Obstructive sleep apnea syndrome is associated with overactive bladder and urgency incontinence in men.

STUDY OBJECTIVE: To investigate the incidence of overactive bladder (OAB) and urgency incontinence (UI) in men with obstructive sleep apnea syndrome (OSAS). DESIGN: Prospective questionnaire study SETTING: Saarland University Hospital PATIENTS: All male patients who underwent full-night in-laboratory polysomnography between November 2006 and April 2007. INTERVENTIONS: Overactive bladder symptom score (OABSS) and International Consultation on Incontinence Questionnaire, Short-Form (ICIQ-SF). MEASUREMENTS AND RESULTS: OSAS severity was assessed according to the apnea-hypopnea-index (AHI). Return rate of questionnaires was 100% (n=100). Patients with upper airway resistance syndrome (UARS) served as controls. Evaluation of OABSS revealed that patients with moderate and severe OSAS presented with a significantly higher incidence of symptoms of OAB than patients with mild OSAS and UARS (P<0.05). Further, the ICIQ-SF revealed a higher occurrence of UI in patients with severe OSAS than in those with mild OSAS and UARS (P<.05). CONCLUSIONS: Increasing severity of OSAS appears to be associated with an increasing occurrence of overactive bladder and urgency incontinence in men. This relationship may have clinical implications for the treatment of affected patients.

The relationship between sleep apnea and overactive bladder.

Approximately 4% to 5% of middle-aged men are affected by obstructive sleep apnea (OSA) syndrome, which is known to cause urologic disorders, cardiovascular diseases, and an increased risk of stroke. The correlation between OSA, erectile dysfunction, and nocturia is well known; a recent study demonstrated the association between overactive bladder and urgency incontinence. This article discusses the current literature and therapeutic options, as well as our own experiences and consequences for affected patients.

Nephrectomy, work bench surgery, and autotransplantation: a case of a solitary left kidney with an extensive centrally located renal cell carcinoma and a tumour thrombus entering the vena cava.

OBJECTIVES: In patients with imperative indication, organ preserving kidney tumour surgery is state of the art. We present our management of an extensive centrally located renal cell carcinoma. METHODS: The patient was suffering from a 8x6x6cm centrally located tumour in the solitary left kidney which infiltrated the lower pole of the kidney, the hilum and built a large tumour thrombus entering the vena cava inferior. We performed a radical nephrectomy with cavotomy, tumour trombectomy and tumour resection in cold ischemia at the work bench (R0). RESULTS: Total ischemic time took 4 h, warm ischemic time 60 min. The pathological tumour stage was pT3b, pN0, R0. During 17 mo of aftercare, the patient was free of metastatic disease and without complaints (serum creatinine actually 1.6 mg/dl). CONCLUSIONS: Hemodialysis reduces the quality of life for 30-40%, the mean mortality rate on hemodialysis is 13% per patient year. To prevend patients from hemodialysis, nephrectomy, work bench surgery and autotransplantation, even in large centrally located tumours and multimorbid patients should be considered to maintain quality and to extend expectancy of life.

Binding of Escherichia coli hemolysin and activation of the target cells is not receptor-dependent.

Production of a single cysteine substitution mutant, S177C, allowed Escherichia coli hemolysin (HlyA) to be radioactively labeled with tritiated N-ethylmaleimide without affecting biological activity. It thus became possible to study the binding characteristics of HlyA as well as of toxin mutants in which one or both acylation sites were deleted. All toxins bound to erythrocytes and granulocytes in a nonsaturable manner. Only wild-type toxin and the lytic monoacylated mutant stimulated production of superoxide anions in granulocytes. An oxidative burst coincided with elevation of intracellular Ca(2+), which was likely because of passive influx of Ca(2+) through the toxin pores. Competition experiments showed that binding to the cells was receptor-independent, and preloading of cells with a nonlytic HlyA mutant did not abrogate the respiratory burst provoked by a subsequent application of wild-type HlyA. In contrast to a previous report, expression or activation of the beta(2) integrin lymphocyte function-associated antigen-1 did not affect binding of HlyA. We conclude that HlyA binds nonspecifically to target cells and a receptor is involved neither in causing hemolysis nor in triggering cellular reactions.