Can higher doses of oxybutynin improve efficacy in neurogenic bladder? 2004

Nelson Bennett, and Margie O'Leary, and Ankur S Patel, and Macrina Xavier, and Janet R Erickson, and Michael B Chancellor
Department of Urology, University of Pittsburgh School of Medicine, Pennsylvania 15213, USA.

OBJECTIVE We evaluated the efficacy and tolerability of higher dose oxybutynin chloride in patients with neurogenic bladder and multiple sclerosis, spinal cord injury or Parkinson's disease. METHODS The study design was a prospective, 12-week dose titration trial of controlled release oxybutynin (OXY-XL). A 7-day washout period was used before initiation of the starting dose of 10 mg OXY-XL. Doses of OXY-XL were increased by 5 mg at weekly intervals to a maximum dose of 30 mg per day guided by patient perception of efficacy versus side effect. Voiding diaries were completed at baseline, and weeks 6 and 12. Post-void residuals were recorded. Criteria for study admission included post-void residual less than 200 ml. RESULTS Of the 39 patients enrolled in the study 22 had multiple sclerosis, 10 had spinal cord injury and 7 had Parkinson's disease. There were 29 women (74%) and 10 men (26%). Within 1 week a decrease in the number of voids per day was seen in greater than 50% of the subjects. At the end of the study statistically significant decreases in the number of voids in 24 hours, episodes of nocturia and incontinence episodes were observed. Residual urine remained unchanged from 33.9 +/- 7.6 ml at baseline to 51.3 +/- 10.4 ml after 12 weeks at the final dose (p = 0.17). No patient experienced serious adverse events and none dropped out during the course of the 12-week study. At the end of the study 20.5% of subjects remained on 30 mg, 15.4% on 25 mg, 23.1% on 20 mg, 15.4% on 15 mg and 25.6% on 10 mg OXY-XL. CONCLUSIONS Aggressive dosing of OXY-XL is safe and effective in patients with neurogenic bladder. Compared with nonneurogenic overactive bladder, higher doses of OXY-XL (15 mg daily or greater) were requested by 74.4% of the patients in our study. The onset of clinical efficacy can occur within 1 week, and doses up to 30 mg are well tolerated and effective in this population.

UI MeSH Term Description Entries
D008297 Male Males
D008333 Mandelic Acids Analogs or derivatives of mandelic acid (alpha-hydroxybenzeneacetic acid). Acids, Mandelic
D008875 Middle Aged An adult aged 45 - 64 years. Middle Age
D011446 Prospective Studies Observation of a population for a sufficient number of persons over a sufficient number of years to generate incidence or mortality rates subsequent to the selection of the study group. Prospective Study,Studies, Prospective,Study, Prospective
D001750 Urinary Bladder, Neurogenic Dysfunction of the URINARY BLADDER due to disease of the central or peripheral nervous system pathways involved in the control of URINATION. This is often associated with SPINAL CORD DISEASES, but may also be caused by BRAIN DISEASES or PERIPHERAL NERVE DISEASES. Bladder Disorder, Neurogenic,Neurogenic Bladder,Bladder Neurogenesis,Bladder, Neurogenic,Neurogenic Bladder Disorder,Neurogenic Bladder, Atonic,Neurogenic Bladder, Spastic,Neurogenic Bladder, Uninhibited,Neurogenic Dysfunction of the Urinary Bladder,Neurogenic Urinary Bladder Disorder,Neurogenic Urinary Bladder, Atonic,Neurogenic Urinary Bladder, Spastic,Neurogenic Urinary Bladder, Uninhibited,Neuropathic Bladder,Urinary Bladder Disorder, Neurogenic,Urinary Bladder Neurogenesis,Urinary Bladder Neurogenic Dysfunction,Atonic Neurogenic Bladder,Neurogenesis, Bladder,Neurogenesis, Urinary Bladder,Neurogenic Bladder Disorders,Neurogenic Urinary Bladder,Spastic Neurogenic Bladder,Uninhibited Neurogenic Bladder
D005260 Female Females
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000328 Adult A person having attained full growth or maturity. Adults are of 19 through 44 years of age. For a person between 19 and 24 years of age, YOUNG ADULT is available. Adults
D018727 Muscarinic Antagonists Drugs that bind to but do not activate MUSCARINIC RECEPTORS, thereby blocking the actions of endogenous ACETYLCHOLINE or exogenous agonists. Muscarinic antagonists have widespread effects including actions on the iris and ciliary muscle of the eye, the heart and blood vessels, secretions of the respiratory tract, GI system, and salivary glands, GI motility, urinary bladder tone, and the central nervous system. Antimuscarinic,Antimuscarinic Agent,Antimuscarinic Agents,Cholinergic Muscarinic Antagonist,Muscarinic Antagonist,Antimuscarinics,Cholinergic Muscarinic Antagonists,Agent, Antimuscarinic,Agents, Antimuscarinic,Antagonist, Cholinergic Muscarinic,Antagonist, Muscarinic,Antagonists, Cholinergic Muscarinic,Antagonists, Muscarinic,Muscarinic Antagonist, Cholinergic,Muscarinic Antagonists, Cholinergic

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