Laparoscopic transabdominal preperitoneal repair of spigelian hernia-closure of the fascial defect is not necessary.

INTRODUCTION: Spigelian hernia (SH) is rare and is traditionally repaired using an open technique. There has been an increasing popularity of laparoscopic methods, with transabdominal preperitoneal (TAPP) repair being one of the popular techniques. Currently, most surgeons using the TAPP technique close the fascial defect prior to mesh placement. Here we report our experience with a TAPP repair that deliberately excludes approximation of the fascial defect. SUBJECTS AND METHODS: Prospective data were collected on consecutive patients undergoing elective SH repair under the care of a single surgeon between 2001 and 2012. Diagnosis was confirmed preoperatively using ultrasonography or computerized tomography. A laparoscopic TAPP repair was used without closing the defect. Following discharge all patients were followed up at 3 and 12 months. The clinical records were reviewed at the time this article was written. The technique, epidemiological characteristics, operative findings, hospital stay, morbidity, and follow-up are presented. RESULTS: Twenty-six patients (16 males) with a median age of 63 years were operated on. The follow-up period ranged between 6 months and 11 years (median, 4 years). Hernia defect size ranged from 2 to 10 cm. Mean operating time for unilateral defects was 45 minutes; that for bilateral defects was 70 minutes. Twenty-two patients were discharged on the same day. There were no postoperative complications or recurrences. CONCLUSIONS: Laparoscopic TAPP repair of SH without closing the defect is safe, effective, and durable. There is no additional benefit from routine closure of the fascial defect. On the contrary, there may be potential advantages in leaving the defect unopposed.

Evaluation of the 4q32-34 locus in European familial pancreatic cancer.

BACKGROUND: Familial pancreatic cancer (FPC) describes a group of families where the inheritance of pancreatic cancer is consistent with an autosomal-dominant mode of inheritance. The 4q32-34 region has been previously identified as a potential locus for FPC in a large American family. METHODS: The region was allelotyped in 231 individuals from 77 European families using nine microsatellite markers, and haplotyping was possible in 191 individuals from 41 families. Families were selected based on at least two affected first-degree relatives with no other cancer syndromes. RESULTS: Linkage to most of the locus was excluded based on LOD scores less than -2.0. Eight families were excluded from linkage to 4q32-34 based on haplotypes not segregating with the disease compared with a predicted six to seven families. Two groups of families were identified, which seem to share common alleles within the minimal disease-associated region of 4q32-34, one group with an apparently earlier age of cancer death than the other pancreatic cancer families. Four genes were identified with potential tumor suppressor roles within the locus in regions that could not be excluded based on the LOD score. These were HMGB2, PPID, MORF4, and SPOCK3. DNA sequence analysis of exons of these genes in affected individuals and in pancreatic cancer cell lines did not reveal any mutations. CONCLUSION: This locus is unlikely to harbor a FPC gene in the majority of our European families.