Differences in inflammatory bowel disease phenotype between South Asians and Northern Europeans living in North West London, UK.

OBJECTIVES: The incidence and prevalence of inflammatory bowel disease (IBD) is increasing throughout Asia. Since the 1950s, there has been substantial migration from South Asia (India, Pakistan, and Bangladesh) to the United Kingdom. The aim of this study was to define the clinical phenotype of IBD in UK South Asians living in North West London, and to compare the results with a white Northern European IBD cohort. METHODS: The phenotypic details of 367 South Asian IBD patients (273 ulcerative colitis (UC) and 94 Crohn's disease (CD)), undergoing active follow-up in five North West London hospitals, were compared with those of 403 consecutively collected white Northern European IBD patients (188 UC and 215 CD). RESULTS: The phenotype of IBD differed significantly between the two populations. 63.0% of South Asian UC patients had extensive colitis compared with 42.5% of the Northern European cohort (P < 0.0001). Proctitis was uncommon in South Asian UC patients (9.9 vs. 26.1% in Northern European patients, P<0.0001). In the South Asian CD cohort, disease location was predominantly colonic (46.8%). CD behavior differed significantly between the groups, with less penetrating disease compared with Northern Europeans (P=0.01) and a reduced need for surgery (P=0.003). CONCLUSIONS: The phenotype of IBD in South Asians living in North West London is significantly different from that of a white Northern European IBD cohort. Knowledge of ethnic variations in disease phenotype may help to identify key genetic, environmental, and behavioral factors contributing to the development of IBD.

The effect of hypnosis on systemic and rectal mucosal measures of inflammation in ulcerative colitis.

OBJECTIVES: Hypnotherapy is effective in several diseases with a psychosomatic component. Our aim was to study the effects of one session of hypnosis on the systemic and rectal mucosal inflammatory responses in patients with active ulcerative colitis (UC). METHODS: In total, 17 patients with active UC underwent a 50-min session of gut-focused hypnotherapy. Before and after each procedure, the systemic inflammatory response was assessed by serum interleukin (IL)-6 and IL-13 concentrations, tumor necrosis factor-alpha (TNF-alpha) and IL-6 production by lipopolysaccharide (LPS)-stimulated whole blood, leukocyte count, natural killer (NK) cell number, platelet activation, and platelet-leukocyte aggregate formation. Rectal inflammation was assessed by mucosal release of substance P (SP), histamine, IL-13 and TNF-alpha, reactive oxygen metabolite production, and mucosal blood flow. Eight patients with active UC underwent a control procedure. RESULTS: Hypnosis decreased pulse by a median 7 beats per minute (bpm) (P= 0.0008); it also reduced the median serum IL-6 concentration by 53% (P= 0.001), but had no effect on the other systemic variables assessed. Hypnosis reduced rectal mucosal release of SP by a median 81% (P= 0.001), histamine by 35% (P= 0.002) and IL-13 by 53% (P= 0.003), and also, blood flow by 18% (P= 0.0004). The control protocol had no effect on any of the variables assessed. CONCLUSIONS: Hypnosis reduced several components of the systemic and mucosal inflammatory response in active ulcerative colitis toward levels found previously in the inactive disease. Some of these effects may contribute to the anecdotally reported benefits of hypnotherapy and provide a rationale for controlled trials of hypnotherapy in UC.

Optimizing quality of outpatient care for patients with inflammatory bowel disease: the importance of specialist clinics.

BACKGROUND: Most patients with inflammatory bowel disease (IBD) undergo long-term outpatient follow up. However, quality of care provided by specialist and non-specialist IBD clinics is rarely critically audited. OBJECTIVE: To compare the standard of outpatient care provided by general gastroenterology and specialist IBD clinics within a single hospital using defined quality criteria. METHODS: The case notes of 60 consecutive patients with IBD attending general gastroenterology clinics and of 100 patients attending the specialist IBD clinic were reviewed for fulfillment of six quality criteria over the preceding 18 months. RESULTS: The proportion of patients fulfilling all six criteria was higher in the specialist IBD clinic. In the specialist IBD clinic, compared with the general gastroenterology clinics, blood tests were performed with appropriate frequency during the initiation of immunosuppressive treatment in 7/11 versus 2/12 patients (P=0.04) and during maintenance in 24/31 versus 6/21 patients (P=0.001); bone protection with oral steroids were given to 25/53 versus 4/24 patients (P=0.01); a screening colonoscopy at 8-10 years was performed in 25/27 versus 11/20 patients with ulcerative colitis (P=0.004); annual serum urea and creatinine concentrations were measured in 82/89 versus 31/45 patients prescribed 5-aminosalicylates (P=0.001); annual liver function tests were performed in 96/100 versus 38/60 patients (P=0.001); and annual haematinics were measured in 37/47 versus 18/33 patients with Crohn's disease (P=0.03). CONCLUSION: By these criteria, the specialist IBD clinic provided better care than the non-specialist general gastroenterology clinics. Even in the specialist clinic, however, the care of a minority of patients did not fulfil certain criteria, emphasizing the need for a critical audit of outpatient management of IBD.

The role of psychological stress in inflammatory bowel disease.

Inflammatory bowel disease (IBD) is an idiopathic inflammatory condition of the gastrointestinal tract whose natural history is one of periods of remission and relapse. The aetiology is complex and reflects an interaction between genes and environment. Psychological stress has long been reported by both doctors and patients as worsening disease activity in IBD. Prospective studies of the relationship between disease relapse and adverse life events have produced conflicting results, in part due to the inherent difficulties of such studies. However, several more recent analyses have suggested that both adverse life events and chronic perceived stress can contribute to disease relapse. There is also an increasing body of evidence to suggest that experimental stress can increase mucosal inflammation both in patients with IBD and in animal models of colitis. Despite this increase in understanding the pro-inflammatory effects of stress in IBD, thus far only a few limited studies have examined stress reduction as a therapeutic modality.

The effect of acute psychologic stress on systemic and rectal mucosal measures of inflammation in ulcerative colitis.

BACKGROUND & AIMS: Recent studies suggest that life events and chronic stress increase the risk of relapse in inflammatory bowel disease. Our aim was to study the effects of acute psychologic stress on systemic and rectal mucosal inflammatory responses in patients with inactive ulcerative colitis (UC). METHODS: Twenty-five patients with inactive UC and 11 healthy volunteers (HV) underwent an experimental stress test. Ten patients with UC and 11 HV underwent a control procedure. Before and after each procedure, systemic inflammatory response was assessed by serum interleukin (IL)-6 and IL-13 concentrations, tumor necrosis factor (TNF)-alpha and IL-6 production by lipopolysaccharide (LPS)-stimulated whole blood, leukocyte count, natural killer (NK) cell numbers, platelet activation, and platelet-leukocyte aggregate (PLA) formation. In patients with UC, rectal mucosal inflammation was assessed by TNF-alpha, IL-13, histamine and substance P release, reactive oxygen metabolite (ROM) production, mucosal blood flow (RMBF) and histology. RESULTS: Stress increased pulse (P < .0001) and systolic BP (P < .0001). In UC, stress increased LPS-stimulated TNF-alpha and IL-6 production by 54% (P = .004) and 11% (P = .04), respectively, leukocyte count by 16% (P = .01), NK cell count by 18% (P = .0008), platelet activation by 65% (P < .0001), PLA formation by 25% (P = .004), mucosal TNF-alpha release by 102% (P = .03), and ROM production by 475% (P = .001) and reduced rectal mucosal blood flow by 22% (P = .05). The control protocol did not change any of the variables measured. There were no differences between the responses of the patients with UC and HV. CONCLUSIONS: Acute psychologic stress induces systemic and mucosal proinflammatory responses, which could contribute to exacerbations of UC in ordinary life.