BACKGROUND: The pathophysiology of hiatal hernias is incompletely understood. This study systematically reviewed the literature of hiatal hernias to provide an evidence-based explanation of the pathogenetic theories and to identify any risk factors at the molecular and cellular levels. METHODS: A systematic search of the Medline and Pubmed databases on the pathophysiology of hiatal hernias was performed to identify English-language citations from the database inception to December 2010. RESULTS: Although few studies have examined the relationship of molecular and cellular changes of the diaphragm to the pathogenesis of hiatal hernias, there appear to be three dominant pathogenic theories: (1) increased intraabdominal pressure forces the gastroesophageal junction (GEJ) into the thorax; (2) esophageal shortening due to fibrosis or excessive vagal nerve stimulation displaces the GEJ into the thorax; and (3) GEJ migrates into the chest secondary to a widening of the diaphragmatic hiatus in response to congenital or acquired molecular and cellular changes, such as the abnormalities of collagen type 3 alpha 1. CONCLUSIONS: The pathogenesis of hiatal hernias at the molecular and cellular levels is poorly described. To date, no single theory has proved to be the definitive explanation for hiatal hernia formation, and its pathogenesis appears to be multifactorial.
BACKGROUND: The pathophysiology of hiatal hernias is incompletely understood. This study systematically reviewed the literature of hiatal hernias to provide an evidence-based explanation of the pathogenetic theories and to identify any risk factors at the molecular and cellular levels. METHODS: A systematic search of the Medline and Pubmed databases on the pathophysiology of hiatal hernias was performed to identify English-language citations from the database inception to December 2010. RESULTS: Although few studies have examined the relationship of molecular and cellular changes of the diaphragm to the pathogenesis of hiatal hernias, there appear to be three dominant pathogenic theories: (1) increased intraabdominal pressure forces the gastroesophageal junction (GEJ) into the thorax; (2) esophageal shortening due to fibrosis or excessive vagal nerve stimulation displaces the GEJ into the thorax; and (3) GEJ migrates into the chest secondary to a widening of the diaphragmatic hiatus in response to congenital or acquired molecular and cellular changes, such as the abnormalities of collagen type 3 alpha 1. CONCLUSIONS: The pathogenesis of hiatal hernias at the molecular and cellular levels is poorly described. To date, no single theory has proved to be the definitive explanation for hiatal hernia formation, and its pathogenesis appears to be multifactorial.
Authors: Lora Melman; Phillip R Chisholm; John A Curci; Batool Arif; Richard Pierce; Eric D Jenkins; L Michael Brunt; Christopher Eagon; Margaret Frisella; Kathleen Miller; Brent D Matthews Journal: Surg Endosc Date: 2010-01-07 Impact factor: 4.584
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