Objective

To better understand parental beliefs regarding the etiology and treatment of nocturnal enuresis (NE).

Methods

A self-administered survey queried parental NE beliefs including perceived etiologies and home behavioral treatments. We assessed for associations between demographic characteristics and propensity to seek medical care for NE.

Results

Of 216 respondents, 78% were female. The most common causes for NE reported were: deep sleeper (56%), unknown (39%), and laziness (26%). Popular home behavioral therapies included: void prior to sleep (77%) and limiting fluid intake at night (71%). Few reported they would use a bedwetting alarm (6%). Fifty-five percent reported they would seek medical care for NE and 28% reported awareness of effective treatments. On multivariable analysis, females (OR 2.3, 95% CI 1.04-5.0) and those with graduate level education (OR 4.8, 95% CI 1.5-15.7) were more likely to seek medical care for their child with NE.

Conclusions

General parental knowledge of the causes and effective treatments for NE is lacking. Only 55% reported they would seek medical care for their child with NE and only 28% reported awareness of effective treatments. Counseling should focus on dispelling common misconceptions about causes and treatments of NE and focus on proven effective treatments.

We report the first case of post-cryotherapy salvage radical prostatectomy for local recurrence performed laparoscopically with the da Vinci robot. Total operative time was 210 minutes and blood loss was 50ml. There were no intraoperative or postoperative complications. The hospital stay was 24 hours and the Foley catheter was removed on postoperative day 7. The patient achieved a pad free status 4 weeks postoperatively. Pathology showed extensive disease, pT3bN0, Gleason score of 5+3 and positive margins. The patient continued on complete androgen deprivation therapy and his follow up PSA at 10 months was <0.1. Further studies are needed to evaluate both functional and oncological results with this approach.

Patients undergoing radical prostatectomy are at increased risk of development of post-operative inguinal hernias (IH). We present the largest series of transperitoneal combined robotic-assisted laparoscopic prostatectomy (RALP) and IH. After IRB approval, data from patients undergoing RALP at two centers were prospectively entered into a database and analyzed. IH were repaired robotically via a transperitoneal route with mesh. Between June 2002 and May 2007, 837 RALPs were performed, 80 of which included combined IH repair (9.6%), by two surgeons, T.A. and D.S. Forty-two patients (52.5%) had IH on pre-operative exam. Twenty-four hernias were left, 32 right, and 24 bilateral. Twenty-two patients had prior ipsilateral or contralateral herniorrhaphy. After dissection of the hernia sac, a swatch of flat Marlex mesh (n = 22), a polypropylene mesh plug (n = 19), an Ultrapro hernia system (n = 7), a Proceed coated mesh (n = 19), a 3D-Max (n = 37), a combination of both umbrella and flat mesh (n = 3), or suture alone (n = 2) was used. Inguinal herniorrhaphy added approximately 15 min of operative time in all cases. There was one hernia recurrence over an average follow-up period of 12.5 months (0.2-52 months). There was one complication attributable to IH repair-a urine leak which was attributed to anastomotic stretch due to reperitonealization. Urological surgeons should perform a thorough inguinal exam during preoperative evaluation and intraoperatively to detect subclinical inguinal hernias. Inguinal herniorrhaphy at the time of RALP is safe and should be routinely performed.

The objective of this study was to perform a comprehensive morphologic analysis of developing mouse external genitalia (ExG) and to determine specific sexual differentiation features that are responsive to androgens or estrogens. To eliminate sex steroid signaling postnatally, male and female mice were gonadectomized on the day of birth, and then injected intraperitoneally every other day with DES (200 ng/g), DHT (1 μg/g), or oil. On day-10 postnatal male and female ExG were dissected, fixed, embedded, serially sectioned and analyzed. We identified 10 sexually dimorphic anatomical features indicative of normal penile and clitoral differentiation in intact mice. Several (but not all) penile features were impaired or abolished as a result of neonatal castration. Those penile features remaining after neonatal castration were completely abolished with attendant clitoral development in androgen receptor (AR) mutant male mice (X(Tfm)/Y and X/Y AR-null) in which AR signaling is absent both pre- and postnatally. Administration of DHT to neonatally castrated males restored development of all 10 masculine features to almost normal levels. Neonatal ovariectomy of female mice had little effect on clitoral development, whereas treatment of ovariectomized female mice with DHT induced partial masculinization of the clitoris. Administration of DES to neonatally gonadectomized male and female mice elicited a spectrum of development abnormalities. These studies demonstrate that the presence or absence of androgen prenatally specifies penile versus clitoral identity. Differentiated penile features emerge postnatally and are sensitive to and dependent upon prenatal or pre- and postnatal androgen. Emergence of differentiated clitoral features occurs postnatally in either intact or ovariectomized females. It is likely that each penile and clitoral feature has a unique time-course of hormonal dependency/sensitivity.

The effect of neonatal exposure to diethylstilbestrol (DES), a potent synthetic estrogen, was examined to evaluate whether the CD-1 (estrogen insensitive, outbred) and C57 (estrogen sensitive, inbred) mouse strains differ in their response to estrogen disruption of male ExG differentiation. CD-1 and C57BL/6 litters were injected with sesame oil or DES (200 ng/g/5 μl in sesame oil vehicle) every other day from birth to day 10. Animals were sacrificed at the following time points: birth, 5, 10 and 60 days postnatal. Neonatally DES-treated mice from both strains had many ExG abnormalities that included the following: (a) severe truncation of the prepuce and glans penis, (b) an abnormal urethral meatus, (c) ventral tethering of the penis, (d) reduced os penis length and glans width, (e) impaired differentiation of cartilage, (f) absence of urethral flaps, and (g) impaired differentiation of erectile bodies. Adverse effects of DES correlated with the expression of estrogen receptors within the affected tissues. While the effects of DES were similar in the more estrogen-sensitive C57BL/6 mice versus the less estrogen-sensitive CD-1 mice, the severity of DES effects was consistently greater in C57BL/6 mice. We suggest that many of the effects of DES, including the induction of hypospadias, are due to impaired growth and tissue fusion events during development.

Potential trans-generational influence of diethylstilbestrol (DES) exposure emerged with reports of effects in grandchildren of DES-treated pregnant women and of reproductive tract tumors in offspring of mice exposed in utero to DES. Accordingly, we examined the trans-generational influence of DES on development of external genitalia (ExG) and compared effects of in utero DES exposure in CD-1 and C57BL/6 mice injected with oil or DES every other day from gestational days 12 to 18. Mice were examined at birth, and on 5-120 days postnatal to evaluate ExG malformations. Of 23 adult (>60 days) prenatally DES-exposed males, features indicative of urethral meatal hypospadias (see text for definitions) ranged from 18% to 100% in prenatally DES-exposed CD-1 males and 31% to 100% in prenatally DES-exposed C57BL/6 males. Thus, the strains differed only slightly in the incidence of male urethral hypospadias. Ninety-one percent of DES-exposed CD-1 females and 100% of DES-exposed C57BL/6 females had urethral-vaginal fistula. All DES-exposed CD-1 and C57BL/6 females lacked an os clitoris. None of the prenatally oil-treated CD-1 and C57BL/6 male and female mice had ExG malformations. For the second-generation study, 10 adult CD-1 males and females, from oil- and DES-exposed groups, respectively, were paired with untreated CD-1 mice for 30 days, and their offspring evaluated for ExG malformations. None of the F1 DES-treated females were fertile. Nine of 10 prenatally DES-exposed CD-1 males sired offspring with untreated females, producing 55 male and 42 female pups. Of the F2 DES-lineage adult males, 20% had exposed urethral flaps, a criterion of urethral meatal hypospadias. Five of 42 (11.9%) F2 DES lineage females had urethral-vaginal fistula. In contrast, all F2 oil-lineage males and all oil-lineage females were normal. Thus, prenatal DES exposure induces malformations of ExG in both sexes and strains of mice, and certain malformations are transmitted to the second-generation.