ABSTRACT
Primary treatment of liver hydatidosis is surgical, but the recurrence rate is about 10%. To minimize the risk of recurrence, 67 consecutive patients with liver hydatidosis were prospectively treated by mebendazole or albendazole for 5 days before surgery. During the operation the viability of the protoscoleces was assessed. Seventeen patients who had viable protoscoleces at the time of the operation received the same benzimidazole one extra month postoperatively, while the remaining 50 patients who had dead protoscoleces didn't receive postoperative therapy. None of the patients developed recurrence of the disease after a follow-up period of 15-67 months (average 41 months). These results suggest that a 5-day preoperative benzimidazole therapy either combined or not with a monthly postoperative course according to the viability of the protoscoleces at the time of operation, may erase the risk of recurrence after surgical treatment of the liver hydatidosis.
Subject(s)
Anticestodal Agents/administration & dosage , Benzimidazoles/administration & dosage , Echinococcosis, Hepatic/surgery , Premedication , Adolescent , Adult , Aged , Aged, 80 and over , Anticestodal Agents/adverse effects , Benzimidazoles/adverse effects , Child , Combined Modality Therapy , Dose-Response Relationship, Drug , Drug Administration Schedule , Female , Follow-Up Studies , Humans , Male , Middle AgedSubject(s)
Cholangitis, Sclerosing/chemically induced , Echinococcosis, Hepatic/drug therapy , Formaldehyde/adverse effects , Cholangitis, Sclerosing/drug therapy , Female , Follow-Up Studies , Formaldehyde/therapeutic use , Humans , Middle Aged , Ursodeoxycholic Acid/administration & dosage , Ursodeoxycholic Acid/therapeutic useABSTRACT
OBJECTIVE: To assess the effect of trimetazidine (an anti-anginal drug that acts as a scavenger of oxygen free radicals) in the protection of hepatocytes after a 90 minute period of warm ischaemia followed by reperfusion in rats. DESIGN: Prospective study. MATERIAL: 80 Wistar rats. INTERVENTIONS: 20 Rats were given a single dose of trimetazidine 2.5 mg/kg intravenously 30 minutes before the induction of ischaemia; 20 received the same dose intraperitoneally twice a day for five days before the experiment and one dose intravenously 30 minutes before; 20 were given a single dose of 2.5 mg/kg intravenously after reperfusion had been started; and 20 acted as controls. All rats underwent liver biopsy through a laparotomy incision on postoperative days 2, 7, and 21, and the activities of liver enzymes in their blood were measured before induction of ischaemia and two, seven, 14, and 21 days afterwards. OUTCOME MEASURES: Histological changes and serum enzyme activities. RESULTS: The amount of centrilobular necrosis of hepatocytes, and the activity of hepatic enzymes were greatest on day 2, as was the reduction in superoxide dismutase activity in the erythrocytes. A single dose of trimetazidine, whether given before or after the ischaemic episode, gave significant protection to hepatocytes, but pretreatment for five days was even more effective. CONCLUSION: Trimetazidine protected rats' livers from injury after a period of warm ischaemia and reperfusion.
Subject(s)
Ischemia/prevention & control , Liver/blood supply , Reperfusion Injury/prevention & control , Trimetazidine/therapeutic use , Animals , Liver/drug effects , Liver/enzymology , Liver/pathology , Prospective Studies , Rats , Rats, Wistar , Reperfusion Injury/pathology , Trimetazidine/pharmacologyABSTRACT
The effectiveness of superoxide dismutase (SOD), catalase (CAT), dimethyl sulphoxide (DMSO) and allopurinol in prevention of peritoneal adhesion formation induced by complete vascular obstruction and reperfusion of an ileal segment was investigated in rats. The ischaemic period was 30 min. Group A (n = 20) were controls, group B (n = 15) received SOD 15,000 U/kg i.v. and group C (n = 17) the same dose of CAT immediately before induction of ischaemia. In group D (n = 20) DMSO 20 mg/kg was given i.v. 5 min before ischaemia, and group E (n = 20) received allopurinol orally 50 mg/kg daily for 2 days and also 2 hours before ischaemia. Ten days later adhesions had developed in 80% of group A, 40% of group B, 47% of group C and 45% of groups D and E (p less than 0.05). The severity of the adhesions was significantly less in the pretreated groups than in the controls. Oxygen-derived free radicals may be pathogenetically important for such adhesion formation. Xanthine oxidase is the principal source of oxygen radicals after a 30-min period of complete regional intestinal ischaemia.
Subject(s)
Free Radicals/therapeutic use , Ileum/blood supply , Peritoneal Diseases/prevention & control , Reperfusion Injury/complications , Allopurinol/therapeutic use , Animals , Catalase/therapeutic use , Dimethyl Sulfoxide/therapeutic use , Drug Evaluation , Female , Rats , Rats, Inbred Strains , Superoxide Dismutase/therapeutic use , Tissue Adhesions/prevention & controlABSTRACT
The role of oxygen derived free radicals in gastric lesions induced by haemorrhagic shock and the protective effect of oxygen radical scavengers, allopurinol and ranitidine, were investigated. Forty five rabbits underwent haemorrhagic shock for 30 minutes and reinfusion of shed blood. They were killed 30 minutes later. The animals were divided in five groups: A (n = 10): Control, B (n = 10): intravenous ranitidine pretreatment, C (n = 10): oral allopurinol, 24 and 2 h before surgery; D (n = 10): intravenous pretreatment with superoxide Dismutase plus catalase, E (n = 5): 60 minute haemorrhagic shock without reinfusion and treatment. Erosions and/or petechiae in all animals in Group A were observed. Three animals in group B and C and 2 in group D (p less than 0.005, p less than 0.001) had gastric lesions. The lesions in the pretreatment groups were significantly smaller than in controls. Oxygen radicals plus HCl play an important role in shock induced gastric lesions. Oxygen radical antagonists show a significant protective role.
