Incisional hernia recurrence after open elective repair: expertise in abdominal wall surgery matters.

BACKGROUND: Recurrence after incisional hernia repair is one of the major problems related with this operation. Our objective is to analyze the influence of abdominal wall surgery expertise in the results of the open elective repair of incisional hernia. METHODS: We have compiled the data of a cohort of patients who received surgery for an incisional hernia from July 2012 to December 2015 in a University Hospital. Data were collected prospectively and registered in the Spanish Register of Incisional Hernia (EVEREG). The short- and long-term complications between the groups of patients operated on by the Abdominal Wall Surgery (AWS) unit and groups operated on by surgeons outside of the specialized abdominal wall group (GS) were compared. RESULTS: During the study period, a total of 237 patients were operated on by the open approach (114 AWS; 123 GS). One hundred seventy-five patients completed a median follow-up of 36.6 months [standard deviation (SD) = 6]. Groups were comparable in terms of age, sex, body mass index (BMI), comorbidities, and complexity of hernia. Complications were similar in both groups. Patients in the AWS group presented fewer recurrences (12.0% vs. 28.9%; P = 0.005). The cumulative incidence of recurrence was higher in the GS group [log rank 13.370; P < 0.001; odds ratio (OR) = 37.8; 95% confidence interval (CI) = 30.3-45.4]. In the multivariate analysis, surgery performed by the AWS unit was related to fewer recurrences (OR = 0.19; 95%CI = 0.07-0.58; P < 0.001). CONCLUSION: Incisional hernia surgery is associated with better results in terms of recurrence when it is performed in a specialized abdominal wall unit.

Regulation of manganese superoxide dismutase (MnSOD) in chronic experimental alcoholism: effects of vitamin E-supplemented and -deficient diets.

In order to investigate the pathogenic mechanism responsible for liver injury associated with chronic alcoholism, we studied the effects of different dietary vitamin E levels in chronically ethanol (EtOH)-fed rats on the activity and mRNA regulation of the manganese superoxide dismutase (MnSOD) enzyme. Evidence is accumulating that intermediates of oxygen reduction may in fact be associated with the development of alcoholic liver disease. Since low vitamin E liver content seems to potentiate EtOH-linked oxidative stress, we studied the effect of EtOH treatment in livers from rats fed a diet deficient or supplemented with vitamin E. Chronic EtOH feeding enhanced hepatic consumption of vitamin E in both groups of EtOH-treated animals, irrespectively of the vitamin E level of the basal diet and the effect was observed in both the microsomal and mitochondrial fractions. Both EtOH-fed groups exhibited increased MnSOD gene expression, while the enzyme activity was enhanced only in the vitamin E-deprived group of EtOH-treated animals. The significant increase in manganese liver content found only in this last group could explain the rise of enzyme activity. In fact, in the absence of a parallel increase of the prosthetic ion manganese, MnSOD mRNA induction was not accompanied by a higher enzymatic activity. These findings support the role of oxidative alteration in the EtOH-induced chronic hepatotoxicity in which MnSOD response might represent a primary defence mechanism against the damaging effect of oxygen radical species.

Regression of morphological alterations and oxidative stress-related parameters after acute lindane-induced hepatotoxicity in rats.

Changes in rat liver oxidative stress-related parameters, morphological alterations, as well as circulating and tissue levels of lindane were studied 1-7 days after the administration of a single dose of 60 mg of lindane/kg. One day after lindane treatment, a significant enhancement in the oxidative stress status of the liver was observed, characterized by an increase in thiobarbituric acid reactants production and in the microsomal generation of superoxide radical (O.-2) coupled to cytochrome P450 induction, and a decrement in the activity of superoxide dismutase (SOD) and catalase. Consequently, the O.-2 production/SOD activity ratio was enhanced two-fold. In this condition, light microscopy studies revealed the incidence of liver lesions in periportal areas, together with significant changes at the mitochondrial level observed by electron microscopy, which coincide with the maximal levels of lindane in the liver, adipose tissue, plasma and whole blood. Changes in oxidative stress-related parameters observed after 1 day of lindane treatment regressed to normal from the third day and thereafter, together with the decrement in circulating and tissue levels of the insecticide. It is concluded that morphological and oxidative stress-related changes induced in the liver by acute lindane intoxication are readily reversible, depend on the hepatic content of the insecticide, and seem to be conditioned by the changes in O.-2 generation.

Resistance of rat kidney mitochondrial membranes to oxidation induced by acute iron overload.

The effect of iron-overload on rat kidney was studied after a single injection of iron-dextran. Total iron content in kidney and isolated kidney mitochondria was markedly elevated over control values. To assess mitochondrial damage by iron overload, succinate-cytochrome c reductase and NADH-cytochrome c reductase activities as well as the rate of succinate-dependent hydrogen peroxide generation were measured. None of these activities were significantly affected by acute iron overload. The net content and the rate of TBARS (thiobarbituric acid reactive species) formation in kidney homogenates from iron-treated rats was significantly higher than that of control animals. Total superoxide dismutase activity in the homogenates from iron overloaded kidney was decreased by 26%, as compared to controls. Catalase, glutathione peroxidase, and Mn-superoxide dismutase activities were not affected by the treatment. The content of alpha-tocopherol was consistently decreased in whole kidney homogenates (-31%), mitochondria from kidney medulla (-31%) and cortex (-34%), from iron-overloaded rats. Our data suggest that iron dextran treatment does not affect kidney integrity, even though increases in lipid peroxidation occur. Vitamin E appears to be effective in controlling iron-dextran dependent radical generation in kidney.