Outcomes in coeliac disease: a qualitative exploration of patients' views on what they want to achieve when seeing a dietitian.

BACKGROUND: Coeliac disease (CD) is managed by life-long adherence to a gluten-free diet and dietitians have the potential to facilitate this. Patient involvement through shared decision-making is central to behaviour-change skills used by dietitians, although there is little evidence supporting its inclusion in evaluating dietetic interventions. The present study aimed to explore patients' preferences for diet and nutrition-related outcomes in CD. METHODS: Adults with CD or adult carers of children with CD were invited through support networks. Participants took part in a telephone, face-to-face interview or focus group which was audio-recorded and transcribed. Themes were developed using a framework method. Ethical approval was obtained. RESULTS: Twenty-nine adult patients and five parents of CD children participated 0-34 years after diagnosis. Four main outcome-related themes emerged: (i) Participants wanted information specific to their lifestyle and time since diagnosis, focussing on food containing gluten, practical issues, prescribable items and general nutrition. (ii) The degree of satisfaction with the consultation process impacted on participants' experience, including the dietitian's CD expertise, consistency of the dietitian seen, and the frequency and length of appointments. (iii) Health concerns were important to participants and focussed on risk of osteoporosis, unwanted weight gain, and the fat and sugar content of manufactured gluten-free products. (iv) Clinical monitoring, including bone scans and antibody measurements, was mentioned but was not described as being of importance for most participants. CONCLUSIONS: The outcomes preferred by CD patients and carers focussed primarily on information and resources received and satisfaction with their dietetic consultation.

Role of prostaglandin E(2) and Ca(2+) in bradykinin induced contractions of guinea-pig gallbladder in vitro.

In this study, we investigated the contribution of prostaglandin E(2) to bradykinin induced contractions of guinea-pig gallbladder in vitro and characterized the sources of activator Ca(2+) for the bradykinin mediated contractions. Contractions induced by bradykinin in guinea-pig gallbladder smooth muscle strips were significantly attenuated by the cyclooxygenase inhibitor piroxicam (10 microM). In the presence of piroxicam, a threshold concentration of prostaglandin E(2) (1 nM) significantly enhanced the contractile response to subsequent challenge with bradykinin. Contractile responses to bradykinin were abolished in a Ca(2+)-free medium plus EDTA. The inhibitor of receptor mediated Ca(2+) entry, SK&F 96365 (1-[beta-[3-(4-methoxyphenyl)-propoxy]-4-methoxyphenethyl]-1H-imidazole hydrochloride, 10-50 microM) dose dependently abolished the response to bradykinin, while this response was only partially attenuated by nifedipine (10-50 microM; a voltage-operated Ca(2+) channel antagonist). Thapsigargin (an inhibitor of the sarcoplasmic reticulum calcium ATP-ase pump, 1 microM) produced sustained contractions of guinea-pig gallbladder strips that were dependent on extracellular Ca(2+). After incubation of strips in a Ca(2+)-free medium with thapsigargin, replacement of Ca(2+) caused a large sustained contraction. We conclude that the contractile response of guinea-pig gallbladder to bradykinin is modulated by prostaglandin E(2). Bradykinin induced contractions of guinea-pig gallbladder are highly dependent on extracellular Ca(2+) which enters through store-operated Ca(2+) channels and partially through voltage-operated Ca(2+) channels.

Sources of calcium in neurokinin A-induced contractions of human colonic smooth muscle in vitro.

OBJECTIVES: Tachykinins have been implicated in the pathogenesis of colonic dysmotility. The sources of activator calcium for neurokinin A (NKA)-induced contraction of human colonic smooth muscle have not been assessed. We evaluated the contribution of extracellular and intracellular Ca2+ to NKA-induced contractions. METHODS: Circular smooth muscle strips of human colon were suspended under 1 g of tension in organ baths containing Krebs solution at 37 degrees C gased with 95% O2/5% CO2. Contractile activity was recorded isometrically. RESULTS: Cumulatively applied NKA (0.1 nmol/L-0.3 micromol/L), produced concentration-dependent contractions of human colonic smooth muscle strips that were not affected by tetrodotoxin (1 micromol/L). The contractile response to NKA was abolished in a Ca2+-free medium containing ethylenediaminetetraacetate (EDTA) (1 mmol/L). Pretreatment of muscle strips with nifedipine (1 micromol/L), an L-type voltage-operated Ca2+ channel antagonist, abolished the contractile responses to NKA. Pretreatment with SK&F 96365 (10 micromol/L and 30 micromol/L), a putative receptor-activated and voltage-operated Ca2+ channel antagonist, attenuated the contractile responses. Depletion of intracellular Ca2+ stores with thapsigargin (1 micromol/L), an inhibitor of the sarcoplasmic reticulum Ca2+ ATP-ase, had no effect on NKA-induced contractions. CONCLUSIONS: NKA-mediated contraction of human colonic smooth muscle is dependent on an influx of extracellular Ca2+ through L-type voltage-operated Ca2+ channels. Intracellular Ca2+ release seems to have little role to play in NKA-mediated contractions.

A 3-month, double-blind, controlled trial of feeding with sucrose polyester in human volunteers.

Sucrose polyester (SPE) is a tasteless, odourless substance which reduces plasma cholesterol concentrations and may therefore be valuable as a fat substitute in human foodstuffs. It has recently been approved for use in snack foods by the United States Federal Drug Administration. The current study was designed to investigate its effects on gastrointestinal physiology and nutrient absorption in human subjects. A 6-month (2 x 3-month periods) double-blind, placebo-controlled, randomized, cross-over trial of SPE and control fat was performed in healthy free-living volunteers. Subjects consumed 20-40 g of SPE daily (mean 26.8 (SE 6.8) g) which reduced the intake of total and saturated fat but had no effect on energy intake or body weight. Plasma cholesterol and triacylglycerols were reduced. The frequency of bowel movements and their urgency were increased and anal leakage occurred in 7.2% of subjects. Abdominal pain was more frequent in subjects receiving SPE and was significantly greater than in the control group after 8 weeks feeding. The plasma concentrations of vitamin E and six carotenoids were significantly reduced. Routine haematology and biochemistry, other vitamins, intestinal biopsies, bile-salt retention, rectal prostaglandins, fractional Ca absorption and aminopyrine metabolism were unaffected. The ingestion of foods containing 20-40 g SPE daily provoked significant gastrointestinal problems. This intake is greater than that to be expected from the use of SPE in savoury snack foods, for which it has been approved by the United States Federal Drug Administration. However, the favourable effects on lipid profiles must be balanced against the reduction in the concentrations of vitamins and carotenoids, as these compounds may have beneficial effects on health through protection from free-radical oxidative stress.

A review of associations between Crohn's disease and consumption of sugars.

OBJECTIVES: To critically review the available literature reporting associations between the onset of Crohn's disease and intakes of sugars or sugar-containing foods. To evaluate published evidence on the use of dietary manipulation of sugars in the treatment of Crohn's disease. DESIGN: All publications from refereed journals which reported intakes of sugars and sugar-containing foods in the context of Crohn's disease onset or treatment were selected. CONCLUSION: Evidence suggesting a relationship between sugars and onset of Crohn's disease was inconsistent and subject to important methodological limitations. There was a clear lack of distinction between reporting of current, as opposed to, retrospective intakes. There appeared to be no clinical advantage to the use of reduced sugar diets in Crohn's disease treatment.

Long-chain triglycerides reduce the efficacy of enteral feeds in patients with active Crohn's disease.

Elemental diets are effective treatments for active Crohn's disease. To determine which dietary constituents are of therapeutic importance, the effectiveness of four separate feeds was related to their compositions, and the findings substantiated by meta-analysis of previous dietary studies. 76 patients with active Crohn's disease were recruited. 17 were randomised to an amino acid-based elemental diet (E028), 22 to E028 with added long-chain triglyceride (E028 LCT), 18 to a semi-elemental, peptide based diet (Pepdite 2+) and 19 received E028 with added medium-chain triglyceride (E028 MCT). Disease activity fell in all groups and remission rate was negatively correlated with the amount of energy derived from LCT (r = -0.97, p = 0.016). Inflammatory indices fell in the groups (E028 + E028 MCT) containing least LCT. No other dietary constituents correlated with remission rate. A meta-analysis of published studies confirmed a negative correlation between remission rate and LCT (r = -0.63, p = 0.006) but not other constituents. The association between dietary LCT and remission rate may have pathogenic significance and allow the development of more effective enteral feeds.

Treatment of active Crohn's disease by exclusion diet: East Anglian multicentre controlled trial.

Elemental diet is as effective in producing remission of Crohn's disease (CD) as is corticosteroid treatment, but most patients relapse soon after resumption of a normal diet. We have investigated the efficacies of dietary modification and oral corticosteroids in maintaining remission achieved with elemental diet. In a multicentre trial, 136 patients with active CD were started on elemental diet and other treatment was withdrawn. 43 (31%) declined to continue elemental diet for 14 days, but 78 (84%) of the remaining 93 achieved remission and were randomly assigned corticosteroids (38) or diet (40). Corticosteroid treatment started at 40 mg prednisolone daily, which was tapered and stopped after 12 weeks; that group received dietary advice on healthy eating. The diet group received "tapered" placebo and were instructed to introduce one new food daily, excluding any that precipitated symptoms. Assessment of progress for up to 2 years was made by physicians unaware of group assignment. Intention-to-treat analysis showed median lengths of remission of 3.8 (interquartile range 5.0) months in the corticosteroid group and 7.5 (15.3) months on diet, and relapse rates at 2 years, adjusted for withdrawals, of 79% and 62%, respectively (p = 0.048). Clinical improvement in the diet group was associated with significant changes in plasma albumin and alpha 1-antichymotrypsin concentrations and erythrocyte sedimentation rate. Food intolerances discovered were predominantly to cereals, dairy products, and yeast. Diet provides a further therapeutic strategy in active Crohn's disease.