Laparoscopic exploration of the common bile duct with a rigid scope in patients with problematic choledocholithiasis.

BACKGROUND: The development of laparoscopic cholecystectomy as a minimally invasive approach to eliminate gallstones, in conjunction with increasingly sophisticated techniques for removal of common bile duct (CBD) stones by endoscopic sphincterotomy, has revolutionized the treatment of choledocholithiasis. We describe a new technical approach to laparoscopic exploration of the CBD after unsuccessful endoscopic stone extraction. METHODS: Eleven patients were subjected to laparoscopic exploration of the CBD with choledochotomy using a rigid scope (24-Fr nephroscope) during the last 2 years. Of these patients, 10 had unsuccessful preoperative (7 cases) or intraoperative (3 cases) stone extraction, and 1 case had a single impacted stone 2.3 cm in diameter. Five patients had a single bile duct stone and 6 patients had multiple stones. The size of the stones ranged from 9.5 to 24 mm (mean = 12.6 +/- 4 mm). RESULTS: Balloon dilation of the papilla of Vater was done in all patients. Most of the stones were fractured and pushed into the duodenum with rigid grasping forceps but a lithotripter was required in 2 patients. Stone clearance was 100%; complications related to the procedure were not observed. After CBD clearance, primary closure of the choledochotomy was achieved in 10 patients. In 1 patient who had CBD perforation during a previous procedure, choledochotomy was closed over a T-tube. The mean operative time was 124 +/- 26.7 min (range = 84-165 min) and the mean postoperative hospital stay was 4 +/- 1.7 days (range = 3-7 days). CONCLUSIONS: Laparoscopic exploration of the CBD with a rigid scope is an efficacious procedure in dealing with unsuccessful endoscopic stone extraction.

Central form of multiple symmetric lipomatosis: a case report.

Multiple symmetric lipomatosis (also known as Madelung's disease, Launois-Bensaude syndrome or benign symmetric lipomatosis) is a rare disease, the etiology of which is unknown. Multiple, symmetric, non-encapsulated lipomatous masses on the face, neck, upper arms, and upper trunk are typical in most cases. Five out of the 200 cases reported in the literature were the distal form of the disease; the rest were proximal. We describe, for the first time, a central form of the disease, simultaneously involving the lower trunk, arms and upper legs.

Laparoendoscopic "rendezvous" versus laparoscopic antegrade sphincterotomy for choledocholithiasis.

BACKGROUND: The ideal management of common bile duct stones in the era of laparoscopic cholecystectomy is controversial. With rapid advances in technology and more experience in laparoscopic skills, many surgeons are now routinely performing single-stage procedures and questioning the wisdom of preoperative endoscopic retrograde cholangiopancreotography, with or without sphincterotomy. The purpose of this study was to compare the success rate, duration of operating time, clinical results, and duration of hospital stay of a laparoendoscopic "rendezvous" technique versus antegrade sphincterotomy in patients with cholecystitis-choledocholithiasis. METHODS: Patients with gallbladder and common bile duct stones undergoing laparoscopic cholecystectomy plus retrograde sphincterotomy (group A; n = 35) were compared retrospectively with those undergoing laparoscopic cholecystectomy plus antegrade sphincterotomy (group B; n = 41) at a single institution. RESULTS: Ductal stone clearance was equivalent in the 2 groups (94% vs 95%; P = .979), as was morbidity (9% vs 5%; P = .545) and conversion (6% vs 5%; P = .877). The median operating time was less in group B (89 vs 117 minutes; P < .0001). There was no significant difference in hospital stay between the 2 groups (P = .140). CONCLUSION: This study suggests that intraoperative sphincterotomy with a combined endoscopic-laparoscopic approach for the removal of common bile duct stone(s) is safe and effective in routine surgical practice. Ductal stone(s) clearance, morbidity, and conversion were equivalent in the 2 groups; antegrade sphincterotomy had a shorter operative time compared with the rendezvous technique.

Liver tissue inducible nitric oxide synthase (iNOS) expression and lipid peroxidation in experimental hepatic ischemia reperfusion injury stimulated with lipopolysaccharide: the role of aminoguanidine.

BACKGROUND: Hepatic ischemia-reperfusion (HIR) is a severe condition that is seen after hepatic arterial injury and in hepatic grafts in living donor transplantation. HIR not only causes liver injury by lipid peroxidation, but also stimulates systemic and portal endotoxemia. Also, lipopolysaccharide (LPS) induces hepatic injury mediated by inducible nitric oxide synthase (iNOS). There is little knowledge on the role of specific iNOS inhibitors in prevention of HIR injury followed by LPS administration. The aim of this study on a LPS induced HIR model was to investigate the effect of aminoguanidine (AG) administration on hepatic tissue iNOS expression and lipid peroxidation when given before or after LPS. METHODS: Six groups were designed; A: Sham, B: HIR, C: HIR + AG, D: HIR + LPS, E: HIR + LPS + AG, F: HIR + AG + LPS. No substance was given to the rats in Group A and B. HIR injury was induced with vascular occlusion for 45 min and reperfusion for 45 min. Drugs were given intraperitoneally 10 min before reperfusion. Serum and tissue analysis for myeloperoxidase (MPO), and malondialdehyde (MDA), and tissue NA+/K+ adenosine 5'triphosphatases (ATPase) and tissue iNOS staining were performed. Permission for this study was obtained from the local Ethics Committee. RESULTS: The level of MPO, MDA, and iNOS staining scores in Group B were significantly higher than Group A and ATPase was lower in Group B (P < 0.05). Contrary to results in Group C, results of MPO, MDA, and iNOS staining scores of Group D was higher than Group B (P < 0.05); however, although iNOS in Group C was lower than Group B, the difference was not significant (P > 0.05). MPO and MDA levels of Groups E and F were significantly lower than Group D. Level of ATPase in Group F was significantly different from Groups D and E. iNOS scoring was low in Group F compared with Group D (P < 0.05). MDA, MPO, and iNOS levels of Group F was lower than Group E, and ATPase of Group F was higher than Group E (P < 0.05). CONCLUSIONS: The results of this study in a LPS induced HIR model showed that LPS after HIR aggravated HIR injury by increasing neutrophil activation and lipid peroxidation both in serum and liver tissue and iNOS in liver, and depleting energy in liver. AG, a selective iNOS inhibitor, ameliorated the negative effects of endotoxemia induced by LPS after HIR; however, energy depletion and iNOS expression in liver tissue were attenuated only when AG was administered prior to LPS. The findings of this study supported the hypothesis that LPS after HIR would aggravate HIR injury and AG would ameliorate this aggravated injury.

Effect of N-acetylcysteine on blood and tissue lipid peroxidation in lipopolysaccharide-induced obstructive jaundice.

In obstructive jaundice, free radical production is increased and antioxidative activity is reduced. N-Acetylcysteine (NAC) has a beneficial effect with anti-inflammatory and antioxidant activity, acting as a free radical scavenger. NAC inhibits inducible nitric oxide synthase, suppresses cytokine expression/release, and inhibits adhesion molecule expression and nuclear factor kappa B. The aim of this study was to investigate the effects of NAC on liver/renal tissue and serum lipid peroxidation in lipopolysaccharide (LPS)-induced obstructive jaundice. We randomized 60 rats into 6 groups: group 1, Sham; group 2, obstructive jaundice (OJ) induced after bile-duct ligation; group 3, OJ + NAC (100 mg kg- 1 subcutaneously); group 4, OJ + LPS (10 mg kg-1); group 5, OJ + NAC + LPS; and group 6, OJ + LPS + NAC. For each group, the biochemical markers of lipid peroxidation and the antioxidant products were measured in serum and liver/renal tissue after sacrifice. Almost all lipid peroxidation products levels were increased and antioxidant products levels were decreased in groups who received LPS (groups 4, 5, and 6), but the effect was less remarkable when NAC was administered before LPS (group 5). The same trend was seen for groups with OJ +/- LPS who did not received NAC or received it after induced toxemia (groups 2, 4, and 6) as compared to groups 1 and 3. Moreover, in the case of OJ + LPS, rats treated with NAC before LPS (group 5) had lower lipid peroxidation products levels and higher antioxidant products levels as compared to those who did not received NAC (group 4). This phenomenon was not reproducible with NAC administered after LPS (group 6). Thus, results of this study showed that NAC prevents the deleterious effects of LPS in obstructive jaundice by reducing lipid peroxidation in serum and liver/renal tissue if administered before LPS. Nonetheless, NAC failed to prevent the lipid peroxidation in the case of established endotoxemia in obstructive jaundice.

The effect of aminoguanidine on blood and tissue lipid peroxidation in jaundiced rats with endotoxemia induced with LPS.

Obstructive jaundice (OJ) is a severe condition that leads to several complications. One of the important problems in OJ is the increased incidence of endotoxemia, which is the result of bacterial translocation (BT) and defective host immune response. Lipid peroxidation (LP) is an important problem in OJ and sepsis in which nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) activity are increased and antioxidative activity is decreased. Formation of peroxynitrite (ONOO(-)) anion leads to cellular damage and apoptosis. In this experimental study, we explore the effect of specific iNOS inhibitor aminoguanidine (AG) on blood and tissue (liver and renal) LP and iNOS levels in jaundiced rats with endotoxemia induced with lipopolysaccharide (LPS). Rats were randomized into six groups; group A, sham; group B, obstructive jaundice (OJ); group C, OJ + LPS; group D, OJ + AG; group E, OJ + LPS + AG; group F, OJ + AG + LPS. Serum malondialdehyde (MDA) and serum myeloperoxidase (MPO) activity and liver and renal tissue MDA, MPO, and Na(+)/K(+)-ATPase activity levels were detected in biochemical methods. Liver and renal tissue iNOS levels were examined immunohistopathologically. Serum and tissue MDA and MPO levels and tissue iNOS expression were increased significantly in groups B, C, and E, while tissue ATPase levels were decreased significantly in the same groups. In the group treated with AG (group D), serum and tissue MDA and MPO levels and tissue iNOS expression were decreased while tissue ATPase levels were increased significantly. In group F, if AG was administrated before LPS, we observed that serum and tissue MDA and MPO levels and tissue iNOS expression were decreased while tissue ATPase levels were increased significantly. Thus, our study showed that AG had a protective effect when it was administrated before LPS, but it failed to prevent tissue iNOS expression and LP if there was established endotoxemia in OJ.

The effect of PARS inhibition on ileal histopathology, apoptosis and lipid peroxidation in LPS-induced obstructive jaundice.

In our experimental study, we investigated the protective effect of 3-aminobenzamide (3-AB), the poly (ADP-ribose) synthetase (PARS inhibitor), on the ileal histopathology and the apoptosis in lipopolysaccharide (LPS)-induced inflammation in rats with obstructive jaundice (OJ). We randomized 40 rats into five groups. Group 1: sham group; Group 2: OJ group; Group 3: OJ+LPS; Group 4: OJ+3-AB+LPS; Group 5: OJ+LPS+3-AB. At the fifth day; the rats were jaundiced. In Group 3; 10 mg kg(-1) LPS was injected intraperitoneally at the fifth day and then after 6h the rats were sacrificed. In Group 4; 10 mg kg(-1) 3-AB was administrated intraperitoneally at the fifth day and repeated daily for 3 days and at the eighth day, 10 mg kg(-1) LPS was injected intraperitoneally. In Group 5, 10 mg kg(-1) LPS was injected intraperitoneally at the fifth day and after 6h 10 mg kg(-1) 3-AB was administrated intraperitoneally and repeated daily for 3 days. At the eighth day, rats were sacrificed. Blood samples were taken for detection of serum MDA levels. Ileum samples were taken after relaparotomy for histopathological examination to evaluate the endotoxin-related intestinal injury and Caspase-3 apoptosis and for detection of tissue MDA and ATPase activities. There was marked destruction of villous and crypt epithelial cells and extensive apoptosis in Groups 3 and 5 in histopathological examination. In Group 4, the scores of intestinal mucosal damage and apoptotic cells were reduced significantly (P<0.05). On the other hand, the scores of intestinal mucosal damage and apoptotic cells were not improved in Group 5. After the administration of 3-AB (Group 4), serum and ileal MDA levels decreased, ileal ATPase increased as compared to Groups 1 and 2. Our study showed that 3-AB prevented the mucosal damage and apoptotic loss of intestinal epithelial cells significantly if it was administrated before LPS. However, 3-AB failed to prevent the mucosal damage and apoptotic loss of intestinal epithelial cells significantly if there was established endotoxemia in OJ.

Efficacy of topical nonsteroidal antiinflammatory drugs in mastalgia treatment.

BACKGROUND: The aim of the study was to investigate the effects of topical nonsteroidal antiinflammatory drugs (NSAIDs) on mastalgia. STUDY DESIGN: A prospective, randomized, blinded, placebo-controlled study was performed to evaluate the effects of topical NSAIDs on cyclic and noncyclic mastalgia. A total of 108 patients, 60 with cyclic (group I) and 48 with noncyclic (group II) breast pain were enrolled. Patients within each group were randomly assigned to receive either topical NSAIDs or placebo three times daily for at least 6 months. Severity of pain was measured before and after 6 months of treatment. RESULTS: The pain score decreased significantly when the mean initial breast pain score was compared with the sixth-month breast pain score of the treatment or the placebo group of cyclic (p = 0.0001 and p = 0.0001, respectively) or noncyclic mastalgia (p = 0.0001 and p = 0.0001, respectively). Significant differences were found when the mean within-person change in pain values in each treatment group were compared with the change in the respective placebo group for either cyclic or noncyclic mastalgia (p = 0.0001 and p = 0.0001, respectively). Changes in pain within treatment groups or placebo groups for cyclic versus noncyclic mastalgia were not found to be statistically different (p = 0.53 and p = 0.96, respectively). No side effect was seen in any group. CONCLUSIONS: Topical application of NSAIDs was effective in both cyclic and noncyclic mastalgia with minimal side effects.