Faculty Bibliography

PURPOSE: To evaluate the effect of increasing age of urology patients on the outcome of laparoscopic procedures. PATIENTS AND METHODS: We performed a retrospective review of patients undergoing laparoscopic urologic procedures from 1998 to 2005, comparing patients 75 or older with all other patients undergoing the same procedures. Data were available on 175 patients. Length of hospitalization, complications, estimated blood loss (EBL), operative time, ASA class, and the Charlson comorbidity index (CCI) were taken from hospital and outpatient records. Subgroup analysis was performed on older patients, one group aged 65 to 74 years and the other > or =75 years. Statistical analysis was done using a two-tailed t-test and chi-square test. RESULTS: Patients aged 75 or older had no statistically significant differences in operative time (318 minutes v 319 minutes; P = 0.967), EBL (271 mL v 331 mL; P = 0.487), or complication rate (14.6% v 12.9%; P = 0.434). However, there was a significant increase in the length of stay (6.06 days v 3.74 days; P = 0.0015). In the subgroup analysis of patients 65 to 74 years v > or =75 years, a significant increase in the length of hospitalization was still present despite controlling for complications. CONCLUSIONS: Laparoscopic procedures in patients 75 years and older entail a significantly longer hospital stay than in younger patients despite similar medical comorbidities. Overall, there was no significant increase in perioperative complications related to age.

Reactivation of latent human cytomegalovirus is of significant concern in immunocompromised transplant patients and is likely to occur through transcriptional activation of immediate early (ie) gene expression through mechanisms that are not well understood. TNF-mediated activation of NF-kappaB has been proposed to be one pathway leading to transcriptional activation of CMV ie gene expression. Using transgenic mice carrying a lacZ reporter gene under the control of the HCMV major ie promoter/enhancer (MIEP-lacZ mice) and MIEP-lacZ mice deficient in TNF receptor 1 and TNF receptor 2 (MIEP-lac Z TNFR DKO mice), we demonstrate that renal ischemia/reperfusion (I/R) injury activates the HCMV enhancer independently of TNF. Induction of MIEP-lacZ expression was preceded by TNFR-independent formation of reactive oxygen species (ROS), weak and transient activation of NF-kappaB and strong and sustained activation of AP-1. Our studies show that, in addition to TNF-mediated signaling, TNF-independent signaling induced by I/R injury can contribute to the activation of the HCMV enhancer. This likely occurs through ROS-mediated activation of AP-1. Targeting MAP kinase signaling pathways as well as NF-kappaB may be of therapeutic value in patients with CMV infection.