An Inflammatory Axonopathy of the Myenteric Plexus Producing a Rapidly Progressive Intestinal Pseudoobstruction

Krishnamurthy, Shoba; Schuffler, Michael D.; Belic, Lanie; Schweid, Abraham I.

doi:10.1016/0016-5085(86)91134-0

Cited by 23 publications

(12 citation statements)

References 12 publications

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“…59,62,66 The associated neoplasms include small cell lung carcinoma, thymoma, gynaecological and breast tumours. 55,56,[66][67][68] It is hypothesized that these autoantibodies are directed against antigens shared by tumour cells and by enteric neurones (onconeural antigens). 69 In vitro studies show that serum from patients with circulating antibodies may reduce neuromuscular function in rat intestinal muscle strips.…”

Section: Inflammatory Neuropathiesmentioning

confidence: 99%

Human enteric neuropathies: morphology and molecular pathology

Giorgio

Camilleri

2004

Neurogastroenterology Motil

203

210

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The aim of this study is to review current understanding of the molecular and morphological pathology of the enteric neuropathies affecting motor function of the human gastrointestinal tract and to evaluate the described pathological entities in the literature to assess whether a new nosology may be proposed. The authors used PUBMED and MEDLINE searches to explore the literature pertinent to the molecular events and pathology of gastrointestinal motility disorders including achalasia, gastroparesis, intestinal pseudo-obstruction, colonic inertia and megacolon in order to characterize the disorders attributable to enteric gut neuropathies. This scholarly review has shown that the pathological features are not readily associated with clinical features, making it difficult for a patient to be classified into any specific category. Individual patients may manifest more than one of the morphological and molecular abnormalities that include: aganglionosis, neuronal intranuclear inclusions and apoptosis, neural degeneration, intestinal neuronal dysplasia, neuronal hyperplasia and ganglioneuromas, mitochondrial dysfunction (syndromic and non-syndromic), inflammatory neuropathies (caused by cellular or humoral immune mechanisms), neurotransmitter diseases and interstitial cell pathology. The pathology of enteric neuropathies requires further study before an effective nosology can be proposed. Carefully studied individual cases and small series provide the basic framework for standardizing the collection and histological evaluation of tissue obtained from such patients. Combined clinical and histopathological studies may facilitate the translation of basic science to the clinical management of patients with enteric neuropathies.

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Section: Inflammatory Neuropathiesmentioning

confidence: 99%

Human enteric neuropathies: morphology and molecular pathology

Giorgio

Camilleri

2004

Neurogastroenterology Motil

203

210

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“…First, they identify mucosal inflammation and immune activation as putative causes of motility disturbances. While this is not necessarily new in the context of enteric infections, it provides insights into symptom generation in inflammatory bowel disease (Kern et al 1951, Rao et al 1987 as well as in cases of intestinal pseudo-obstruction in which immune cells have been identified in the neuromuscular layers of the gut (Krishnamurthy et al 1986). Second, these data illustrate that the motility apparatus of the gut is altered in the presence of inflammation that is ostensibly limited to the mucosa.…”

Section: Introductionmentioning

confidence: 98%

“…1951 , Rao et al . 1987 ) as well as in cases of intestinal pseudo‐obstruction in which immune cells have been identified in the neuromuscular layers of the gut ( Krishnamurthy et al . 1986 ).…”

Section: Introductionmentioning

confidence: 99%

The effect of nematode infection upon intestinal smooth muscle function

Collins

1998

Parasite Immunology

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Nematode infections are useful in studying both host defence and inflammation induced changes in intestinal physiology, including increased contraction by intestinal muscle. Our initial studies of the heightened muscle function found during T. spiralis infection led to investigations of the role of immune and inflammatory cells and mediators in the immunodulation of intestinal muscle function. By infecting various immunodeficient mouse strains, as well as gene transfer to the intestine, T lymphocytes, and in particular the CD4+ve subset were found to be responsible for altering smooth muscle function. However, eosinophils as well as the cytokine interleukin-4 may also be involved. Investigations also indicate a potential role for increased muscle function and propulsive activity in expelling nematode parasites. Mutant mice which suffer aberrant intestinal propulsion, or based upon an immunodeficiency, undergo reduced changes in muscle function during infection, undergo prolonged infections. While increased muscle function may be an adaptive host response, the changes in muscle function may persist long after the resolution of the infection. Thus understanding the mechanisms behind the immunomodulation of intestinal muscle function may also impact upon clinical gastroenterology, since motility disturbances in man often occur following enteric infections, or other inflammatory conditions of the bowel.

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“…The primary sporadic visceral neuropathies can be either degenerative non‐inflammatory or degenerative inflammatory according to the histopathological alterations of the ENS 2 . In primary inflammatory neuropathies, the infiltrate in the myenteric plexus is predominantly lymphocytic 2,5–9 or, in rare cases, eosinophilic 10 . The clinical manifestations depend on the segment of the gut involved 11 .…”

Section: Introductionmentioning

confidence: 99%