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We read with great interest the article by Roberts and co-authors (Gut 2006;55:1697–703) who reported a case–control study of oesophageal pathology in systemic sclerosis. Their findings and conclusions are an important contribution to the better understanding of the pathomechanisms of scleroderma-related oesophageal dysmotility.
As we have been investigating full-thickness biopsies of the bowel in various forms of intestinal dysmotility for more than two decades we were particularly interested in the changes of the myenteric plexus in their control material. Our interest derives from the paucity of data on the normal enteric nervous system due to the difficulties obtaining bowel tissue from healthy individuals.
The findings of “myenteric plexus-associated lymphocytes” in their control material and the interpretation of these cells seem to us a bit problematic. Our remarks and questions relate, therefore, to (1) the nature of the controls and (2) the presence of inflammatory cells at the myenteric plexus.
The controls were the next non-scleroderma autopsy cases matched by sex, race and decade of age. Autopsy is performed on previously sick people who died of their disease. Therefore, their control material cannot be regarded as “normal control” regarding the presence/absence of inflammatory cells in the region of the myenteric plexus. To be able to judge the nature of these controls the reader needs the pathological diagnoses obtained following the autopsies. We do not know how many of the autopsied patients in the control group had, for instance, malignant tumours, other autoimmune diseases or inflammatory disorders. It is well known that both in malignant tumours (lung carcinoma) and inflammatory bowel disease, lymphocytic ganglioneuritis can be found in otherwise normal parts of the gastrointestinal wall. Unfortunately, the authors did not provide a table with the main diseases found at autopsy. Due to this fact we do not think that their control material represents true controls and therefore it should not be regarded as such.
Their use of the term “cellular infiltrates” is also problematic. Inflammatory cellular infiltrates means, according to classic pathological teaching, the presence of various inflammatory cells outside the blood and lymphatic vasculature, ie, infiltrating the tissue, coming into close contact with the tissue specific or connective tissue cells. The authors wrote: “...lymphatic vessels surrounded the myenteric plexus. Lymphatic vessels may account for the trivial cellular infiltrates…”. Indeed, three lymphocytes in a row can be seen within a lymphatic vessel in the middle of fig 4A of the paper by Roberts et al, and similarly another lymphocyte in the bottom of this photograph surrounded by a “halo” probably representing the lumen of a small lymphatic capillary. Such inflammatory cells should absolutely not be regarded and interpreted as “cellular infiltrates”.
The situation is a little different regarding intraganglional lymphocytes in the close vicinity of neurons. Roberts and colleagues found “intraneural infiltrate” in one case at the gastro-oesophageal junction and one case in the distal oesophagus. They did not give information whether the inflammatory cells were within the myenteric ganglion or within the nerves. The absence of inflammatory cells within the myenteric ganglia in 72/74 control patients is otherwise an important finding, which supports our own observation.
We have not found a single lymphocyte or other inflammatory cell within the myenteric ganglia in our autopsy control material of 15 cases.1 We have seen a few intraganglional inflammatory cells only in one case when the patient died of septicaemia. Therefore we think that the presence of lymphocytes or other inflammatory cells within ganglia should be interpreted as abnormal.
Competing interests: None.
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