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Lymphocytic Oesophagitis Preliminary Ultrastructural Observations
Carlos A Rubio1, Elisabeth Villnow2, Peter T Schmidt3
1Department of Pathology, Karolinska University Hospital, Stockholm, Sweden Carlos.Rubio@ki.se.
Insights
Lymphocytic oesophagitis (LyE) shows significant ultrastructural damage in esophageal cells and intraepithelial lymphocytes. These changes, including cell disintegration and edema, are linked to intercellular fluid accumulation.
Area of Science:
- Gastroenterology
- Pathology
- Cell Biology
Background:
- Lymphocytic oesophagitis (LyE) is defined by a high count of intraepithelial lymphocytes (IELs) in the esophageal epithelium (≥40 CD3+IELs/HPF).
- The underlying ultrastructural changes in LyE are not well understood.
Purpose of the Study:
- To investigate the ultrastructural alterations in LyE using transmission electron microscopy (TEM).
Main Methods:
- Esophageal biopsies from seven patients were analyzed.
- Included were four LyE cases, one reflux oesophagitis, one eosinophilic oesophagitis (EoE), and one normal control.
Main Results:
- LyE exhibited marked intercellular edema (spongiosis) and regressive changes in squamous cells, including cytoplasmic edema, vacuolization, and cell disintegration.
- Intraepithelial lymphocytes (IELs) also displayed regressive changes, such as ballooning and intracytoplasmic disintegration.
Conclusions:
- Spongiosis in LyE may impair cell nutrition and introduce noxious molecules, contributing to observed TEM alterations.
- These findings offer novel insights into the ultrastructural pathology of LyE in both squamous cells and IELs.
Background/Aim:
Lymphocytic oesophagitis (LyE) is a newly described entity characterized by a high number of intraepithelial lymphocytes/ high power field (≥40 CD3+IELs/HPF) in the oesophageal epithelium. The aim of the study was to investigate possible ultrastructural changes taking place in LyE at the transmission electron microscopic (TEM) level.
Materials And Methods:
Oesopageal biopsies from seven patients were investigated: four were consecutive patients with LyE, one with reflux oesopagitis, one with eosinophilic oesopagitis (EoE) and one with histologically normal squamous epithelium.
Results:
In LyE, marked intercellular oedema (spongiosis) and a gamut of regressive changes were found in squamous cells, ranging from cytoplasmic oedema and vacuolization, to total cell disintegration. IELs also showed regressive changes ranging from ballooned, oedematous cytoplasm to signs of intracytoplasmatic disintegration.
Conclusion:
Besides hampered cell nutrition conveyed by spongiosis, putative noxious molecules contained in the intercellular spongiotic oedema might account for the dramatic TEM alterations found in LyE. The present findings provide, for the first time, "inside information" on the ultrastructural alterations taking place in LyE, both in squamous cells and in IELs.
