Eosinophilic cystitis caused by Candida glabrata: A case report.

Eosinophilic cystitis is a rare disease of the bladder, for which there is no clear cause or standard treatment. We report the case of a 61 year old man who presented with irritative voiding symptoms and gross hematuria. Cystoscopy showed diffuse urothelial erythema and a posterior bladder wall ulcer. Bladder biopsy revealed marked eosinophilic cystitis with ulceration. Urine culture grew Candida glabrata. After treatment with oral fluconazole, his voiding symptoms resolved and subsequent bladder biopsy revealed a complete dearth of eosinophils. This is the first case report linking eosinophilic cystitis to Candida glabrata.

A case of ectopic dysplastic kidney and ectopic ureter diagnosed by MRI.

BACKGROUND: A 14-year-old girl with a solitary right kidney had continuous urinary incontinence. Four months previously she had undergone surgical resection of a vaginal septum associated with uterus didelphys, which was causing obstructed menstrual flow. She was toilet trained at the age of 2 years, had a normal voiding pattern, and had no history or family history of incontinence. INVESTIGATIONS: Pelvic examination, abdominal and pelvic ultrasonography, renal scintigraphy, voiding cystourethrography, abdominal and pelvic MRI, fluoroscopic retrograde vaginography, vaginoscopy, cystourethroscopy after administration of indigo carmine, laparoscopy, and pathologic examination of the excised specimen. DIAGNOSIS: Ectopic ureter draining into the vagina associated with a contralateral dysplastic kidney. MANAGEMENT: Laparoscopic nephrectomy of the left renal remnant and ligation of the left distal ureter.

Predicting blood loss and transfusion requirements during radical prostatectomy: the significant negative impact of increasing body mass index.

PURPOSE: Radical retropubic prostatectomy (RRP) has been associated with significant blood loss and/or transfusion requirement. While still a concern, routine autologous blood donation has not been standard at our institution for more than a decade. We assessed recent blood loss and transfusion requirements in contemporary patients undergoing RRP and examined the possible predictive impact of preoperative variables. MATERIALS AND METHODS: A retrospective review of 436 consecutive patients who underwent RRP between July 1999 and December 2001 was performed with the primary purpose of analyzing estimated blood loss (EBL) and blood transfusion requirements as well as possible preoperative risk factors, including clinical demographic characteristics, body mass index (BMI), defined as weight in kg/height in m, comorbidities, American Society of Anesthesiologists classification and Charlson index score. RESULTS: A total of 436 consecutive patients with a mean age of 60 years (range 39 to 78) underwent RRP under general anesthesia. Mean American Society of Anesthesiologists class was 2.3 (range 1 to 3) and the mean BMI was 27.7 (range 18.2 to 44.3). Mean preoperative and postoperative hematocrit was 43.9% and 32.5%, respectively. Overall mean EBL was 603 cc (range 100 to 3500) and the transfusion rate was 4.8%. On multivariate analysis the only significant correlative predictor of EBL was BMI. There was a significantly lower EBL in patients with an acceptable BMI (less than 25) vs overweight (25 to 30) and obese (greater than 30) patients (p = 0.021). Likewise the rate of transfusion was significantly higher in the overweight (6.9%) and obese (5.6%) groups compared to the normal BMI group (1.9%) (p = 0.009). CONCLUSIONS: Our series demonstrates that blood loss during RRP continues to decrease. The respectable blood loss and low transfusion rates in this series were due to refinements in surgical technique rather than to perioperative modifications. To our knowledge the identification of BMI as a predictor of blood loss and transfusion is novel. These data serve as a benchmark for future comparisons and argue for continued refinements in techniques to decrease blood loss, particularly in overweight and obese patients.

Ureteroneocystostomy without urethral catheterization shortens hospital stay without compromising postoperative success.

PURPOSE: We determine whether routinely performing catheterless ureteroneocystostomy would minimize hospital stays without compromising postoperative outcomes. MATERIALS AND METHODS: Between May 1996 and February 2002 patients who underwent ureteroneocystostomy at a single major tertiary care institution were identified. Patients who underwent additional, simultaneous surgical procedures were excluded from the study. Data recorded included patient demographics, reflux grade, use of a bladder catheter, length of hospital stay, medication use, postoperative complications and subsequent rehospitalization. RESULTS: Of the 300 patients included in the study 266 were girls and 34 were boys, with a median age of 4 years (range 3 months to 19 years). Reimplantation was bilateral in 215 cases and unilateral in 85. Reflux was grade I in 1% of cases, grade II in 18%, grade III in 47%, grade IV in 25% and grade V in 9%. Similar distributions were observed among the 76 patients who received bladder catheters and the 224 who did not. The average length of postoperative hospitalization for patients who received catheters compared to those who did not was 2.1 versus 1.4 days (p <0.001), and the rate of prolonged hospitalization are 18% versus 5%, respectively (p <0.01). Postoperative complication rates were 17% versus 8% (p <0.05) for patients who received catheters compared to those who did not. There was no statistically significant difference in the rate of rehospitalization whether urethral catheters were used (1.3% vs 4.9%, respectively, p = 0.07). Furthermore, there was no statistically significant difference in the amount of either ketorolac or oxybutynin used by patients who received catheters compared to those who did not. CONCLUSIONS: Surgical repair of vesicoureteral reflux via catheterless ureteroneocystostomy can reduce hospital stay without adversely affecting complication rates, rehospitalization rates and the amount of medications needed postoperatively.

Elements of the glucocorticoid and retinoic acid response units are involved in cAMP-mediated expression of the PEPCK gene.

Although many genes are regulated by the concerted action of several hormones, hormonal signaling to gene promoters has generally been studied one hormone at a time. The phosphoenolpyruvate carboxykinase (PEPCK) gene is a case in point. Transcription of this gene is induced by glucagon (acting by the second messenger, cAMP), glucocorticoids, and retinoic acid, and it is dominantly repressed by insulin. These hormonal responses require the presence of different hormone response units (HRUs), which consist of constellations of DNA elements and associated transcription factors. These include the glucocorticoid response unit (GRU), cAMP response unit (CRU), retinoic acid response unit (RARU), and the insulin response unit. HRUs are known to have functional overlap. In particular, the cAMP response element of the CRU is also a component of the GRU. The purpose of this study was to determine whether known GRU or RARU elements or transcription factors function as components of the CRU. We show here that the glucocorticoid accessory factor binding site 1 and glucocorticoid accessory factor binding site 3 elements, which are components of both the GRU and RARU, are an important part of the CRU. Furthermore, we find that the transcription factor, chicken ovalbumin upstream promoter-transcription factor, and two coactivators, cAMP response element-binding protein-binding protein and steroid receptor coactivator-1, participate in both the cAMP and glucocorticoid responses. This provides a further illustration of how the PEPCK gene promoter integrates different hormone responses through overlapping HRUs that utilize some of the same transcription factors and coactivators.

Insulin inhibits hepatocellular glucose production by utilizing liver-enriched transcriptional inhibitory protein to disrupt the association of CREB-binding protein and RNA polymerase II with the phosphoenolpyruvate carboxykinase gene promoter.

Hormones regulate glucose homeostasis, in part, by controlling the expression of gluconeogenic enzymes, such as phosphoenolpyruvate carboxykinase (PEPCK). Insulin and glucocorticoids reciprocally regulate PEPCK expression primarily at the level of gene transcription. We demonstrate here that glucocorticoids promote, whereas insulin disrupts, the association of CREB-binding protein (CBP) and RNA polymerase II with the hepatic PEPCK gene promoter in vivo. We also show that accessory factors, such as CCAAT/enhancer-binding protein beta (C/EBP beta), can recruit CBP to drive transcription. Insulin increases protein levels of liver-enriched transcriptional inhibitory protein (LIP), an inhibitory form of C/EBP beta, in a phosphatidylinositol 3-kinase-dependent manner. LIP concomitantly replaces liver-enriched transcriptional activator protein on the PEPCK gene promoter, which can abrogate the recruitment of CBP and polymerase II, culminating in the repression of PEPCK expression and the attenuation of hepatocellular glucose production.