title: Treatment outcomes according to neuropathic bladder sphincter dysfunction type after treatment of oxybutynin chloride in children with myelodysplasia.
abstract: OBJECTIVE
  We investigated the treatment outcomes according to neuropathic bladder sphincter dysfunction (NBSD) type after oral oxybutynin (OBT) treatment in children with NBSD caused by myelodysplasia.
  
  
  METHODS
  Among 334 pediatric patients who were diagnosed with NBSD caused by myelodysplasia, only children treated with oral OBT for more than 1 year with pre- and post-treatment urodynamic studies and dimercaptosuccinic acid (DMSA) were retrospectively reviewed. We compared pre- and post-treatment urodynamic parameters including maximum cystometric capacity (MCC), MCC/estimated bladder capacity (EBC), and compliance by NBSD type in children. We also compared renal scarring on pre- and post-treatment DMSA by NBSD type in children.
  
  
  RESULTS
  Our study population was comprised of 81 children (45 boys and 36 girls), with a mean age of 4.2 ± 3.4 years. The mean follow-up duration was 4.5 (range 1.0-15.1) years. After OBT treatment, MCC was increased significantly in all types of NBSD from 110.3 ± 62.2 to 202.3 ± 103.9 ml (p < 0.05), compliance was significantly improved from 6.4 ± 6.1 to 11.1 ± 9.6 ml/cmH2O (p < 0.05), but MCC/EBC was slightly decreased from 75.2 ± 46.9 to 69.8 ± 33.3 % (p = 0.40). Sub-analyzed by NBSD type, the pre-treatment compliance of children with acontractile detrusor with spastic sphincter (n = 16) was markedly decreased compared with other types of NBSD. Acontractile detrusor with spastic sphincter demonstrated the worst renal deterioration on DMSA.
  
  
  CONCLUSIONS
  Although increases in MCC/EBC were limited, oral OBT treatment markedly improved MCC and compliance in all NBSD types. Children who had acontractile detrusor with spastic sphincter had a relatively high probability of renal deterioration and required specific attention.
authors.affiliation: Department of Urology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
authors.forename: Minki
authors.initials: M
authors.lastname: Baek
authors.forename: Jung Yoon
authors.initials: JY
authors.lastname: Kang
authors.forename: Jeongyun
authors.initials: J
authors.lastname: Jeong
authors.forename: Dae Kyung
authors.initials: DK
authors.lastname: Kim
authors.forename: Kwang Myung
authors.initials: KM
authors.lastname: Kim
mesh_terms: D000284:Administration, Oral; D002675:Child, Preschool; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008333:Mandelic Acids / Q000008:administration & dosage*; D018727:Muscarinic Antagonists / Q000008:administration & dosage; D009436:Neural Tube Defects / Q000150:complications*; D012189:Retrospective Studies; D013997:Time Factors; D016896:Treatment Outcome; D001750:Urinary Bladder, Neurogenic / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D014563:Urodynamics
chemical_list: D008333:Mandelic Acids; D018727:Muscarinic Antagonists; C005419:oxybutynin
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