Schistosomiasis-A Disobedient Ureter, a Disobedient Diagnosis.

Background: Schistosomiasis is rare in western countries, but remains a potentially serious disease. It is known to result in severe urogenital complications; prompt diagnosis can therefore significantly affect outcomes. Case Presentation: We report the case of a 41-year-old male with pleuritic chest pain and visible hematuria who had emigrated from Zimbabwe to the United Kingdom 20 years previously. CT imaging revealed a hydronephrotic right pelvicaliceal system, with a dilated ureter to its distal portion. Preliminary tests for schistosomiasis, including terminal urine microscopy and serology, were negative. An initial ureteroscopy was challenging owing to a tight ureteral stricture such that a retrograde stent insertion and not ureteroscopic visualization or biopsy was carried out. A relook ureteroscopy after 6 weeks revealed a dense distal ureteral stricture, biopsies were taken, the stricture was ablated with LASER, and a retrograde stent was placed. Microscopic examination of the biopsies confirmed Schistosomiasis haematobium. Treatment consisted of a divided dose of praziquantel and a reducing dose of steroids. At a third look ureteroscopy the stricture was ablated with LASER again, and the stent was removed. Subsequent renograms indicated recurrent obstruction despite LASER treatment and a retrograde ureteral stent was replaced. The patient ultimately had a Boari flap ureteral reimplant with good results. Conclusion: This case illustrates the clinical challenges of diagnosing and treating ureteral schistosomiasis. It shows that all the initial tests can be negative, but where the clinical picture points toward schistosomiasis it is worth persevering and a good tissue biopsy may be the only way to verify an otherwise elusive diagnosis.

A simple two-stage "bailout" technique for the removal of an unyielding ureteric stent.

OBJECTIVE: To describe a simple technique that can be used to manage an unexpected mildly to moderately (<10 mm) encrusted ureteric stent with consummate ease when time, equipment, or experience are unavailable. METHODS: We present a series of 5 patients with impacted ureteric stents that were difficult to remove owing to presumed encrustation of the upper end. The indwelling time for the stent ranged from 8 to 16 weeks. All 5 patients were managed by insertion of a second ureteric stent alongside the original one. RESULT: The encrusted stents were successfully retrieved in all 5 patients at a subsequent visit after the insertion of the second stent, without the need for further specialist equipment or expertise. CONCLUSION: Insertion of a second stent next to an unyielding, encrusted ureteric stent is a safe, simple, and effective technique to aid in its retrieval. We propose that it should be considered in select patients where encrustation is unexpected and an experienced endourologist is unavailable.

Intravesical instillation of mitomycin C: a cause of delayed bladder perforation?

We present a case of bladder perforation secondary to intravesical instillation of mitomycin C following transurethral resection of bladder tumour (TURBT) and the role of early detection leading to successful conservative management. We also review the key relevant literature.

beta-Actin regulates platelet nitric oxide synthase 3 activity through interaction with heat shock protein 90.

Cytoskeletal proteins are crucial in maintaining cellular structure and, in certain cell types, also play an essential role in motility and shape change. Nitric oxide (NO) is an important paracrine mediator of vascular and platelet function and is produced in the vasculature by the enzyme NO synthase type 3 (NOS-3). Here, we demonstrate in human platelets that the polymerization state of beta-actin crucially regulates the activation state of NOS-3, and hence NO formation, through altering its binding of heat shock protein 90 (Hsp90). We found that NOS-3 binds to the globular, but not the filamentous, form of beta-actin, and the affinity of NOS-3 for globular beta-actin is, in turn, increased by Hsp90. Formation of this ternary complex among NOS-3, globular beta-actin, and Hsp90, in turn, results in an increase in both NOS activity and cyclic guanosine-3',5'-monophosphate, an index of bioactive NO, as well as an increased rate of Hsp90 degradation, thus limiting the duration for which NOS-3 remains activated. These observations suggest that beta-actin plays a critical role in regulating NO formation and signaling in platelets.