Familial transmission of urogenital prolapse and incontinence.
OBJECTIVE
To summarize recent evidence suggesting a genetic basis for the development of urogenital prolapse and stress urinary incontinence.


RESULTS
Epidemiological evidence suggests that some women have a genetic predisposition to the development of urogenital prolapse and stress incontinence. Abnormal expression of various structural proteins is thought to be the molecular genetic mechanism for the development of these conditions. A group of families with an autosomal dominant pattern of transmission of urogenital prolapse with high penetrance has been identified. No similar cohort of families with familial stress incontinence currently exists, although candidate genes have been identified that appear to predispose women to urogenital prolapse and stress incontinence. Additionally, animal models of urogenital prolapse have been developed that closely parallel the development of prolapse in humans.


CONCLUSIONS
A growing body of evidence suggests a genetic basis for the development of urogenital prolapse and stress incontinence. Candidate genes have been identified that may result in alteration of the normal metabolism of various structural proteins which may ultimately predispose some women to both urogenital prolapse and stress incontinence. Further research into the genetic basis of these conditions may provide a comprehensive understanding of the biological basis of these disorders.
Twiss
Christian
C
Department of Urology, University of California, Los Angeles, California , USA. ctwiss@mednet.ucla.edu
Triaca
Veronica
V
Rodríguez
Larissa V
LV
D000818:Animals; D015331:Cohort Studies; D005192:Family Health; D005260:Female; D005799:Genes, Dominant; D020022:Genetic Predisposition to Disease; D006801:Humans; D051379:Mice; D018345:Mice, Knockout; D008957:Models, Genetic; D011300:Preoperative Care; D012307:Risk Factors; D001745:Urinary Bladder Diseases / Q000175:diagnosis* / Q000235:genetics* / Q000628:therapy; D014596:Uterine Prolapse / Q000175:diagnosis* / Q000235:genetics* / Q000628:therapy