The role of glial cells and apoptosis of enteric neurones in the neuropathology of intractable slow transit constipation

Bassotti, Gabrio

doi:10.1136/gut.2005.073197

Cited by 169 publications

(163 citation statements)

References 51 publications

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“…Only a few specific histopathological abnormalities have been found and described to date [12] . Concerning ICCs, there have been two studies of patients with idiopathic megabowl [5,13] and four studies of patients with idiopathic constipation with decreased ICC density [6,[14][15][16] . By contrast, another study of 63 patients with megacolon has shown no consistent alterations in colonic ICC histology [17] .…”

Section: Discussionmentioning

confidence: 99%

Therapy-refractory gastrointestinal motility disorder in a child with c-kit mutations

Breuer

Oh²,

Molderings³

et al. 2010

WJG

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Constipation and fecal impaction are frequent and distressing complaints in pediatric gastroenterology. Especially in neurologically handicapped children, treatment of severe forms of slow-transit constipation (STC) can be difficult. In the majority of cases, STC is of unknown etiology. However, in recent years, there is growing evidence that interstitial cells of Cajal (ICCs), which serve as electrical pacemakers and generate spontaneous electrical slow waves in the gastrointestinal tract, might play an important role in the pathophysiology of STC. It remains unclear whether morphological ICC alterations seen in affected patients are based on congenital developmental anomalies, or whether they are a consequence of long-term constipation with secondary damage of the gastrointestinal nervous system. To the best of our knowledge, we present the first case of a patient with histological alterations in ICC morphology who displayed multiple alterations of c-kit at the level of mRNA. The protein encoded by c-kit is the receptor tyrosine kinase Kit (CD117), which is crucial for development and function of ICCs. Therefore, these findings provide a new explanation for congenital alterations of ICC development that result in gastrointestinal motility disorders.

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Section: Discussionmentioning

confidence: 99%

Therapy-refractory gastrointestinal motility disorder in a child with c-kit mutations

Breuer

Oh²,

Molderings³

et al. 2010

WJG

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“…[23][24][25][26] After removal, the surgical specimens were immediately fixed in 10% neutral-buffered formalin for 24 h, then 12-20 full-thickness samples from the whole ablated colon were taken and transversal sections obtained. For conventional histology 5 mm paraffin sections were stained with Hematoxylin-Eosin, Pas and Trichrome stain.…”

Section: Methodsmentioning

confidence: 99%

Colonic neuropathological aspects in patients with intractable constipation due to obstructed defecation

et al. 2007

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One of the most frequent subtypes of constipation is represented by obstructed defecation, and it has recently been reported that these patients may have colonic motor abnormalities in addition to alterations of the anorectal area. However, it is unknown whether these patients display abnormalities of the enteric nervous system, as reported in other groups of constipated subjects. For this reason, we evaluated the neuropathologic aspects of the enteric nervous system in a homogeneous group of patients with obstructed defecation. Colonic specimens from 11 patients (nine women, age range 39-66 years) undergoing surgery for symptoms refractory to any therapeutic measure, including biofeedback training, were obtained and examined by means of conventional histological methods and immunohistochemistry (NSE, S100, c-Kit, formamide-mAb, Bcl-2, CD34, alfa-actin). Analysis of the specimens showed that the enteric neurons were significantly decreased only in the submucosal plexus of patients (Po0.0001 vs controls), whereas the enteric glial cells of constipated patients were reduced in both the myenteric (P ¼ 0.018 vs controls) and the submucosal plexus (P ¼ 0.004 vs controls). No difference between patients and controls were found concerning c-Kit and CD34 expression, and the number of apoptotic neurons. These findings support the concept that at least a subgroup of patients with obstructed defecation and severe, intractable symptoms display abnormalities of the enteric nervous system, mostly related to the enteric glial cells. These findings might explain some of the pathophysiological abnormalities, and help to better understand this condition.

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“…On the other hand, the patients with STC, in whom one would expect the best response, actually had the worst outcome. This fact, however, is not completely unexpected, since these are the patients who most frequently have features of intractable constipation, including a true colonic inertia [13], often due to important abnormalities of the enteric nervous system [14,15]. These abnormalities led to the reclassification of many form of constipation (especially the more severe ones) as true enteric neuro-gliopathies [16,17].…”

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confidence: 99%

The use of prucalopride in real life for the treatment of constipation subtypes: ups and downs

Bassotti

Bellini

2013

Tech Coloproctol

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The role of glial cells and apoptosis of enteric neurones in the neuropathology of intractable slow transit constipation

Cited by 169 publications

References 51 publications

Therapy-refractory gastrointestinal motility disorder in a child with c-kit mutations

Therapy-refractory gastrointestinal motility disorder in a child with c-kit mutations

Colonic neuropathological aspects in patients with intractable constipation due to obstructed defecation

The use of prucalopride in real life for the treatment of constipation subtypes: ups and downs

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