Parastomal hernia repair: laparoscopic ventral hernia meshplasty with stoma relocation. The current state and a clinical case presentation.

BACKGROUND: Parastomal hernia is a frequent complication after performing an ostomy, and although different technical options have been described, it lacks an ideal intervention to resolve it. The use of meshes and the laparoscopic approach, has led to a significant advance in resolving this condition. However, the ideal technique should guarantee must ensure integral repair of the abdominal wall, taking into account the functionality of the stoma. In large parastomal eventrations the repairing of the ventral hernia with a mesh and relocating the stoma in another quadrant may be an intervention that fulfills both principles, and open approach being described. METHODS: We review the current state of surgical management of this condition and analyze the different technical options. Present the first description for using a laparoscopic technique with meshplasty and stoma relocation in an obese patient with a complex parastomal hernia, with results in the 18 month follow up. CONCLUSIONS: Surgical technique repair of the parastomal hernia is sometimes a complex issue, which possibly requires different solutions according to the characteristics of the hernia and patient. The technique described of meshplasty with stoma relocation by laparoscopic approach has been revealed as an affordable technique, with minor inconvenience to the patient, absence of complications and good functional results in the long term, benefiting from the advantages of minimally invasive surgery itself.

Dual effect of insulin on in vitro leptin secretion by adipose tissue.

Although it is widely accepted that insulin stimulates leptin secretion, a dual action was observed using a validated in vitro system, i.e., an early (less than 48 h) inhibitory action, followed later (48-96 h) by a clear-cut stimulation. While the inhibitory phase was observed at every glucose concentration tested (from 1 to 25 mM), the stimulatory phase required the presence of physiological or supraphysiological glucose concentrations. In fact, leptin secretion was virtually eliminated in the presence of glucose uptake inhibitors. This dual effect of insulin was not due to modifications of the ob mRNA levels, suggesting that it depends entirely on posttranslational mechanisms. In conclusion, insulin appears to induce an early inhibition of leptin secretion by the adipose cell, followed later by a stimulatory effect secondary to the metabolic changes triggered by the insulin-induced increase in glucose uptake.