Abstract：
BACKGROUND: This systematic review aims to identify genetic and biologic markers associated with abdominal hernia formation.
METHODS: Following PRIMSA-guidelines, we searched PubMed, MEDLINE, Embase, Scopus, and COCHRANE databases.
RESULTS: Of 5946 studies, 65 were selected, excluding parastomal hernias due to insufficient data. For inguinal hernias, five studies unveiled 92 susceptible loci across 66 genes, predominantly linked to immune responses. Eleven studies observed elevated MMP-2 levels, with seven highlighting greater MMP-2 in direct compared to indirect inguinal hernias. One incisional hernia study identified unique gene-expression profiles in 174 genes associated with inflammation and cell-adhesion. In hiatal hernias, several genetic risk loci were identified. For all hernia categories, type I/III collagen ratios diminished.
CONCLUSIONS: Biological markers in inguinal hernias appears consistent. Yet, the genetic predisposition in incisional hernias remains elusive. Further research to elucidate these genetic and biological intricacies can pave the way for more individualized patient care.
METHODS: Following PRIMSA-guidelines, we searched PubMed, MEDLINE, Embase, Scopus, and COCHRANE databases.
RESULTS: Of 5946 studies, 65 were selected, excluding parastomal hernias due to insufficient data. For inguinal hernias, five studies unveiled 92 susceptible loci across 66 genes, predominantly linked to immune responses. Eleven studies observed elevated MMP-2 levels, with seven highlighting greater MMP-2 in direct compared to indirect inguinal hernias. One incisional hernia study identified unique gene-expression profiles in 174 genes associated with inflammation and cell-adhesion. In hiatal hernias, several genetic risk loci were identified. For all hernia categories, type I/III collagen ratios diminished.
CONCLUSIONS: Biological markers in inguinal hernias appears consistent. Yet, the genetic predisposition in incisional hernias remains elusive. Further research to elucidate these genetic and biological intricacies can pave the way for more individualized patient care.
摘要：
背景：本系统综述旨在确定与腹部疝形成相关的遗传和生物学标志物。
方法：遵循PRIMSA指南，我们搜索了PubMed,MEDLINE,Embase,Scopus,和COCHRANE数据库。
结果：在5946项研究中，65人被选中，由于数据不足，排除了造口旁疝。腹股沟疝,五项研究揭示了66个基因的92个易感基因座，主要与免疫反应有关。11项研究观察到MMP-2水平升高，与间接腹股沟疝相比，直接突出了七个更高的MMP-2。一项切口疝研究在与炎症和细胞粘附相关的174个基因中确定了独特的基因表达谱。在食管裂孔疝中，确定了几个遗传风险位点。对于所有疝气类别，I型/III型胶原比值减少。
结论：腹股沟疝的生物学标记似乎是一致的。然而，切口疝的遗传易感性仍然难以捉摸。进一步研究阐明这些遗传和生物复杂性可以为更个性化的患者护理铺平道路。
方法：遵循PRIMSA指南，我们搜索了PubMed,MEDLINE,Embase,Scopus,和COCHRANE数据库。
结果：在5946项研究中，65人被选中，由于数据不足，排除了造口旁疝。腹股沟疝,五项研究揭示了66个基因的92个易感基因座，主要与免疫反应有关。11项研究观察到MMP-2水平升高，与间接腹股沟疝相比，直接突出了七个更高的MMP-2。一项切口疝研究在与炎症和细胞粘附相关的174个基因中确定了独特的基因表达谱。在食管裂孔疝中，确定了几个遗传风险位点。对于所有疝气类别，I型/III型胶原比值减少。
结论：腹股沟疝的生物学标记似乎是一致的。然而，切口疝的遗传易感性仍然难以捉摸。进一步研究阐明这些遗传和生物复杂性可以为更个性化的患者护理铺平道路。
