A road map for the management of a pregnancy complicated by maternal bladder exstrophy.

Bladder exstrophy (BE) is a congenital genito-urinary malformation where there is a defect in the abdominal wall resulting in a protruding open bladder with exposed mucosa (Resnik R.P. et al. Creasy and Resnik's maternal-fetal medicine: principles and practice. Elsevier, 2019). Several reconstructive procedures are required to correct the anomalies, resulting in an ileal conduit which is an alternate urinary reservoir reconstructed from the terminal ileum (Madersbacher S, et al. J Urol 169(3):985-90, 2003). We describe the care of a pregnant woman with BE and outline the principles of management of her pregnancy with a multidisciplinary team. Timely pre-operative planning is advised to minimise intraoperative complications in the event of a caesarean section. The woman went on to have an uncomplicated classical caesarean section at term by midline laparotomy with a good outcome for both mother and baby.

Perioperative outcome of initial 190 cases of robot-assisted laparoscopic radical prostatectomy - A single-center experience.

OBJECTIVE: To analyze the perioperative outcome of the first 190 cases of robot-assisted laparoscopic radical prostatectomy performed at our center from July 2006 to December 2010. MATERIALS AND METHODS: Operative and recovery data for men with localized prostate cancer undergoing robot-assisted radical prostatectomy at our center were reviewed. All surgeries were performed using the 4-arm da Vinci-S surgical robot. Preoperative data included age, body mass index (BMI), prostate specific antigen (PSA) level, prostate weight, biopsy Gleason score and TNM staging, while operative and recovery data included total operative time, estimated blood loss, complications, hospital stay and catheter time. These parameters were evaluated for the safety and efficacy of this procedure in our center. RESULTS: The mean age of our patients was 65 ± 1.2 years. The mean BMI was 25.20 ± 2.88 and the median PSA was 14.8 ng/ml. Majority of our patients belonged to clinical stage T2 (51.58%). The mean total operative time was 166.44 ± 11.5 min. Six patients required conversion to open procedure and there was one rectal injury. The median estimated blood loss was 302 ± 14.45 ml and the median duration of hospital stay was 4 days. The overall margin positivity rate was 12.63%. CONCLUSION: Despite our limited robotic surgery experience, our perioperative outcome and complication rate is comparable to most contemporary series. Robot-assisted laparoscopic prostatectomy (RALP) is easy to learn and provides the patient with the benefits of minimally invasive surgery with minimal perioperative morbidity.

Correlation between the preoperative serum prostate specific antigen, Gleason score, and clinical staging with pathological outcome following robot-assisted radical prostatectomy: an Indian experience.

OBJECTIVES: To correlate the preoperative serum prostate specific antigen (PSA), Gleason score, and clinical staging with pathological outcome following robot-assisted radical prostatectomy (RARP) in Indian men with clinically localized cancer prostate. MATERIALS AND METHODS: A prospective study analysis was done for 166 consecutive patients of prostate cancer who underwent RARP at our center from June 2006 to October 2009. Preoperative workup included serum PSA, biopsy Gleason score, and clinical staging. The preoperative parameters were correlated with final Gleason score, capsular penetration, seminal vesicle involvement, and lymph node status on final histopathology. RESULTS: The mean age was 64 years (range: 50-76 years) with mean and median PSA of 17.98 ng/ml (range: 0.3-68.3 ng/ml) and 12.1 ng/ml, respectively. With increase in preoperative Gleason score, chance of organ confinement decreases (P=0.002) and capsular penetration increases (P=0.004) linearly. With increasing serum PSA, there is linear decrease in trend of organ-confined disease (P=0.03) and increased chances of seminal vesicle involvement (P=0.02). Patients with higher clinical stage have less probability of localized disease (P=0.007) and more chances of capsular penetration (P=0.04) and seminal vesicle involvement (P=0.004). CONCLUSION: Our data suggest that patients with higher preoperative serum PSA, Gleason score, and clinical stage have more chances of advanced pathological stage following RARP.

Pitfalls of subcapsular nephrectomy: report of a case with point of technique to avoid urinary fistula formation.

Nephrectomy after pyonephrosis, repeated acute pyelonephritis or chronic pyelonephritis is a challenge for any surgeon, owing to adhesions around the kidney. We encountered an unusual case of post-nephrectomy urinary fistula, as a complication of subcapsular nephrectomy. This occurred as a result of residual renal tissue after nephrectomy, which was subsequently excised using methylene blue as an aid to ensure complete excision. Such a complication has never been reported in existing literature. We reviewed the literature for any such related complications to gather an insight to its occurrence and also present a simple point of technique to avoid such a catastrophe.

Hyperparathyroidism induced by hypothyroidism.

The coexistence of hyperparathyroidism and thyroid tumors and/or chronic thyroiditis has raised the possibility of an etiologic relationship. The present study was designed to test the hypothesis that the chronic elevation of thyroid-stimulating hormone (TSH) is related to the development of hyperparathyroidism. Three groups of 24 rats each were treated for 12 weeks as follows: group 1 received propylthiouracil (PTU) in their deionized water; group 2 received PTU and thyroid hormone to suppress TSH and to serve as a control group for possible direct effects of PTU; and group 3 was not treated at all and served as another control group. At 12 weeks, 95% of group 1 rats (PTU only) showed hyperplasia of the parathyroids with a 30% mean increase in circulating parathormone.

High phosphate diet-induced primary hyperparathyroidism: an animal model.

Primary hyperparathyroidism (PHPT) is increasing in incidence and detection, primarily because of the aging of our population and the widespread use of automated serum calcium determination. As a result, a substantial number of "early" cases or "biochemical" PHPT are being detected. The indications for parathyroidectomy in such early cases of PHPT are currently under debate, primarily because of economic issues. These factors underscore the importance of research into the basic mechanisms and natural history of PHPT. We investigated an animal model of diet-induced PHPT that retains two crucial aspects of PHPT: elevation of endogenously produced parathyroid hormone (PTH), accompanied by gross and microscopic changes in the native parathyroid glands. Female Long-Evans rats were divided into six groups of 15 each and fed a control diet (Ca/P of 1:2) or a high-phosphate diet (Ca/P of 1:7) for 1-, 2-, or 3-month intervals. Compared with the control animals, serum PTH levels were elevated at all three time intervals in the experimental group, whereas serum calcium levels were decreased at all time intervals. Serum creatine levels were also elevated at all time intervals, whereas serum phosphorus levels did not change. Parathyroid histopathologic studies demonstrated no change at 1 month, whereas nine of 15 experimental animals showed mild hyperplasia at 2 months and 13 of 14 showed mild to moderate hyperplasia with gland enlargement at 3 months compared with control animals. Histopathologic examination of the kidneys showed no change at 1 month but focal parenchymal inflammation with calcium deposition at 2 and 3 months in the experimental groups. In conclusion, the high-phosphate diet successfully induced the earliest changes of PHPT: elevated PTH levels and parathyroid hyperplasia. However, because renal function was mildly compromised early on, some element of early secondary (renal) hyperparathyroidism may have supervened quickly. Because this model is simple, it may be useful to investigate this complex syndrome further, as well as its natural history and the complications it produces in other organs such as the kidneys.

Renal lesions in young rats induced by Salmonella enteritidis endotoxin.

Sepsis in newborns and infants is a major pediatric problem often associated with renal dysfunction. The present report deals with changes in renal tissue induced by Salmonella enteritidis endotoxin in 10- and 28-day-old Sprague-Dawley rats. Our studies revealed a 90% lethality within 24 h of 0.1 mg/kg and 35 mg/kg S. enteritidis endotoxin injection in 10- and 28-day-old rats, respectively. The 10- and 28-day-old animals received a single intraperitoneal injection of the 90% lethality dose and were sacrificed at different intervals for histopathological evaluation of kidneys by light and electron microscopy. The glomeruli showed visceral epithelial and endothelial cell swelling and polymorphonuclear leukocyte and platelet accumulation in the capillary lumina. Cortical and medullary tubules showed edematous separation, mild focal epithelial cell damage and focal intertubular hemorrhage. Renal sections of 28-day-old experimental rats showed increased numbers of polymorphs in the glomerulus and enlarged mesangial matrix. These sections also showed an increase in the number of hemorrhagic foci in 10 x field compared with the 10-day-old experimental rats. Endothelial cells of renal vasculature showed cytoplasmic swelling, vacuolization, autophagic vesicle formation and presence of secondary lysosomes. Changes in the endothelial cells of peritubular microvasculature were extensive, resulting in focal degeneration and partial loss of endothelial lining. These studies show that infant rats are extremely sensitive to S. enteritidis endotoxin requiring 1/350 the dose given to young adults to induce histopathological changes in kidney; the endothelial cells of microvasculature appear to be the primary targets of endotoxic injury irrespective of age.

Anatomical and functional effects of estrogen-induced prolactinomas on the rat hypothalamus.

Although estrogen-induced prolactinomas have been widely studied, little attention has been accorded to local pressure effects of the tumor on the hypothalamus and portal vasculature. To portray the magnitude of this phenomenon, four groups of 12-13-week-old female Fisher 344 rats were studied. Group 1 was an intact control receiving a subcutaneously (SC) placed placebo pellet; group 2 was an ovariectomized control with a SC placed placebo pellet; group 3 was ovariectomized with a 10 mg SC placed diethylstilbestrol (DES) pellet; and group 4 was ovariectomized receiving both 10 mg DES and 10 mg SC placed bromocriptine pellets. Blood samples were obtained at 4 weeks, and the animals were sacrificed at 8 weeks after pellet implantation at which time blood, pituitary and hypothalami were obtained. At 4 weeks serum prolactin levels were similarly and significantly elevated above the control groups in both the DES and DES/bromocriptine groups. By 8 weeks, however, serum prolactin level(s) in the DES-treated animals had tripled from the 4-week value, while levels in the DES/bromocriptine-treated animals were unchanged from the 4-week values. This finding matched the observation that the DES-treated animals had pituitaries 2.5-fold heavier than the DES/bromocriptine animals. The gross and histologic structure of the hypothalami and portal vessels were markedly disrupted in DES-treated rats and much less so in the DES/bromocriptine-treated group. These findings lead us to speculate that the pathogenesis of DES-induced prolactinomas proceeds in two phases: First, there is an early chemical induction phase in which estrogen directly and indirectly stimulates lactotrope proliferation and, second, a mechanical disinhibition phase, where tumor-induced destruction of the hypothalamus and portal vessels unleashes the pituitary from the dopaminergic restraining effects of the hypothalamus.

Microvascular endothelium: a major target site of endotoxin induced injury in 10 day old rat.

We have studied the effects of two endotoxins, S enteritidis and E coli on liver, pancreas, intestine, lung and kidney of 10 day old Sprague Dawley rat at light and electron microscope levels. One group of experimental animals (N = 31) received a single intraperitoneal injection of 0.1 mg/kg of S enteritidis endotoxin. The second experimental group (N = 34) received multiple intraperitoneal injections of 5 to 10 mg/kg of E coli endotoxin at 15 minute intervals over a period of 75 minutes. Within four hours of injections, histopathologic evaluation of all the tissues revealed interstitial edema, widening of blood capillary lumina, accumulation of polymorphonuclear leukocytes and platelets in capillary lumina and marked swelling, vacuolization and focal desquamation of endothelial cells in microvasculature. Hepatocytes showed loss of glycogen, vacuolization and degeneration in the centro-portal region. Islet cells of pancreas also revealed swelling and vacuolization. In the small intestine, hemorrhagic pools of blood were frequently seen in lamina propria and the apical portion of villi showed degeneration and breakdown. Lungs showed focal hemorrhage, collapse of alveolar architecture and swelling of endothelium in larger artereoles. Based on these studies, we suggest that endothelial cells of microvasculature in various tissues of 10 day old rat are extremely sensitive to endotoxins, irrespective of source, and cells derived from reticuloendothelial system may play an important role in the endotoxicosis.

Age related correlation between serum TSH and thyroid C cell hyperplasia in Long-Evans rats.

The purpose of the present investigation was to determine whether there is a correlation between the serum levels of thyroid stimulating hormone (TSH), parafollicular cell (C) population in the thyroid and calcitonin (CT) secretion in aging Long-Evans (L-E) rats. Serum TSH and CT values were determined in 50 male rats at ages 2, 6, 12, 18 and 24 months and 50 female rats at 18, 21 and 24 months. The animals were sacrificed at the end of the experiment to evaluate thyroid C cell pathology. Male rats showed an increase in the serum TSH values at 6 and 12 months of age, a decline at 18 months and a significant increase from 18 to 24 months of age. In female rats, a significant increase in serum TSH concentration was also noted from 18 to 24 months of age. In both sexes, 24 month old animals with thyroid C cell hyperplasia (CH+ group) had a significantly higher level of serum TSH as compared to animals with normal distribution of C cells (CH- group). Concentration of serum CT showed a progressive increase with age in both sexes. Male rats with thyroid C cell pathology had significantly higher levels of serum CT at 24 months of age as compared to rats with normal C cell distribution. In female rats, however, serum CT concentrations in two groups were not statistically significant. We conclude from these studies that in aged L-E rats, serum TSH concentration has an influence on thyroid C cell population.

Radioiodine sensitivity of parafollicular C cells in aged Long-Evans rats.

An earlier study from our laboratory demonstrated that the incidence of thyroid C cell neoplasia in aging Long-Evans rats was high. When radioactive iodine was administered to 8-week-old Long-Evans rats, this incidence was reduced, although thyroid follicular cell neoplasia was increased. The aim of this study was to determine whether iodine-131 (131I) administered to an aged population of Long-Evans rats with established C cell hyperplasia would have a C cell ablative effect as pronounced as that observed in studies of young rats. For this study, 180 18-month-old Long-Evans rats (90 male and 90 female) were used. Baseline serum calcitonin levels were determined, and control and experimental groups containing equal numbers of animals were designated. 131I was administered by intraperitoneal injection to the experimental group, while equal volumes of saline solution were given to the control group. Blood samples for determination of serum calcitonin levels were obtained at 6-week intervals until the rats were 24 months old. Thyroid glands were then removed, and tissues were fixed, sectioned, and stained with hematoxylin and eosin and with peroxidase-antiperoxidase (PAP) using an anticalcitonin antibody. Examination of thyroid tissues showed that the incidence of C cell neoplasia was significantly reduced in irradiated animals as compared with nonirradiated controls (chi 2 analysis, p less than 0.05). PAP staining demonstrated diminished intracytoplasmic calcitonin in the radiation-treated group. Analysis of serum calcitonin levels over time showed significantly lower levels in the irradiated rat group than in the nonirradiated group (p less than 0.006).

Testosterone enhancement of thyroid carcinoma in rats: the role of TSH.

Radiation treatment of Long-Evans male rats (40 mu Ci Na131I at the age of 2 months) led to a high incidence of thyroid follicular carcinomas at the age of 24 months; castration of males before irradiation caused a significant reduction in incidence of this tumor. In this study, replacement testosterone (T) was administered to castrated male rats by means of implanted, slow-release hormone-containing pellets (T-physiologic dose). Three testosterone doses (0.1T, 1.0T, and 30T) were used to treat groups of castrated irradiated and castrated nonirradiated rats from 2 to 18 months of age. The incidence of thyroid follicular carcinoma at 18 months in irradiated rats depended on the dose of replacement testosterone used. Tumor incidence was 8%, 14%, 41%, and 50% after treatment with 0T, 0.1T, 1.0T, and 30T, respectively. The incidence of thyroid follicular carcinoma in nonirradiated rats ranged from 0 to 7%. Mean serum thyroid-stimulating hormone (TSH) values in irradiated animal groups were elevated significantly above those for age-matched nonirradiated animals. The degree of TSH elevation in irradiated animals was related directly to the testosterone-replacement level. All rat groups showed age-dependent decreases in serum T4 levels, and T4 levels were also lowered by replacement testosterone in nonirradiated castrated animals. In aging irradiated animals, serum T4 levels were similarly decreased by testosterone, despite elevated TSH levels in these groups. In this study, testosterone appeared to act indirectly to promote development of irradiation-induced thyroid tumors by early and prolonged elevation of TSH levels.

Androgen-mediated development of irradiation-induced thyroid tumors in rats: dependence on animal age during interval of androgen replacement in castrated males.

When male Long-Evans rats at age 8 weeks were radiation treated (40 microCi Na131I), thyroid follicular adenomas and carcinomas were observed at age 24 months with a high incidence of 94%. Castration of males prior to irradiation significantly reduced this tumor incidence to 60%. When testosterone (T) was replaced in castrated, irradiated male rats, differentially increased incidences of thyroid tumors occurred, depending on the time interval for hormone replacement. Immediate (age 2-6 mo) or early (age 6-12 mo) T replacement at approximate physiologic levels led to thyroid follicular tumor incidences of 100 and 82%, respectively, whereas intermediate (12-18 mo) or late (18-24 mo) T treatment led to only 70 and 73% incidences, respectively. Continuous T replacement (2-24 mo) in castrated irradiated male rats raised thyroid tumor incidence to 100%. Since elevated thyroid-stimulating hormone (TSH) is a reported requisite for development of radiation-associated thyroid tumors, the effects of T on serum TSH levels were examined. Mean serum TSH values in all irradiated animal groups were significantly elevated above age-matched nonirradiated animals at 6, 12, 18, and 24 months. Serum TSH levels were higher in continuous T-replaced irradiated castrates than in intact, irradiated males, whereas such intact male TSH levels were greater than those for irradiated castrates without T treatment. Interval T replacement in castrated male rats was generally associated with increased serum TSH levels during the treatment interval and with lowered TSH levels after discontinuation of T treatment, particularly in irradiated rats. However, when irradiated, castrated males received late T replacement (age 18-24 mo), there was no elevation of TSH at the end of the treatment interval. Thus an indirect effect of T via early stimulation of TSH may be at least partly responsible for the high incidence of irradiation-induced thyroid tumors in rats.

Age effects on the reactivity of antistreptococcal cell membrane antisera to murine glomerular basement membrane. In vitro versus in vivo analysis.

Antisera to the streptococcal cell membrane (SCM) were evaluated for their reactivity to murine glomerular basement membrane (GBM) in four strains of mice. Animals were studied on a daily basis from birth through 3 months and weekly thereafter through 18 months. Paired animals were compared for in vivo binding of antibody versus an indirect fluorescent antibody technique on fresh kidney sections. The findings demonstrated a granular type GBM staining for all anti-SCM which were positive. Nonspecific background staining accompanied most of the indirect fluorescent antibody sections tested while being totally absent for the direct fluorescent test on tissue from in vivo challenge of the primary antibody. The in vitro testing showed tissue from young mice (0-6 days old) to be most reactive, while the strongest reactivity was seen in the age group of 10-20 days for in vivo testing. These cross-reactive antibodies, i.e., GBM-binding anti-SCM, are best evaluated by in vivo methods where tissue is taken 4 days after antiserum injection. Animals of the age range 6-8 weeks were often negative, indicating that this age range selected for many studies may not be the most favorable one via either in vitro or in vivo studies.

The role of visceral epithelial, endothelial and mesangial cells in the formation and turnover of glomerular basement membrane.

Incorporation of 3H-proline in the mouse kidney was studied by electron microscopic radioautography in a pulse-chase mode to establish the role of visceral epithelial, endothelial, and mesangial elements in the synthesis and turnover of glomerular basement membrane. Visceral epithelial and endothelial cells were found to play a significant role in the formation of glomerular basement membrane components, and turnover time for one of the components was found to be under 2 h. The synthesis of second component is slow and make take 8-24 h. The mesangial cells appear to play a significant role in the reabsorption of the component with a faster turnover rate.