Risk factors of recurrence after incisional hernia preperitoneal repair: a long-term retrospective single-center cohort study.

PURPOSE: To explore the risk factors for incisional hernia (IH) recurrence following open prepertioneal repair. METHODS: Patients diagnosed with primary IH who underwent open preperitoneal repair at our hospital were enrolled. Patients were assessed, and perioperative factors were collected. Recurrence surveys were performed at regular intervals throughout the long-term postoperative follow-up. The risk factors for IH recurrence were identified using univariate and multivariate analyses. RESULTS: This study included 145 patients. Significant differences were found between recurrence and non-recurrence patients regarding pulmonary ventilation function (PVT), age, body mass index (BMI), mesh materials, type of surgery (clean, clean-contaminated, or contaminated), surgical site infections (SSIs), maximum width of the hernia defect (MWHD), and site of incisional hernia (P < 0.01). The univariate survival analysis revealed that PVT abnormalities, age > 70 years, BMI > 27 kg/m2, porcine small intestine submucosal (PSIS) mesh, non-clean surgery, SSIs, MWHD > 10 cm, and location in the lateral zones were significant factors for IH recurrence after open preperitoneal repair. The multivariate survival analysis showed that PVT abnormalities, age > 70 years, BMI > 27 kg/m2, and PSIS mesh were independent risk factors for IH recurrence after open preperitoneal repair. CONCLUSIONS: We identified PVT abnormalities, age > 70 years, BMI > 27 kg/m2, and PSIS mesh as novel risk factors for IH recurrence after open preperitoneal repair.

A transcriptomic analysis of incisional hernia based on high-throughput sequencing technology.

PURPOSE: Incisional hernia is a common postoperative complication; however, few transcriptomic studies have been conducted on it. In this study, we used second-generation high-throughput sequencing to explore the pathogenesis and potential therapeutic targets of incisional hernias. METHODS: Superficial fasciae were collected from 15 patients without hernia and 21 patients with an incisional hernia. High-throughput sequencing of the fascia was performed to generate an expression matrix. We analyzed the matrix to identify differentially expressed genes (DEGs) and performed gene ontology and enrichment analyses of these DEGs. Additionally, an external dataset was utilized to identify key DEGs. RESULTS: We identified 1,823 DEGs closely associated with extracellular matrix (ECM) imbalance, bacterial inflammatory response, and fibrillar collagen trimerization. TNNT3, CMAY5, ATP1B4, ASB5, CILP, SIX4, FBN1 and FNDC5 were identified as key DEGs at the intersection of the two expression matrices. Moreover, non-alcoholic fatty liver disease-related, TNF, and IL-17 signaling pathways were identified as key enrichment pathways. CONCLUSIONS: We identified eight key DEGs and three pathways associated with incisional hernias. Our findings offer new insights into the pathogenesis of incisional hernias and highlight potential targets for their prevention and treatment.