290
| Thus, as anticipated by the authors of the last case report
(Magalhães et al., 2024 ), we are facing the eternal question of what came first, intestinal inflammation or enteric neuritis. Possibly there is no definitive answer as in single cases different mechanisms may lead to the same result. While some authors (Blake et al., 2012 ; Chénier et al., 2011 ) put
forward the hypothesis of primary ganglionitis with subsequent in- testinal dysfunction supported by the fact that in some cases a de- creased neuronal density was found in the absence of concurrent inflammatory process (Schusser et al., 2000 ), others believe that ganglionopathy could be secondary to diffuse severe gut inflamma- tion (Ortolani et al., 2021 ). Herpesviruses have received significant attention on this as-
pect due to their demonstrated enteric neurotropism (De Giorgio et al., 2002 ; Giessler et al., 2020 ). If we add that the predominant cells found around the myenteric plexus are lymphocytes, it is rea- sonable to suspect a viral origin of the disease, even in the cases in which it was not confirmed by PCR (Burns et al., 1990 ; Chénier et al., 2011 ). On the other hand, if we consider the myenteric ganglionitis associated with A. perfoliata it becomes evident that, in this case, it is the severe local inflammation triggered by the parasite that causes a secondary neuronal degeneration (Pavone et al., 2011 ). However, in many cases, the reasoning cannot be so obvious,
especially if time has passed from the initial insult and the neuronal degeneration. Inflammatory infiltrates in the gut mucosa are a nonspecific
pattern of hyper- reactivity thus, it is often challenging to find out the exact cause. The immunohistochemical examination could add relevant information, as T cells are the predominant component of an immune- mediated mechanism but might still not clarify the exact underlying cause of such a mechanism. It is time to consider IBD diagnosed with the classical diagnos-
tic work- up (Vitale, 2022 ) as a clinical manifestation rather than a definitive diagnosis, as it can assemble different forms, degrees and causes of intestinal dysfunction. In particular, the mucosal infiltrates found on noninvasive biopsies may or may not be the cause or the consequence of neuronal dysfunction. The authors of the recent clinical report (Magalhães et al., 2024 )
highlight the limitations of partial thickness rectal or duodenal biop- sies as they do not permit the evaluation of the myenteric plexus. Although a reasonable step in the work- up of a case, in patients non- responsive to classical management and with recurrent episodes of intestinal obstruction, we should not delay a full- thickness biopsy to reach a comprehensive diagnosis and better define the progno- sis. From a research perspective, elucidating which microorganisms or immune- mediated reactions contribute to these forms of enteric neuropathies would be extremely interesting. However, in prac- tice, understanding the pathophysiological mechanism at the basis of the intestinal inflammation/dysfunction is more important than identifying a specific pathogen or antigen. Extensive neuronal dam- age is irreversible, leading to a poor long- term outcome (Chénier et al., 2011 ) and opening the way to alternative treatments that
VITALE
may help to regulate neuronal survival, development and function (Magalhães et al., 2024 ).
FUNDING INFORMATION There are no funders to report for this clinical commentary.
CONFLICT OF INTEREST STATEMENT No conflicts of interest have been declared.
ETHICS STATEMENT Not applicable to this clinical commentary.
ORCID Valentina Vitale
https://orcid.org/0000-0003-2273-5377
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