Heartburn pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: José Eduardo Riceto Loyola Junior, M.D.[2]

Overview

The sensation of heartburn is caused by exposure of the lower esophagus to the acidic contents of the stomach. Normally, the lower esophageal sphincter (LES) separating the stomach from the esophagus is supposed to contract to prevent this situation. If the sphincter relaxes for any reason (as normally occurs during swallowing), stomach contents, mixed with gastric acid, can return into the esophagus. This return is also known as reflux, and may progress to gastroesophageal reflux disease (GERD) if it occurs frequently. If this is the case, the gastric acid and pepsin now located in the esophagus can injure the tight junction proteins in the esophageal epithelium. This results in increased paracellular permeability and dilated intercellular space and edema in the submucosa, which is amplified by an immunological mechanism mediated by inflammatory cytokines.[1]

Pathophysiology

  • With the most recent research findings, it is believed that the gastric acid does not directly cause heartburn, but causes it using a myriad of inflammatory mechanisms which are being elucidated and may be targets of new therapeutic drugs in the future.[1]
Source by:BruceBlaus - Own work, CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=44923646

Pathology


Many changes have been reported in the esophageal epithelium in patients with gastroesophageal reflux disease, as a response to damage. These changes have been summarized in the Esohisto project:

Histologic criteria for the recognition and assessment of microscopic lesions related to gastroesophageal reflux disease (GERD) – the Esohisto project criteria[3]
Proliferative changes of the squamous epithelium Criterion Definition and method of assessment Severity score
Basal cell layer Hyperplasia Basal cell layer thickness in μm as a proportion (%) of total epithelial thickness (10×) 0 (<15%)

1 (15–30%)

2 (>30%)

Papillary Elongation Papillary length in μm as a proportion (%) of total epithelial thickness (10×) 0 (<50%)

1 (50–75%)

2 (>75%)

Dilated intercellular spaces Identify as irregular round dilations or diffuse widening of intercellular space (40×) 0 (absent)

1 (<1 lymphocyte)

2 (≥1 lymphocyte)

Inflammatory infiltrate Intraepithelial Eosinophils Count in the most affected high-power field (4×0) 0 (absent)

1 (1–2 cells)

2 (>2 cells)

Inflammatory infiltrate Intraepithelial Neutrophils Count in the most affected high-power field (40×) 0 (absent)

1 (1–2 cells)

2 (>2 cells)

Inflammatory infiltrate Intraepithelial mononuclear cells Count in the most affected high-power field (40×) 0 (0–9 cells)

1 (10–30 cells)

2 (>30 cells)

References

  1. 1.0 1.1 1.2 1.3 Miwa H, Kondo T, Oshima T (2016). "Gastroesophageal reflux disease-related and functional heartburn: pathophysiology and treatment". Curr Opin Gastroenterol. 32 (4): 344–52. doi:10.1097/MOG.0000000000000282. PMID 27206157.
  2. De Giorgi F, Palmiero M, Esposito I, Mosca F, Cuomo R (October 2006). "Pathophysiology of gastro-oesophageal reflux disease". Acta Otorhinolaryngol Ital. 26 (5): 241–6. PMC 2639970. PMID 17345925.
  3. Yerian L, Fiocca R, Mastracci L, Riddell R, Vieth M, Sharma P; et al. (2011). "Refinement and reproducibility of histologic criteria for the assessment of microscopic lesions in patients with gastroesophageal reflux disease: the Esohisto Project". Dig Dis Sci. 56 (9): 2656–65. doi:10.1007/s10620-011-1624-z. PMID 21365241.