Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C1510475 (diverticular disease)
 2,138 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Some patients with colonic diverticula suffer recurrent abdominal pain and exhibit visceral hypersensitivity, though the mechanism is unclear. Prior diverticulitis increases the risk of being symptomatic while experimental colitis in animals increases expression of neuropeptides within the enteric nervous system (ENS) which may mediate visceral hypersensitivity. Our aim was to determine the expression of neuropeptides within the ENS in diverticulitis (study 1) and in patients with symptomatic disease (study 2). Study 1 - Nerves in colonic resection specimens with either acute diverticulitis (AD, n = 16) or chronic diverticulitis (CD, n = 16) were assessed for neuropeptide expression recording % area staining with protein gene product (PGP9.5), substance P (SP), neuropeptide K (NPK), pituitary adenylate cyclase activating polypeptide (PACAP), vasoactive intestinal polypeptide (VIP) and galanin. Study 2 - Seventeen symptomatic and 15 asymptomatic patients with colonic diverticula underwent flexible sigmoidoscopy and multiple peridiverticular mucosal biopsies. Study 1- Neural tissue, as assessed by PGP staining was increased to a similar degree in circular muscle in both AD and CD. The CD specimens showed significant increases in the immunoreactivity of SP, NPK and galanin in both mucosal and circular muscle layer compared with controls. Study 2 - Mucosal histology was normal and PGP9.5 staining was similar between groups however patients with symptomatic diverticular disease demonstrated significantly higher levels of SP, NPK, VIP, PACAP and galanin within the mucosal plexus. Patients with symptomatic diverticular disease exhibit increased neuropeptides in mucosal biopsies which may reflect resolved prior inflammation, as it parallels the changes seen in acute and chronic diverticulitis.
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PMID:Post inflammatory damage to the enteric nervous system in diverticular disease and its relationship to symptoms. 1945 15

The pathogenesis of diverticular disease is still poorly understood and considered to be multifactorial. Whereas classical pathogenetic concepts have focused on risk factors including increasing age, low-fiber diet and connective tissue disorders, novel concepts take into account that patients with diverticular disease exhibit disturbed intestinal motility patterns (that may result in functional obstruction and painful sensations) therefore postulating an underlying enteric neuro-/myopathy. Recent studies including quantitative evaluations of the enteric nervous system (ENS) in diverticular disease yielded hypoganglionic conditions of both myenteric and submucosal plexus as well as a nerve tissue remodeling in chronic diverticular disease. The disturbed neuromuscular communication was proven by demonstrating alterations in several enteric neurotransmitter systems, exemplified for the cholinergic, serotonergic, nitrergic system as well as for vasointestinal peptide, galanin and tachykinins. Novel lines of evidence have added the involvement of neurotrophic factors such as glial cell line-derived neurotrophic factor which is supposed to regulate ENS development and maintenance and which is downregulated in patients with diverticular disease. Consistent with the hypothesis of an enteric myopathy, deficits in smooth muscle integrity and composition such as hypertrophy, fibrotic transformation and gene expression deficits could be delineated. Taken together, the structural and functional findings on alterations of the ENS and the enteric musculature in diverticular disease provide evidence to strengthen the hypothesis that an enteric neuro-/myopathy may contribute to the development of colonic diverticula and the generation of symptoms in the course of the disease.
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PMID:Abnormalities of neuromuscular anatomy in diverticular disease. 2257 80