Analysis of risk factors for complications in 262 cases of laparoscopic colectomy.

BACKGROUND: The aim of the study was to critically review the experience of our unit to identify all the risk factors that can predict the intra-operative and post-operative complications, early and late, that are related to the procedure. MATERIALS AND METHODS: We retrospectively reviewed 293 patients who had undergone laparoscopic colectomy at the General Surgery and Organ Transplantation Unit of the University Hospital of Parma between January 2001 and September 2009. Preoperative tumour staging was performed for all patients by pancolonoscopic examination, performed preferably by the operating surgeon, thoracic-abdominal-pelvic CT, and, for rectal neoplasia, with further input from endoscopic ultrasound and/or pelvic magnetic resonance (MR) imaging. The parameters evaluated for each patient included age, sex, body mass index (BMI), ASA score, preoperative blood tests, associated comorbidities, cancer, others surgical procedures, operative time, laparotomy conversion rate, intra- and post-operative complications, any returns to the operating theatre, length of hospital stay and mortality. RESULTS: A total of 293 laparoscopic colectomy procedures were performed in our unit between January 2001 and September 2009; we analysed 262 of the 293 cases treated, since the data were incomplete and not correctly stored for 31 cases. The overall rate of intra- and post-operative complications was 22.9% (60/262). In 40 cases (40/262, 15.26%), the complications were surgical, and in the other 20 cases (7.63%) they were medical; mortality rate of 0.38% (1/262). CONCLUSIONS: Rectal resection is significantly associated with a greater number of intra- and post-operative complications than the other surgical procedures examined. The laparoscopic approach maintains its benefits even in patients with known preoperative comorbidities and constitutes a feasible procedure even in patients who are obese and/or with ASA status > or = III.

Defunctioning stoma in high-risk rectal anastomosis.

BACKGROUND: Ileostomy in rectal surgery is not always indicated for protecting the anastomosis. METHODS: We examined patients who underwent low rectal resection surgery for carcinoma between June 2005 and December 2007. We categorized the patient's characteristics according to the American Society of Anesthesiologists (ASA). We estimated hospital stay, and postoperative Dukes stage. RESULTS: 68 patients, 47 males and 21 females (mean age 67.8 years, range 40-85 years) treated with low rectal resection for carcinoma. An ileostomy was performed in 29 out of 68 patients (42.6%). Six postoperative ileostomy cases led to the appearance of peritonitis from anastomotic fistula. Among the patients with ileostomy 19 pts. (65.5%) belonged to ASA II and 10 pts.(34.5%) to ASA III; among those patients without ileostomy, 32 (82.05%) ASA II and 7 (17.95%) ASA III (p = n.s.). Of patients who underwent the first protective surgical procedure, 4 belonged to ASA II (66.6%) and 2 to ASA III (33.3%). The mean hospital stay for the non ileostomy group was 7.64 +/- 0.7 days, while it was 7.36 +/- 0.49 (p = n.s.) for the ileostomy group. The mean stay of postoperative ileostomy for leakage was 10.83 +/- 1.16 days. CONCLUSIONS: Ileostomy cannot completely prevent the onset of leakage, but may reduce overall hospitalization time.

The pyrimidinergic P2Y6 receptor mediates a novel release of proinflammatory cytokines and chemokines in monocytic cells stimulated with UDP.

The human P2Y6 receptor (hP2Y6) is a member of the G protein-coupled pyrimidinergic P2 receptor family that responds specifically to the extracellular nucleotide uridine diphosphate (UDP). Recently, the hP2Y6 receptor has been reported to mediate monocyte IL-8 production in response to UDP or lipopolysaccharide (LPS), but the role of hP2Y6 in regulating other pro-inflammatory cytokines or mediators is largely unknown. We demonstrate here that UDP specifically induces soluble TNF-alpha and IL-8 production in a promonocytic U937 cell line stably transfected with hP2Y6. However, we did not detect IL-1alpha, IL-1beta, IL-6, IL-10, IL-18, and PGE2 in the conditioned media from the same cell line. These results distinguish UDP/P2Y6 signaling from LPS signaling. Interestingly, UDP induces the production of IL-8, but not TNF-alpha, in human astrocytoma 1321N1 cell lines stably transfected with hP2Y6. Therefore, the immune effect of UDP/P2Y6 signaling on the production of proinflammatory cytokines is selective and dependent on cell types. We further identify that UDP can also induce the production of proinflammatory chemokines MCP-1 and IP-10 in hP2Y6 transfected promonocytic U937 cell lines, but not astrocytoma 1321N1 cell lines stably transfected with hP2Y6. From the Taqman analysis, UDP stimulation significantly upregulates the mRNA levels of IL-8, IP-10, and IL-1beta, but not TNF-alpha. Taken together, these new findings expand the pro-inflammatory biology of UDP mediated by the P2Y6 receptor.

Antagonist-induced micro-opioid receptor up-regulation decreases G-protein receptor kinase-2 and dynamin-2 abundance in mouse spinal cord.

Chronic treatment with opioid receptor antagonists has been shown to increase the density of micro-, delta- and kappa-opioid receptors in cell culture and in the intact animal. Although opioid receptor antagonist-induced up-regulation is a robust phenomenon, the mechanisms responsible for the increase in receptor density remain unclear. In the present study, changes in a kinase and a GTPase that have been implicated in G-protein-coupled receptor regulation were examined following opioid receptor antagonist treatment. Mice were implanted s.c. with a naltrexone pellet or placebo pellet. On the eighth day following implantation, spinal cord was removed and G-protein receptor kinase-2 (GRK-2) and dynamin-2 abundance were determined using a quantitative immunoblot approach. Changes in micro-opioid receptor density were also determined. Naltrexone treatment produced a significant (145%) increase in micro-opioid receptor density. Naltrexone treatment was associated with a significant 36% decrease in GRK-2 and 30% decrease in dynamin-2 abundance in spinal cord. These data raise the possibility that opioid receptor antagonist-induced micro-opioid receptor up-regulation in the intact animal may be due to a reduction in constitutive internalization of opioid receptors.

Mu-opioid receptor down-regulation and tolerance are not equally dependent upon G-protein signaling.

In the present study, the contribution of pertussis toxin (PTX)-sensitive G(i/o)-proteins to opioid tolerance and mu-opioid receptor down-regulation in the mouse were examined. Mice were injected once intracerebroventricularly and intrathecally with PTX (0.1 microg/site). Controls were treated with saline. On the 10th day following PTX treatment, continuous subcutaneous infusion of etorphine (150 or 200 microg/kg/day) or morphine (40 mg/kg/day+25 mg slow-release pellet) was begun. Control mice were implanted with inert placebo pellets. Pumps and pellets were removed 3 days later, and mice were tested for morphine analgesia or mu-opioid receptor density was determined in the whole brain, spinal cord, and midbrain. Both infusion doses of etorphine produced significant tolerance (ED50 shift=approximately 4-6-fold) and down-regulation of mu-opioid receptors (approximately 20-35%). Morphine treatment also produced significant tolerance (ED50 shift= approximately 5-8-fold), but no mu-opioid receptor down-regulation. PTX dramatically reduced the acute potency of morphine and blocked the further development of tolerance by both etorphine and morphine treatments. However, PTX had no effect on etorphine-induced mu-opioid receptor down-regulation in brain, cord, or midbrain. These results suggest that PTX-sensitive G-proteins have a minimal role in agonist-induced mu-opioid receptor density regulation in vivo, but are critical in mediating acute and chronic functional effects of opioids such as analgesia and tolerance.