at inconvenient and unpredictable times. This urgency can interfere with daily routines, intimacy, and sexual function, all of which can lead to embarrassment, low self-esteem, and a diminished quality of life.

OAB affects men and women equally. Of an estimated 33.3 million adults in the U.S., 12.2 million have incontinence and 21.2 million do not.

Tolterodine tartrate (Pharmacia) and oxybutynin chloride (Ortho-McNeil) are anticholiner-gic drugs that are currently used for the treatment of OAB. Both of these drugs are potent, competitive antimuscarinic receptor antagonists. However, the need for compounds that are as effective at relieving symptoms of OAB as these, but with fewer unpleasant side effects, has triggered the development of a new anticholinergic agent, trospium chloride (Sanctura™, Indevus/Odyssey).

The Food and Drug Administration (FDA) approved trospium, an anti-spasmodic, antimuscarinic agent, in May 2004 for the treatment of OAB with symptoms of urge urinary incontinence, urgency, and urinary frequency. Key factors that characterize the older agents (and oxybutynin) include extensive metabolism via the CYP-450 system and the formation of pharmacologically active metabolites, thus increasing the likelihood of metabolic drug interactions.

Table 1 Mean (± SD) Pharmacokinetic Parameters in Healthy Subjects Receiving a Single 20-mg Dose of Trospium Chloride

Cmax

AUC0_.

Tmax

Tl/2

(ng/ml)

(ng/ml • hour)

(hour)

(hour)

3.5 ± 4.0

36.4 ±21.8

5.3 ± 1.2

18.3 ± 3.2

Crosses the blood-brain barrier, inducing distinct central nervous system (CNS) effects and thereby affecting patients’ daily routines; in contrast, tolterodine canadian and trospium lack distinct CNS effects, suggesting that they both act primarily in the periphery. In doses of 20 mg twice daily, trospium has demonstrated a better risk-benefit profile for long-term therapy than 5-mg, twice-daily doses of oxybutynin canadian.

ETIOLOGY

For proper urination to take place, the urinary tract and brain must work cohesively to control and initiate the process. The slight need to void urine is stimulated when the urine volume reaches about one-half of the bladder’s capacity. The need to void urine is suppressed by the brain until a person initiates micturition.

Normally, when urination has been initiated, the CNS signals the detrusor muscle to contract into a “V” shape and expel urine. As the pressure in the bladder increases, the detrusor muscle remains contracted until the bladder empties. Upon emptying, pressure falls, and the bladder relaxes and returns to its normal muscle tone. However, people with OAB experience a malfunctioning de-trusor muscle, resulting in spastic and uncontrollable urination.

OAB is not a disease state; it is a symptom associated with the following underlying conditions:

  • nerve damage caused by abdominal trauma, pelvic trauma, or surgery
  • bladder stones
  • adverse drug effects (ADEs)
  • neurological disease (e.g., multiple sclerosis, Parkinson’s disease, stroke, or spinal cord lesions)
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Another condition that produces symptoms similar to those experienced with OAB is a urinary tract infection (UTI), which most commonly occurs in women.


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