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Biomedical subjects

Robin Spiller

Publications and source records attributed to Robin Spiller.

17 recordsLinked to original sources

How inflammation changes neuromuscular function and its relevance to symptoms in diverticular disease.

Diverticulosis is largely asymptomatic but recent evidence suggests that episodes of acute diverticulitis double the risk of subsequently suffering from recurrent noninflammatory pain. Numerous animal models demonstrate how inflammation is followed by circular muscle hypertrophy, abnormalities of innervation, and increased sensitivity to cholinergic agents. There is also an impairment of norepinephrine and acetylcholine release and damage to nitrergic neurons. These changes are also associated with visceral hypersensitivity. Many of the features, including visceral hypersensitivity are also seen in symptomatic patients with diverticulosis. The trinitrobenzene sulfonic acid colitis model demonstrates that inflammation is followed by long lasting increases in tachykinin and other neuropeptide immunoreactivity. These changes occur both in the mucosa and myenteric plexus and parallel changes seen in resections and mucosal biopsies in diverticular patients. These neural abnormalities may be responsible for the visceral hypersensitivity, which explains why symptoms correlate poorly with objective abnormalities such as intraluminal pressure or motor patterns. Treatment of visceral hypersensitivity might be more effective than current therapies that often leave pain unaltered.

Animals↗

Post-infectious irritable bowel syndrome.

PURPOSE OF REVIEW: Irritable bowel syndrome patients form a heterogeneous group with a variable contribution of central and peripheral components. The peripheral component is prominent in irritable bowel syndrome developing after infection (post-infectious irritable bowel syndrome) and this has proved a profitable area of research. RECENT FINDINGS: Recent studies have overthrown the dogma that irritable bowel syndrome is characterized by no abnormality of structure by demonstrating low-grade lymphocytic infiltration in the gut mucosa, increased permeability and increases in other inflammatory components including enterochromaffin and mast cells. Furthermore, increased inflammatory cytokines in both mucosa and blood have been demonstrated in irritable bowel syndrome. While steroid treatment has proved ineffective, preliminary studies with probiotics exerting an anti-inflammatory effect have shown benefit. SUMMARY: The study of post-infectious irritable bowel syndrome has revealed the importance of low-grade inflammation in causing irritable bowel syndrome symptoms. It has suggested novel approaches to irritable bowel syndrome including studies of serotonin and histamine metabolism which may be relevant to other subtypes of the disease.

Animals↗

Impact of bitter taste on gastric motility.

BACKGROUND: Unexplained nausea and vomiting is often associated with delayed gastric emptying in patients with functional dyspepsia. We hypothesized that the experience of an unpleasant, nauseating taste could lead to a delay in gastric emptying. METHODS: Sixteen healthy women consumed a bland liquid test meal on three separate study days. On two of the study days subjects sham fed either a bitter tasting, modified Slim-Fast bar or one with a pleasant strawberry flavour. The time for 50% gastric emptying (GE(50)) was non-invasively assessed by electrical impedance tomography and antral motility by electrogastrography (EGG). RESULTS: Gastric emptying was significantly delayed by sham feeding the bitter compared with the pleasant bar, GE(50) 24.7+/-3.9 versus 17.2+/-1.8 min, P<0.05. EGG power rose significantly during both the pleasant (basal 1.46+/-0.07 to 2.33+/-0.14 log(10) microV(2)/min, P=0.000) and the bitter sham feed (basal 1.64+/-0.09 to 2.35+/-0.11 log(10) microV(2)/min, P=0.000). CONCLUSION: An unpleasant bitter taste delays gastric emptying but does not significantly impair antral motility.

Adult↗

Irritable bowel syndrome: a little understood organic bowel disease?

Irritable bowel syndrome affects 10% of adults with an unexplained female predominance. Although only a few people see their family doctor, the disease causes reduced quality of life and represents a multi-billion pound health-care problem. The disorder clusters in families, which is possibly because of intra-familial learning and a genetic predisposition. Visceral hypersensitivity is a key feature in most patients. Results of imaging studies of regional cerebral blood flow during rectal distension suggest underlying disturbances of central processing of afferent signals, though this is not unique to the disorder, since it is seen in other chronic pain syndromes. Environmental factors that are strongly implicated in at least some patients include gastrointestinal infection and inflammation and chronic stress. Diagnosis is based on positive symptoms and absence of any alarm indicators. Treatment remains unsatisfactory and hinges on an excellent doctor-patient relationship, with drugs for symptom exacerbations. Cognitive behavioural treatment, psychotherapy, and hypnosis could provide long-lasting benefit in some patients. Tricyclic antidepressants in low doses seem to be the most effective class of drugs for the disorder on the basis of limited data.

Brain↗

Serotonergic modulating drugs for functional gastrointestinal diseases.

After many years of basic research we have now begun to learn how to manipulate the serotonergic mechanisms within the gut. This has lead to a number of significant advances including 5HT3 antagonists for the treatment of functional diarrhoea, 5HT4 agonists for the treatment of constipation and 5HT1 agonists for the treatment of impaired fundal relaxation. Initial enthusiasm has been somewhat dented by the withdrawal of alosetron because of ischaemic colitis, but it remains to be seen whether this adverse event will be seen with other 5HT3 antagonists. Finally it should be recognized that, in a substantial proportion of patients attending clinics complaining of functional symptoms, anxiety is a major component. The drugs so far described are by and large devoid of CNS effects. It remains possible therefore that a drug which combines both peripheral and central effects would likely to be beneficial.

Colon↗