Short Term Outcomes of Laparoscopic Intraperitoneal Onlay Mesh With Facial Repair(IPOM-plus) for Ventral Hernia.

2019-10-28 13:56:50 | BioPortfolio


entral hernias are a major cause of functional impairment, abdominal pain, and bowel obstruction. The overall incidence of primary ventral hernia is estimated to be between 4 and 5 % in the literature, and ventral incisional hernia rates vary from 35 to 60 % within 5 years after laparotomy . After laparoscopy, this rate is estimated to decline from 0.5 to 15 % even after two decades, LVHR or open repair (OVHR) is still a matter of debate because of concerns about seroma formation, recurrence rate, and the intraperitoneal mesh position. . The laparoscopic technique for repairing ventral and incisional hernias is now well established. However, several issues related to LVHR, such as the high recurrence rate of hernias with large fascial defects and in extremely obese patients, are yet to be resolved. Additional problems include seroma formation. To solve these problems, laparoscopic fascial defect closure with IPOM reinforcement (IPOM-Plus) has been introduced in the past decade, and a few studies have reported satisfactory outcomes. Although detailed techniques for fascial defect closure and handling of the mesh have been published, standardized techniques are yet to be established.

Study Design




laparoscopic (IPOM) hernioplasty without repair, aparoscopic IIPOM hernioplasty with intracorporeal repair using proline 0 versus stratifix PDS, laparoscopic IPOM hernioplasty with transfacial closure using PDS LOOP 0


Zagazig Unversity




Zagazig University

Results (where available)

View Results


Published on BioPortfolio: 2019-10-28T13:56:50-0400

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Medical and Biotech [MESH] Definitions

The reconstruction of a continuous two-stranded DNA molecule without mismatch from a molecule which contained damaged regions. The major repair mechanisms are excision repair, in which defective regions in one strand are excised and resynthesized using the complementary base pairing information in the intact strand; photoreactivation repair, in which the lethal and mutagenic effects of ultraviolet light are eliminated; and post-replication repair, in which the primary lesions are not repaired, but the gaps in one daughter duplex are filled in by incorporation of portions of the other (undamaged) daughter duplex. Excision repair and post-replication repair are sometimes referred to as "dark repair" because they do not require light.

A DNA repair enzyme that catalyzes DNA synthesis during base excision DNA repair. EC

The repair of DOUBLE-STRAND DNA BREAKS by rejoining the broken ends of DNA to each other directly.

Repair of DNA DAMAGE by exchange of DNA between matching sequences, usually between the allelic DNA (ALLELES) of sister chromatids.

DNA repair proteins that include the bacterial MutL protein and its eukaryotic homologs. They consist of a conserved N-terminal region with weak ATPase activity, an endonuclease motif, and a C-terminal domain that forms MutL homodimers or heterodimers between MLH1 and the PMS1, MISMATCH REPAIR ENDONUCLEASE PMS2; or MLH3 proteins. These complexes function in DNA repair pathways, primarily DNA MISMATCH REPAIR, where MutL/MLH1 and the MUTS DNA MISMATCH-BINDING PROTEIN are targeted to damaged DNA.

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