Bilateral endoscopic total extraperitoneal (TEP) inguinal hernia repair does not induce obstructive azoospermia: data of a retrospective and prospective trial.

BACKGROUND: The endoscopic totally extraperitoneal (TEP) mesh repair is nowadays a well-established tension-free method for inguinal hernia repair. Mainly based on animal studies and case reports, a concern about the risk of postoperative infertility was expressed. This clinical study aimed to evaluate the risk of infertility due to obstructive azoospermia in men of fertile age who underwent a bilateral hernia repair. METHODS: Over 3 years (2005-2008) 59 male patients, 18-60 years of age, underwent a bilateral TEP repair. Twenty-one of them were prospectively ("light mesh") and 38 retrospectively ("heavy mesh") evaluated for testicular volume and perfusion, serum levels of sexual hormones, ejaculate volume, and number of spermatic cells. Those parameters were determined preoperatively (prospective group) and not earlier than 3 months postoperatively (both groups). RESULTS: No significant difference between pre- and postoperative values was detected in the prospectively studied group. All postoperative parameters were within the normal range in the retrospective group. There was no evidence of impaired fertility in any patient due to the operation. CONCLUSION: The standardized TEP technique for simultaneous bilateral inguinal hernia repair in male patients was not associated with a higher risk for postoperative infertility after mesh implantation. The use of heavy-weight meshes had no negative effect on fertility.

Acute liver failure: from bench to bedside.

Acute liver failure constitutes a challenge to clinicians and scientists alike. The course of the disease, usually unpredictable and polarizing, is associated with a high mortality unless liver transplantation is feasible, but can end in a spontaneous restitution. It poses many scientific questions regarding the mechanisms of liver cell damage and regeneration and the possibility of new therapeutic approaches. However, the performance of clinical studies in patients in acute liver failure presents problems because of the varied etiology, the small number of cases, and furthermore due to ethical and logistical difficulties. For this reason experimental investigations have gained a special importance. Arising from the improved understanding of the mechanisms of liver cell damage in acute liver failure, which may be primarily due not to the initial noxious agent alone but may also be triggered secondarily by the release of proinflammatory mediators, there are numerous options for liver cell protection, some of which have already proved successful in experimental studies. New insights into the mechanisms of regulation of liver regeneration and the physiological liver mass, gathered in particular from experimental models of partial hepatectomy and by the use of gene-manipulated animals, have contributed to the development of new therapeutic approaches for the stimulation of liver cell regeneration. Temporary liver support systems have already been successfully employed in some cases under clinical conditions. Although the systematic experimental investigation of many of the questions of acute liver failure has significantly contributed to a better understanding of liver cell damage and regeneration, the application of this new knowledge to clinical practice is to some extent made difficult by the artificial simplification that experimental studies inevitably entail and needs to be validated by controlled clinical studies.

Development and evaluation of an experimental model for investigating the pathogenesis and therapeutic strategies of acute liver failure.

Because of the various etiologies of acute liver failure (ALF) a clinically relevant model must fulfill four criteria--reversibility, reproducibility, ALF-induced death, and a sufficient time interval for diagnosis and therapy between induction and death. In this study an experimental model was evaluated for these criteria. A total of 49 rats were randomized into seven groups: First, a pilot study was performed regarding the survival rate after different treatments: In group I, animals underwent a 70% liver resection. In group II, 70% liver resection was combined with ascending doses of postoperative endotoxin administration up to 400 microg/kg (group IIc). In group III, animals only underwent liver mobilization. In group IV, ALF was induced according to the protocol of group IIc, but with additional treatment of an endothelin-A-receptor (ETAR) antagonist. Animals in group V received only 400 microg endotoxin. After induction of ALF, all animals died within the first day, showing significantly elevated bilirubin and ammonium levels and severe damage to hepatocellular integrity. Application of the ETAR antagonist resulted in the survival of 6/7 animals until the 14th day; the biochemical and histomorphological changes were reversible. All other animals survived to the 14th day. A clinically relevant model of ALF in rats can be created by the combination of 70% liver resection and endotoxin application to produce an inflammatory component.