Uric acid is the final product of purine metabolism in humans. The final two reactions of its production catalyzing the conversion of hypoxanthine to xanthine and the latter to uric acid are catalysed by the enzyme xanthine oxidoreductase, which may attain two inter-convertible forms, namely xanthine dehydrogenase or xanthine oxidase. The latter uses molecular oxygen as electron acceptor and generates superoxide anion and other reactive oxygen products. The role of uric acid in conditions associated with oxidative stress is not entirely clear. Evidence mainly based on epidemiological studies suggests that increased serum levels of uric acid are a risk factor for cardiovascular disease where oxidative stress plays an important pathophysiological role. Also, allopurinol, a xanthine oxidoreductase inhibitor that lowers serum levels of uric acid exerts protective effects in situations associated with oxidative stress (e.g. ischaemia-reperfusion injury, cardiovascular disease). However, there is increasing experimental and clinical evidence showing that uric acid has an important role in vivo as an antioxidant. This review presents the current evidence regarding the antioxidant role of uric acid and suggests that it has an important role as an oxidative stress marker and a potential therapeutic role as an antioxidant. Further well designed clinical studies are needed to clarify the potential use of uric acid (or uric acid precursors) in diseases associated with oxidative stress.

SILS cholecystectomy, as well as the invisible scar, has significantly lower abdominal and shoulder pain scores, especially after the first 24 h postoperatively, when this pain is nonexistent. (Registration Clinical Trial number: NTC00872287, www.clinicaltrials.gov ).

Free radical-induced lipid peroxidation associated with a decrease in plasma antioxidant capacity and UA levels as well as altered hepatic function is observed after deflation of the pneumoperitoneum. These results suggest that free radicals are generated at the end of a laparoscopic procedure, possibly as a result of an ischemia-reperfusion phenomenon induced by the inflation and deflation of the pneumoperitoneum.

After laparoscopic surgery carbon dioxide remains within the peritoneal cavity for a few days, commonly causing pain. This prospective randomized study was performed to determine the efficacy of intraperitoneal infusion of normal saline on postoperative pain after laparoscopic cholecystectomy. Altogether 300 patients were randomly assigned to one of five groups of 60 patients each. Group A: control group, no peritoneal infusion, no subhepatic drain. Group B: no peritoneal infusion but a subhepatic closed brain was left for 24 hours. Group C: normal saline 25 to 30 ml/kg body weight at a temperature of 37 degrees C was infused under the right hemidiaphragm and left in the peritoneal cavity. Group D: normal saline in a room temperature was infused under the right hemidiaphragm and suctioned after the pneumoperitoneum was deflated. Group E: normal saline was infused and suctioned as in group D, but a subhepatic closed drain was left for 24 hours. Postoperatively, analgesic medication usage, nausea, vomiting, and pain scores were determined at 2, 6, 12, 24, 48, and 72 hours (during hospitalization and at home). Postoperative pain was reduced significantly (p < 0.001) in the patients of groups C, D, and E versus controls, whereas no difference was observed between groups A and B. Among groups C < D and E, group E (p < 0.01) had the best results followed by group D and then group C. Intraperitoneal normal saline offered a detectable benefit to patients undergoing laparoscopic cholecystectomy. The beneficial effect was better when the fluid was suctioned after deflation of the pneumoperitoneum and even better when a subhepatic closed drain continued fluid suction during the first postoperative hours.

No abstract

Preincisional local infiltration plus intraperitoneal infusion of ropivacaine at the beginning of LC combined with normal saline infusion at the end of the procedure is a safe and valid method for reducing pain after LC.

Seroma is a frequent complication of laparoscopic or open repair of ventral hernias using expanded polytetrafluoroethylene mesh. Aspiration of this seroma has the risk of introducing bacteria, resulting in infection and the recurrence of the hernia. Between May 1996 and December 2000, 51 patents who underwent 53 laparoscopic ventral hernioplasties (44 incisional, 5 large epigastric, and 4 large umbilical) were randomized to participate in a trial comparing the intraperitoneal onlay mesh repair with or without cauterization of the hernia sac. Group A (26 patients; 28 hernias) patients were operated on by using an expanded polytetrafluoroethylene Dual Mesh patch (Gore and Associates, Flagstaff, AZ, U.S.A.) inserted intraperitoneally and secured by full-thickness stitches and endoscopic clips to cover the hernia defect, while the sac was left intact. Group B (25 patients, 25 hernias) patients were operated on according to the same technique as those in group A, but the hernia sac was cauterized by monopolar cautery (5 cases) or harmonic scalpel (20 cases). After surgery, clinical examination and computed tomography scans were used to confirm or test the existence of seroma and recurrence. In group A, four clinically evident seromas were found. Two of them were resolved with no intervention. In the remaining two cases, multiple aspirations were needed for 4 and 7 months, respectively, but 2 and 3 months, respectively, after resolution of the seroma, a recurrence of the hernia was observed. There was one more recurrence without seroma and three with subclinical seromas (only observed on computed tomography scans). In group B, subclinical seroma (only observed in computed tomography scan) resolved in a few days, and one recurrence without seroma was observed. Although only a small number of patients were studied, our findings suggest that the cauterization of the hernia sac prevents seromas and reduces recurrences in laparoscopic repair of ventral hernias.

Verapamil administered before treatment, but not after treatment, had a beneficial effect on a 90-minute warm ischemia-reperfusion rat liver injury model. The possible activation of proteases converting the xanthine dehydrogenase to xanthine oxidase, the significant mitochondrial calcium loading during the ischemic period, and the potentiation of calcium and oxygen-derived free radicals to promote injury to mitochondria are mechanisms supported by this study, based on both histologic observations and on the pattern of enzyme leak after the acute ischemic event.