1/449. Intravesicular formaldehyde instillation and renal complications. Intravesicular formaldehyde has been used for intractable hemorrhagic cystitis since the late 1960's. Initial reports described few complications, but in the 1970's both ureteral as well renal parenchymal damage were reported in the urology literature. This has been less appreciated by nephrologists perhaps related to the paucity of reports in the nephrology literature. Although the pathogenesis has not been rigorously studied ureteral toxicity may be secondary to intense edema, inflammation and subsequent fibrosis induced by the formaldehyde; while renal tubular injury may be secondary to systemic absorption of formaldehyde. Ureteral reflux as well as dosage of intravesicular formaldehyde seem to be risk factors for acute renal failure. We describe a case of acute renal failure secondary to intravesicular formaldehyde and review pathogenesis as well as potential prophylactic measures to prevent this complication. ( info) |
2/449. Encrusted cystitis: aetiology, clinical aspects and management. Encrusted cystitis is a rare condition characterised by the formation of calcified plaques adherent to or embedded in the bladder mucosa. Although chronic infection with urea-splitting organisms is a prerequisite, other factors seem to play an important role in its development. We report our experience of 4 such cases in which encrusted cystitis presented with various symptoms, produced different pathological abnormalities and was treated by different means in each patient. ( info) |
3/449. Pelvic lipomatosis associated with proliferative cystitis: case report and review of the Japanese literature. PURPOSE: We report only the second known patient with pelvic lipomatosis associated with proliferative cystitis in the Japanese literature, a 43-year-old mildly obese Japanese male who demonstrated radiographic findings characteristic of pelvic lipomatosis. methods: Cystourethrography revealed an elevated pear-shaped bladder and an elongated and anteriorly displaced prostatic urethra. Computed tomography demonstrated excess intrapelvic fat that exhibited a density identical to that of subcutaneous fat tissue. Cystoscopic and histologic examination revealed concomitant proliferative cystitis composed of von Brunn's nest, cystitis cystica and cystitis glandularis, but no malignant cells. RESULTS/CONCLUSIONS: As a result of dietary control for 15 months, the proliferative cystitis improved mildly, but the amount of fat was unchanged. ( info) |
4/449. Gangrenous cystitis: a rare cause of colovesical fistula. A case of gangrenous cystitis presenting as a colovesical fistula in an elderly woman is described. The literature on this rare condition is reviewed. ( info) |
| We report a case of vesical tubulovillous adenoma that occurred in a background of protracted chronic cystitis with intestinal-type glandular metaplasia and extensive cellular atypia (dysplasia) in the flat mucosa. flow cytometry analysis showed dna aneuploidy in the adenoma. Increased expression of the tumor suppresser gene, p53, and also of cellular proliferation markers (proliferating cell nuclear antigen and MIB-1) were detected in the villous adenoma and in the dysplastic regions of the flat metaplastic mucosa. These findings provide insight into the biology of intestinal metaplasia and also lend support to the theory of the chronic irritation-metaplasia-dysplasia-carcinoma sequence. ( info) |
6/449. Pediatric inflammatory bladder tumors: myofibroblastic and eosinophilic subtypes. PURPOSE: Benign bladder tumors are rare in children. A number of descriptive terms have previously been used to describe inflammatory tumors with myofibroblastic proliferation or eosinophilic infiltration. We present our experience with these tumors and review the literature. MATERIALS AND methods: We retrospectively reviewed the records of all children presenting with a benign focal bladder mass during the last 5 years, including 2 girls and 3 boys 2 to 12 years old (mean age 7). RESULTS: Presenting symptomatology included irritative voiding symptoms, suprapubic pain and hematuria. All bladder masses were diagnosed by ultrasonography and all patients underwent transurethral resection. Three children who had an inflammatory bladder tumor with myofibroblastic features required open tumor excision with preservation of the bladder. In the 2 remaining children urine culture was positive preoperatively and the diagnosis was an inflammatory bladder tumor with eosinophilic infiltration. Transurethral resection of the mass was performed without partial cystectomy. CONCLUSIONS: Inflammatory myofibroblastic and eosinophilic tumors represent forms of focal cystitis with a tumefactive component. Differentiation from the malignant bladder neoplasms of childhood has important consequences for therapy. Management of these benign but aggressive inflammatory lesions involves local control by endoscopic or open surgery with bladder preservation. We encourage refined use of the terminology for inflammatory myofibroblastic and eosinophilic tumors. ( info) |
| OBJECTIVE: The purpose of this study was to evaluate the incidence, diagnostic criteria and treatment of eosinophilic cystitis (EC) in denmark during the period 1989-94. MATERIAL AND methods: A questionnaire was sent to all Danish departments of surgery, urology and pathology. RESULTS: Fifty-six cases of EC were diagnosed in the departments of surgery and urology, and 135 patients were diagnosed in the departments of pathology. The therapy was most often steroid instillation in the bladder or peroral antihistamines. Success rates of treatment were reported to be acceptable. CONCLUSION: The questionnaire confirmed that EC is a rare disease, which is often confused with other bladder diseases. We recommend strict histological criteria combined with clinical information when making the diagnosis of EC. Therapy is generally symptomatic. A diagnostic code number from the Danish health Board is needed. ( info) |
8/449. Haemorrhagic cystitis associated with adenovirus in a patient with AIDS treated for a non-Hodgkin's lymphoma. Adenovirus-induced haemorrhagic cystitis has been reported chiefly in bone marrow or kidney transplant recipients. We report here on an hiv-positive patient treated for a Burkitt's lymphoma who developed gross haematuria associated with fever and burning urination. Usual causes of haematuria were ruled out: lithiasis, urinary tract lesions, glomerulonephritis, mycobacterium and schistosoma infections, and drug toxicity. Adenovirus was detected by cellular cultures and BK/jc virus dna sequences were detected using a polymerase chain reaction method. Because BK/JC virus shedding is very common (75%) in hiv patients receiving chemotherapy, our data strongly suggest that adenovirus was responsible for the haemorrhagic cystitis in our patient. In conclusion, adenovirus should be considered as a potential cause of haemorrhagic cystitis in AIDS patients whose immunosuppression is aggravated by cytotoxic drugs. ( info) |
9/449. Tiaprofenic acid-induced cystitis--three cases and a literature review. Tiaprofenic acid is a non-steroidal anti-inflammatory drug that may cause severe non-bacterial cystitis. Three cases are described and the literature is reviewed. ( info) |
| OBJECTIVE: Hemorrhagic cystitis is a well-known complication of cyclophosphamide therapy but extensive involvement of the entire urinary tract is far less common. We report here a patient who developed severe hemorrhagic pyelitis, ureteritis, and cystitis after one cycle of cyclophosphamide-containing combination chemotherapy. METHOD: A patient with synchronous carcinoma of the ovary and the uterus developed severe hemorrhagic pyelitis, ureteritis, and cystitis leading to bilateral hydronephroses and acute renal failure after one cycle of combination chemotherapy containing cyclophosphamide. The blood clots in the upper urinary tract were aspirated endoscopically and bilateral internal ureteric stents were inserted. RESULT: She underwent a prolonged diuretic phase with several episodes of hypokalemia, hypomagnesemia, and hypocalcemia and required intensive fluid and electrolytes replacement. Subsequently, she recovered fully with the ureteric stents removed 26 days later. CONCLUSION: In contrast to previous reports, where 2.8 g of cyclophosphamide was estimated to be the minimum cumulative dose required to cause hemorrhagic cystitis, this case illustrates that severe hemorrhagic complication can occur even after a low dose of cyclophosphamide (600 mg/m(2), total dose of 846 mg). Prompt diagnosis and intervention may be life-saving. ( info) |