Selection of the most appropriate treatment to obtain the best results with the lowest rate of recurrence and minimal morbidity and mortality is mandatory for the management of hepatic hydatid disease. The surgical approach is the mainstay of treatment, and there has been a tendency toward laparoscopic surgery and, more recently, percutaneous treatment (PT), which has become increasingly popular with revolutions in techniques. We aimed to evaluate the results of current therapeutic methods in the context of a 10-year single-institution experience. Between 1992 and 2003, 355 patients with 510 hydatid cysts of the liver were treated by open operation, laparoscopic surgery, or PT. The series included 128 females and 227 males ranging in age from 10 years to 73 years. Preferred treatment modalities, perioperative complications, interventions, recurrences, and length of hospital stay were retrospectively analyzed. There were two postoperative deaths (1.08%) in the open surgery group. Biliary leakage was observed in 28 patients treated with open surgery, in 10 patients after PT, and in 2 after laparoscopic treatment. Recurrence rates were 16.2%, 3.3%, and 3.5% after open surgery, laparoscopic surgery, and percutaneous treatment, respectively. Characteristics of the cyst, presence of cystobiliary communications, and the availability of a multidisciplinary team are the factors that we believe directly affect the results. Radical surgery can be done safely for suitable cases; conventional procedures are associated with greater morbidity. Laparoscopic surgery seems effective and safe, with low morbidity and recurrence rates for type I-III cysts in accessible localizations. Our experience with PAIR (puncture, aspiration, injection, and reaspiration) and catheterization provides evidence that the procedure is an effective and safe option.

NAC treatment had beneficial effects in sodium taurocholate-induced AP in rats. It reduced pancreatic tissue necrosis and lipid peroxidation. In our study, the mechanism underlying the beneficial effects of NAC seemed to be its antioxidant activity, either by increasing hepatic GPx activity, or by a direct scavenging effect on free radicals, thus enhancing the production of and/or inhibiting the degradation of nitric oxide.

The 5-hydroxytryptamine (5-HT) receptors mediating contraction in human isolated mesenteric arteries were characterized. Endothelium-denuded human isolated mesenteric arteries were used. 5-HT induced concentration-dependent contractions in mesenteric arteries (Emax, 127.37 +/- 7.61% of 80 mM KCl maximal contraction; pD2, 6.73 +/- 0.09 [-logEC50]). Sumatriptan, a selective 5-HT1B/1D receptor agonist, induced concentration-dependent contractions in some of the arteries (Emax, 61.82 +/- 10.04%; pD2, 6.56 +/- 0.21, n = 9) but not in the others (Emax < 5%, n = 13), suggesting that functional 5-HT1B/1D receptors exist in some but not in all mesenteric arteries. GR127935 (a selective 5-HT1B/1D receptor antagonist, 3 nM) inhibited sumatriptan-induced contractions in arteries in which sumatriptan responses were strong in an insurmountable manner. GR127935 (10 nM) also inhibited 5-HT responses and shifted the concentration-response curve of 5-HT to the right significantly (p < 0.05; pD2s were 6.54 +/- 0.18 and 5.93 +/- 0.11 in the presence of vehicle and GR127935, respectively). Ketanserin (0.01-1 microM) competitively antagonized 5-HT responses in human mesenteric arteries: pA2 value was 8.40 +/- 0.25 (slope of Schild regression, 1.43 +/- 0.18; r2, 0.98). Tropisetron (5-HT3 receptor antagonist) and prazosin (alpha1-adrenoceptor antagonist) did not affect the contractions induced by 5-HT. These results suggest that 5-HT2A and 5-HT1B/1D receptors, but not 5-HT3 and alpha1-adrenoceptors, are involved in the 5-HT-induced contractions in human isolated mesenteric arteries. Sumatriptan-induced and 5-HT1B/1D receptor-mediated responses vary greatly among patients.

No abstract

No abstract