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Crura ultrastructural alterations in patients with hiatal hernia: a pilot study

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An Erratum to this article was published on 22 June 2007

Abstract

Background

Laparoscopic fundoplication for gastroesophageal reflux disease (GERD) and hiatal hernia has been validated worldwide in the past decade. However, hiatal hernia recurrence still represents the most frequent long-term complication after primary repair. Different techniques for hiatal closure have been recommended, but the problem remains unsolved. The authors theorized that ultrastructural alterations may be implicated in hiatal hernia. Thus, this study was undertaken to investigate the presence of these alterations in patients with or without hiatal hernia.

Methods

Samples from Laimer–Bertelli connective membrane and muscular crura at the esophageal hiatus were collected from 19 patients with GERD and hiatal hernia (HH group), and from 7 patients without hiatal hernia enrolled as the control group (NHH group). Specimens were processed and analyzed by transmission electron microscopy.

Results

Muscle and connective samples from the NHH group did not present any ultrastructural alteration that could be detected by transmission electron microscopy. Similarly, connective samples from the HH group showed no ultrastructural alterations. In contrast, all muscle samples from the HH group exhibited sarcolemmal alterations, subsarcolemmal vacuolar degeneration, extended disruption of sarcotubular complexes, increased intermyofibrillar spaces, and sarcomere splitting.

Conclusion

The evidence of ultrastructural alterations in all the patients in the HH group raises the suspicion that the long-term outcomes of antireflux surgery depend not only on the surgical technique, but also on the underlying muscular diaphragmatic illness.

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Correspondence to L. Fei.

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An erratum to this article can be found at http://dx.doi.org/10.1007/s00464-007-9467-6

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Fei, L., del Genio, G., Brusciano, L. et al. Crura ultrastructural alterations in patients with hiatal hernia: a pilot study. Surg Endosc 21, 907–911 (2007). https://doi.org/10.1007/s00464-006-9043-5

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  • DOI: https://doi.org/10.1007/s00464-006-9043-5

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