In quiescent IBD, IBS-like symptoms related to persistent subclinical inflammation associated with increased colonic paracellular permeability. A persistent increase in TNF-α in colonic mucosa may contribute to the epithelial barrier defects associated with abdominal pain in quiescent IBD, but not in IBS. Optimisation of anti-inflammatory therapy may be considered in quiescent IBD with IBS-like symptoms.
In IBS patients, the presence of an allergic background correlates with a more severe disease and diarrhea predominance, possibly by enhancing mucosal MC activation and paracellular permeability.
Elevated MCs counts are a key feature of the low-grade inflammatory infiltrate in the caecal mucosa of IBS. Fatigue and depression are associated with mucosal cell counts, in particular MCs, suggesting that psychological factors are associated with the low-grade inflammatory infiltrate in IBS.
The prevalence of IBS-like symptoms is elevated in quiescent CD. The presence of IBS-like symptoms in quiescent CD is probably associated with the range of fatigue/depression disorders. The mechanism underlying the occurrence of IBS-like symptoms in quiescent CD needs to be further explored.
HDM, a ubiquitous environmental factor, is present in the human gut where it directly affects gut function through its proteolytic activity. HDM may be an important trigger of gut dysfunction and warrants further investigation.
Neuropathy Target Esterase (NTE) is the molecular target in the nervous system for organophosphorus esters (OP) when they cause delayed polyneuropathy. Some NTE activity was recently found also in blood lymphocytes. An unsuccessful suicide attempt with the widely used pesticide chlorpyrifos (0,0-diethyl-0-3,5,6,-trichloro-2-pyridyl phosphorothioate) is reported, where prior inhibition of lymphocytic NTE correlates with the delayed development of polyneuropathy. A 42-year-old man drank approximately 300 mg/kg chlorpyrifos. The subsequent severe cholinergic syndrome lasted for 17 days with varying degrees of severity. Thirty days after intoxication the clinical and electrophysiological examination of the peripheral nervous system was normal but lymphocytic NTE was about 60% inhibited. On day 43 the patient began to complain of paresthesia and leg weakness. Clinical examination, electrophysiology and a nerve biopsy revealed signs of a peripheral polyneuropathy, axonal in type. This case report indicates that measurement of lymphocytic NTE might be used as a clinical test to predict the development of OP-induced delayed polyneuropathy.
We have shown that while transient functional bowel disorder occurred in 34.7% of patients (eight of 23 patients) recently infected with C difficile, only 4.3% of patients (one of 23 patients) had symptoms indicative of IBS after three months (ie, postinfectious IBS). Because an age-related reduction in immune responsiveness has been documented, it can be speculated that the low incidence of postinfectious IBS may be explained by the older age of the study population. Therefore, it cannot be excluded that the findings may be different in younger patients.
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