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Review |
From the UCSF Children's Hospital, Department of Urology, University of California, San Francisco, California.
| Correspondence to: Laurence S. Baskin, MD, Chief, Pediatric Urology, Professor Urology and Pediatrics, UCSF Children's Hospital, University of California, San Francisco, 400 Parnassus Avenue A640, San Francisco, CA 94143 (e-mail: lbaskin{at}urology.ucsf.edu). |
Hypospadias is one of the most common congenital anomalies in the United
States, occurring in approximately 1 in 125 live male births. Embryological
studies have demonstrated that, depending on where the urethral development
arrests, the meatal opening can be anywhere along the shaft of the penis or,
in more severe forms, within the scrotum or in the perineum. Currently, the
only available treatment is surgery. If left uncorrected, especially in its
severe form, there is risk of infertility and psychological effects, such as
avoidance of intimate relationships. The cause of hypospadias is largely
unknown; however, current epidemiology and laboratory studies have shed new
light into the etiology of hypospadias. With recent advancements in molecular
biology and microarray technology, it appears that hypospadias is potentially
related to disrupted gene expression. Specifically, some of the environmental
chemicals are acting as antiandrogens and interfere directly with the action
of testosterone-related gene expression. In this paper, we briefly review the
normal development of male external genitalia and the prevalence and
environmental risk factors related to hypospadias. In addition, we discuss
some of the recent laboratory findings that contribute to our current
understanding of this disease.
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