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• W2020473612 abstract "Background & Aims: N-3 fatty acids from fish oil, antioxidants, and short-chain fatty acids (SCFAs) produced during the fermentation of soluble fiber may attenuate inflammation associated with ulcerative colitis (UC). We assessed the efficacy of a nutritionally balanced oral supplement enriched with fish oil, fructooligosaccharides, gum arabic, vitamin E, vitamin C, and selenium on disease activity and medication use in adults with mild to moderate UC. Methods: A total of 121 patients with UC and a disease activity index (DAI) from 3–9 on a 12-point scale were block randomized for extent of disease and smoking status. In addition to their usual diet, patients consumed 18 oz of the oral supplement or a carbohydrate-based placebo formula each day for 6 months. Clinical and histologic responses were assessed at 3 and 6 months or at the final visit. A change in average prednisone use between groups was tested by using a linear mixed-effects model. Results: Eighty-six patients completed the study. Baseline characteristics were not different between groups except for a higher total DAI score in the oral supplement group (7.3 ± 1.3; n = 36) compared with the placebo group (6.2 ± 2.0; n = 50) (P < .05). Both groups showed significant and similar degree of improvement at 6 months in DAI (−2.5 for oral supplement and −2.8 for placebo) and histologic index (−1.9 for oral supplement vs. −2.0 for placebo). Both intent-to-treat and completed patients given oral supplement had a significantly greater rate of decrease in the dose of prednisone required to control clinical symptoms over 6 months as compared with the placebo group (P < .001). Conclusions: The improvement in clinical response combined with a decreased requirement for corticosteroids suggest that this enriched oral supplement can be a useful adjuvant therapy in patients with UC. Background & Aims: N-3 fatty acids from fish oil, antioxidants, and short-chain fatty acids (SCFAs) produced during the fermentation of soluble fiber may attenuate inflammation associated with ulcerative colitis (UC). We assessed the efficacy of a nutritionally balanced oral supplement enriched with fish oil, fructooligosaccharides, gum arabic, vitamin E, vitamin C, and selenium on disease activity and medication use in adults with mild to moderate UC. Methods: A total of 121 patients with UC and a disease activity index (DAI) from 3–9 on a 12-point scale were block randomized for extent of disease and smoking status. In addition to their usual diet, patients consumed 18 oz of the oral supplement or a carbohydrate-based placebo formula each day for 6 months. Clinical and histologic responses were assessed at 3 and 6 months or at the final visit. A change in average prednisone use between groups was tested by using a linear mixed-effects model. Results: Eighty-six patients completed the study. Baseline characteristics were not different between groups except for a higher total DAI score in the oral supplement group (7.3 ± 1.3; n = 36) compared with the placebo group (6.2 ± 2.0; n = 50) (P < .05). Both groups showed significant and similar degree of improvement at 6 months in DAI (−2.5 for oral supplement and −2.8 for placebo) and histologic index (−1.9 for oral supplement vs. −2.0 for placebo). Both intent-to-treat and completed patients given oral supplement had a significantly greater rate of decrease in the dose of prednisone required to control clinical symptoms over 6 months as compared with the placebo group (P < .001). Conclusions: The improvement in clinical response combined with a decreased requirement for corticosteroids suggest that this enriched oral supplement can be a useful adjuvant therapy in patients with UC. Ulcerative colitis (UC) is a chronic inflammatory disease of the colon characterized by bloody diarrhea and abdominal pain. Mediators of the immune response associated with UC include cytokines, adhesion molecules, growth factors, and eicosanoids. These factors orchestrate the interaction between leukocytes, vascular endothelium, and colonic epithelium, and result in mucosal injury, which is the hallmark of UC.1Fiocchi C. Inflammatory bowel disease etiology and pathogenesis.Gastroenterology. 1998; 115: 182-205Abstract Full Text Full Text PDF PubMed Scopus (1858) Google Scholar Medical therapy attempts to interrupt this process so that tissue injury is minimized and mucosal healing is promoted. Corticosteroids are highly effective in moderately to severely active UC. Unfortunately, adverse effects are a concern and more than one quarter of patients will relapse when corticosteroid treatment is discontinued.2Truelove S.C. Witts L.J. Cortisone in ulcerative colitis. Final report on a therapeutic trial.BMJ. 1955; 2: 1041-1048Crossref PubMed Scopus (2182) Google Scholar Patients who relapse can be treated with repeated courses of corticosteroids, azathioprine, or 6-mercaptopurine if remission cannot be maintained with sulfasalazine or mesalamine.3Hanauer S.B. Baert F.J. The management of ulcerative colitis.Ann Rev Med. 1995; 46: 497-505Crossref PubMed Scopus (14) Google Scholar Unfortunately, immunosuppressive medications may not be tolerated or may lead to serious adverse effects. Efforts have continued to find new treatments for the management of UC that ideally would be effective, safe, and inexpensive. Evidence that the chronic intake of n-3 fatty acids from fish oil inhibits neutrophil and monocyte function suggests that n-3 fatty acids have anti-inflammatory properties. Beneficial effects of fish oil have been shown in animal models of inflammatory bowel disease (IBD)4Empey L.R. Jewell L.D. Garg M.L. et al.Fish oil-enriched diet is mucosal protective against acetic acid-induced colitis in rats.Can J Physiol Pharmacol. 1991; 69: 480-487Crossref PubMed Scopus (52) Google Scholar, 5Vilaseca J. Salas A. Guarner F. et al.Dietary fish oil reduces progression of chronic inflammatory lesions in a rat model of granulomatous colitis.Gut. 1990; 31: 534-539Crossref Scopus (165) Google Scholar and in small clinical trials that involved patients with UC.6Lorenz R. Weber P.C. Szimnan P. et al.Supplementation with n-3 fatty acids from fish oil in chronic inflammatory bowel disease.J Intern Med Suppl. 1989; 225: 225-232Google Scholar, 7Hillier K. Jewell R. Dorrell L. et al.Incorporation of fatty acids from fish oil and olive oil into colonic mucosal lipids and effects upon eicosanoid synthesis in inflammatory bowel disease.Gut. 1991; 32: 1151-1155Crossref PubMed Scopus (104) Google Scholar, 8Saloman P. Kornbluth A.A. Janowitz M.D. Treatment of ulcerative colitis with fish oil n-3-ω-fatty acid an open trial.J Clin Gastroenterol. 1990; 12: 157-161Crossref PubMed Scopus (120) Google Scholar Short-chain fatty acids (SCFAs) produced from bacterial fermentation also may influence the overall health of colonic mucosa in various colonic disorders. SCFA enemas have been shown to have a beneficial effect in patients with UC.9Senagore A.J. MacKeigan J.M. Scheider M. et al.Short-chain fatty acid enemas a cost effective alternative in the treatment of nonspecific proctosigmoiditis.Dis Colon Rectum. 1992; 35: 923-927Crossref PubMed Scopus (93) Google Scholar, 10Scheppach W. Sommer H. Kirchner T. et al.Effect of butyrate enemas on the colonic mucosa in distal ulcerative colitis.Gastroenterology. 1992; 103: 51-58Abstract PubMed Google Scholar, 11Scheppach W. German-Austrian SCFA Study GroupTreatment of distal ulcerative colitis with short-chain fatty acid enemas.Dig Dis Sci. 1996; 14: 2254-2259Crossref Scopus (169) Google Scholar, 12Breuer I. Soergel K.H. Lashner B.A. et al.Short chain fatty acid rectal irrigation for left-sided ulcerative colitis a randomised, placebo controlled trial.Gut. 1997; 40: 485-491PubMed Google Scholar These compounds cannot be delivered to the colon when taken orally because they are absorbed by the small bowel and metabolized by the liver. Fermentable fiber and nondigestible oligosaccharides taken by mouth increase the densities of beneficial bacteria (Bifidobacterium species) in the gastrointestinal tract13Hidaka H. Tashiro Y. Elda T. Proliferation of bifidobacteria by oligosaccharides and their useful effect on human health.Bifidobact Microflora. 1991; 10: 65-79Crossref Google Scholar, 14Okazai M. Fujikawa S. Matsumoto N. Effect of xylooligosaccharide on the growth of bifidobacteria.Bifidobact Microflora. 1990; 9: 77-86Google Scholar and these bacteria can increase the concentration of SCFAs in the colon.15Gibson G.R. Roberfroid M.B. Dietary modulation of the human colonic microbiota introducing the concept of prebiotics.J Nutr. 1995; 125: 1401-1412Crossref PubMed Scopus (5458) Google Scholar, 16Mitsuoka T. Bifidobacteria and their role in human health.J Indust Microbiol. 1990; 6: 263-268Crossref Scopus (311) Google Scholar Finally, a growing body of data indicate that oxygen-derived free radicals such as superoxide (O2−), hydrogen peroxide (H2O2), and hydroxyl radicals (OH−) have a role in mediating intestinal damage in IBD.17Grisham M.B. Oxidants and free radicals in inflammatory bowel disease.Lancet. 1994; 344: 859-861Abstract PubMed Scopus (466) Google Scholar, 18Buffinton G. Doe W. Depleted mucosal antioxidant defenses in inflammatory bowel disease.Free Radic Biol Med. 1995; 19: 911-918Crossref PubMed Scopus (237) Google Scholar, 19Keshavarzian A. Sedghi S. Kanofsky J. et al.Excessive production or reactive oxygen metabolites by inflamed colon analysis by chemiluminescence probe.Gastroenterology. 1992; 103: 177-185PubMed Google Scholar Considering the compromised antioxidation state of the large bowel of IBD patients, it may be beneficial to increase the intake of vitamins that have antioxidant properties. Considering the potential clinical benefit of these anti-inflammatory nutrients, Grisham et al20Grisham M.B. DeMichele S.J. Garleb K.A. et al.Sulfasalazine or enteral diets containing fish oil or oligosaccharides attenuate chronic colitis in rats.Inflamm Bowel Dis. 1996; 2: 178-188PubMed Google Scholar evaluated fish oil and the fermentable substrates in a rat model of chronic granulomatous colitis. Results showed an enteral diet supplemented with either fish oil and fructooligosaccharides or xylooligosaccharides exhibited anti-inflammatory action that was similar in efficacy to sulfasalazine in this model of colitis. A broad array of nutritional interventions have been used in the management of IBD.21Dudrick S.J. Latifi R. Schrager R. Nutritional management of inflammatory bowel disease.Surg Clin North Am. 1991; 71: 609-623PubMed Google Scholar, 22Burke A. Lichtenstein G.R. Rombeau J.L. Nutrition and ulcerative colitis.Baillieres Clin Gastroenterol. 1997; 11: 153-174Abstract Full Text PDF PubMed Scopus (34) Google Scholar In most cases these therapies, which include diet modification, enteral tube feeding, and parenteral nutrition, have been used to replete nutrient deficiencies or minimize symptoms associated with structural and functional abnormalities in Crohn’s disease. Some of the studies cited in these reviews suggest that enteral nutrition is effective therapy for the treatment of ileal and ileocolonic disease. There is no evidence that any of these nutritional approaches is of benefit in decreasing disease activity in UC. We felt that a specialized enteral formula could serve as a vehicle for the delivery of the previously discussed functional ingredients and that their combination may enhance the therapeutic efficacy in UC. Therefore, we undertook this clinical trial to assess the efficacy of a nutritionally balanced oral supplement with fish oil, fructooligosaccharides, gum arabic, and antioxidants (vitamin E, vitamin C, selenium) on disease activity and prescribed medication use in adults with mild to moderate UC. This study was a randomized, double-blind, placebo-controlled, parallel-group multicenter trial that recruited patients from 5 clinical centers in the United States. Patients meeting entry criteria and without exclusions were assigned to their study group at each center with the use of a permuted-block randomization design stratified for extent of disease (left-sided colitis or pancolitis) and smoking status (never smoked, quit smoking, or are active smokers) to ensure equal distribution for these characteristics among the study groups. The study physician, coordinator, patient caregivers, and patients were blinded as to diet identity throughout the study. The study randomization plan, data management, and statistical analyses were performed by an independent data management and statistical company (STATPROBE, Dublin, OH). The study was approved by the institutional review boards at each site before patient enrollment. Adult patients over the age of 18 years were included if they had UC for at least 6 months, had active inflammation on flexible endoscopic examination, and had symptoms of mild to moderate activity as determined by the disease activity index (DAI) of 3–9 at study entry as described by Sutherland et al23Sutherland L.R. Martin F. Greer S. et al.5-aminosalicylic acid enema in the treatment of distal ulcerative colitis, proctosigmoiditis, and proctitis.Gastroenterology. 1987; 92: 1894-1898Abstract PubMed Google Scholar Exclusion criteria included Crohn’s disease, infectious or ischemic colitis, or disease limited to the rectum. Patients also were excluded if they had severe UC requiring hospitalization or proctocolectomy; a history of bleeding diathesis, blood dyscrasia, or the need for therapeutic anticoagulation; a history of malignancy, human immunodeficiency virus, diabetes mellitus, or significant cardiac, pulmonary, hepatic, renal, or endocrinologic disease. The use of antibiotics and nonsteroidal anti-inflammatory drugs was not allowed within 2 weeks of enrollment and immunosuppressive medications for UC such as azathioprine, 6-mercaptopurine, methotrexate, and cyclosporine were not allowed within 4 weeks of study entry. Eligible patients underwent a complete history and physical examination at the baseline study (screening period) visit. The extent of UC was determined by either colonoscopy or barium enema performed within the previous year. A flexible sigmoidoscopy (or colonoscopy if extent of disease was not known) was performed at the baseline visit to confirm the presence of active disease. A modified Baron et al24Baron J.H. Connell A.M. Lennard-Jones J.E. Variation between observers in describing mucosal appearances in proctocolitis.BMJ. 1964; 1: 89-92Crossref PubMed Scopus (523) Google Scholar scale score of at least 1 out of 3 was required for study entry. This scale corresponds to the following endoscopic features: 0 = vascular pattern present, normal light reflex; 1 = loss of vascular pattern, edema without bleeding; 2 = granularity and friability; 3 = ulceration with spontaneous bleeding. The DAI was calculated to confirm the presence of mild to moderate disease activity. The DAI is based on 4 clinical parameters that include stool frequency, rectal bleeding, appearance of the rectal mucosa, and the physicians’ rating of disease activity. Each parameter is given a numeric score of 0 for normal, 1 for mild, 2 for modest, and 3 for severe activity. A mucosal biopsy specimen was taken above the rectal valves approximately 12–15 cm from the anal verge in an area without mucosal ulceration. A peripheral blood sample was obtained for a complete blood count, coagulation profile, serum chemistries, iron studies, erythrocyte sedimentation rate, plasma phospholipid fatty acids, and plasma concentrations of β-carotene, α-tocopherol, and retinol. Plasma phospholipids were isolated from the total lipids by thin-layer chromatography and quantitated by gas chromatography as previously described.25Huang Y.S. Chaudhary S. Thurmond J.M. et al.Cloning of the delta 12- and delta 6-desaturases from Mortierella alpina and recombinant production of gamma-linolenic acid in Saccharomyces cerevisiae.Lipids. 1999; 34: 649-659Crossref PubMed Scopus (127) Google Scholar Plasma levels of α-tocopherol and β-carotene were measured by Craft Technologies, Inc. (Wilson, NC) using high-performance liquid chromatography with programmed wavelength ultraviolet detection.26Craft N.E. High resolution HPLC method for the simultaneous analysis of carotenoids, retinoids, and tocopherols.FASEB Journal. 1996; 10: A527Google Scholar Stool samples were analyzed for enteric pathogens. A bleeding time also was obtained. Repeat evaluation was performed after 3 and 6 months of treatment. This included interim history, physical examination, flexible sigmoidoscopy with mucosal biopsy examination, and all laboratory tests previously outlined except stool cultures. Mucosal biopsy specimens were processed in Hollande fixative, stained with H&E, and examined by a single blinded pathologist (J.G.) who had no prior knowledge about the treatment or clinical activity of the disease. All slides were scored on a subjective 4-point scale (0–3+) for histologic features of active inflammation and chronicity using histologic criteria that have been associated reliably with UC.27Nostrant T.T. Kumar N.B. Appelman H.D. Histopathology differentiates acute self-limited colitis from ulcerative colitis.Gastroenterology. 1997; 92: 318-328Google Scholar, 28Surawicz C.M. Haggitt R.C. Husseman M. et al.Mucosal biopsy diagnosis of colitis acute self-limited colitis and idiopathic inflammatory bowel disease.Gastroenterology. 1994; 107: 755-763Abstract Full Text PDF PubMed Scopus (160) Google Scholar Markers of active inflammation included the presence or absence of cryptitis and/or crypt abscesses and erosion or ulceration of the surface epithelium. Features of chronicity included the presence or absence of architectural distortion, expansion of the lamina propria, and Paneth’s cell metaplasia. Activity scores (possible total of 6) and chronicity scores (possible total of 9) then were added to calculate a total score in each case (possible score of 15). The placebo formula was a ready-to-feed carbohydrate-based drink containing water, sucrose, flavoring, and color. No protein, fat, vitamins, or minerals were added to this product. The UC nutritional supplement (UCNS) is a nutritionally balanced ready-to-feed calorically dense (1.3 kcal/mL) formula supplemented with a novel oil blend containing fish oil (1.09 g eicosapentaenoic acid [EPA] and .46 g docosahexaenoic acid [DHA] per 8 oz), a fermentable oligosaccharide/fiber system (fructooligosaccharide and gum arabic), and a combination of increased antioxidant vitamins and minerals. A complete analysis of the composition of both study diets is shown in Table 1. Patients randomized to either study group were instructed to drink placebo or UCNS formulation for 6 months in an amount that equaled 33.3% of the patient’s actual energy expenditure approximated by using the Harris-Benedict equation for basal energy expenditure multiplied by an activity factor of 1.3.29Harris J.A. Benedict F.G. A biometric study of basal metabolism in man. Carnegie Institute, Washington, DC1919Google Scholar To make certain that each subject drank a similar formula volume regardless of the treatment arm, the caloric density of 1.3 kcal/mL was used for both formulas to determine the volume of study formula each subject needed to consume.Table 1Composition of Study FormulasNutrientAmount per 8 oz (237 mL)PlaceboaFlavored, colored, 5% sucrose solutions with 1000 PPM xanthan gum added as a thickening agent.UCNSbProtein = 47.5% partially hydrolyzed Na caseinate, 47.5% Na caseinate, 5% whey protein concentrate; fat = 16.2% medium-chain triglyceride, 9.3% canola oil, 65% refined deodorized sardine oil, 5.5% soybean oil, 4% soy lecithin; and carbohydrate = 78.4% maltodextrin, 10% sucrose, 5.98% fructooligosaccharide, 4.68% gum arabic, 0.93% soy polysaccharide.Protein (g)-16.1 (21% of calories)Lipid (g)-6.5 (18% of calories)Carbohydrate (g)1249.7 (61% of calories)Gum arabic (g)-2.2Fructooligosaccharide (g)-2.9Soy polysaccharide (g)-.4Vitaminsβ-carotene (μg)-1185Vitamin A (IU)-1320Vitamin D (IU)-192Vitamin E (IU)-72Vitamin K (μg)-32Vitamin C (mg)-156Folic acid (μg)-456Thiamine (mg)-1.6Riboflavin (mg)-1.2Vitamin B6 (mg)-1.2Vitamin B12 (μg)-4.32Niacin (mg)-9.6Choline (mg)-126Biotin (μg)-187Pantothenic acid (mg)-6MineralsSodium (mg)-360Potassium (mg)-480Chloride (mg)-365Calcium (mg)-432Phosphorus (mg)-300Magnesium (mg)-108Iodine (μg)-42Manganese (mg)-1.5Copper (mg)-.6Zinc (mg)-7.0Iron (mg)-5.3Selenium (μg)-22Chromium (μg)-30Molybdenum (μg)-49.4Carnitine (mg)-36Taurine (mg)-56Energy (kcal)48310UCNS, ulcerative colitis nutritional supplement.a Flavored, colored, 5% sucrose solutions with 1000 PPM xanthan gum added as a thickening agent.b Protein = 47.5% partially hydrolyzed Na caseinate, 47.5% Na caseinate, 5% whey protein concentrate; fat = 16.2% medium-chain triglyceride, 9.3% canola oil, 65% refined deodorized sardine oil, 5.5% soybean oil, 4% soy lecithin; and carbohydrate = 78.4% maltodextrin, 10% sucrose, 5.98% fructooligosaccharide, 4.68% gum arabic, 0.93% soy polysaccharide. Open table in a new tab UCNS, ulcerative colitis nutritional supplement. Patients were instructed to maintain their routine diet throughout the study. They were asked to discontinue oral vitamin and mineral supplements before entrance into the study and throughout the entire duration of the study. Daily diary forms were given to each patient and they were instructed to keep a log of their formula intake, bowel function, and medication use. Patient diary forms were returned to the study coordinator each week to ensure compliance and to make certain significant clinical deterioration did not occur. A nurse contacted the patient by telephone every 2 weeks to encourage adherence with the study formulas and maintenance of the daily diary forms. Treatment compliance was assessed by a count of cans of formula used per 3-month period, daily records of formula consumption, and plasma phospholipid fatty acid levels. Prednisone and/or sulfasalazine or other mesalamine derivatives were permitted during the course of the study. These medications were adjusted throughout the study by the patients’ physician according to patient symptoms using a maximum daily dose of prednisone of 40 mg or .75 mg/kg (whichever was higher) and of mesalamine derivatives of 8 g sulfasalazine. Antibiotics were allowed for treating uncomplicated infections, but only for up to 10 days to avoid alterations in the intestinal microflora. Immunosuppressive drugs (cyclosporine, azathioprine, 6-mercaptopurine, methotrexate) were not permitted during the study. Nonsteroidal anti-inflammatory drugs were not allowed during the course of the study to avoid interaction of these medications with the action of the n-3 fatty acid component of the UCNS. The use of these medications and their amounts were recorded daily during the study. The study initially was sized to enroll a minimum of 45 patients in each treatment group. This estimate was based on detecting a difference between the treatment groups in mean change from baseline for daily dosage of prednisone usage of at least 5.7 mg/day. The associated test statistic was powered at 80% and the level of statistical significance for a nondirectional alternative hypothesis (ie, a 2-sided test) was set at α = .05. The sample size was adjusted upwardly to 120 patients (60 patients per treatment group) for an expected occurrence of early, nontreatment-related dropouts. The primary efficacy end point was to assess the daily dose of medications used to treat UC. These medications included corticosteroids and mesalamine because other immunosuppressive medications were not allowed before or during the study. Secondary analyses were performed on measures of disease activity (ie, DAI total score, modified Baron’s scale,24Baron J.H. Connell A.M. Lennard-Jones J.E. Variation between observers in describing mucosal appearances in proctocolitis.BMJ. 1964; 1: 89-92Crossref PubMed Scopus (523) Google Scholar and total histology index score) to evaluate if treatment differences in prednisone use adversely impacted disease status. Safety was measured by collection of adverse event data, changes in plasma biochemistry and hematologic values, and early study withdrawal caused by adverse events. An analysis of the efficacy data was performed for 2 patient populations: an intent-to-treat group based on all patients who were randomized and an evaluable patient sample that satisfied protocol-specified eligibility criteria. This latter group was labeled as completers. In general, all statistical tests of treatment group differences were 2-sided and results were declared significant at an α level ≤ .05. Treatment differences for the primary efficacy variable were tested using a linear mixed-effects model. Before the analysis, a change from baseline value was calculated per patient separately for each month as ([Σ prednisone dose over the month ÷ number of observation days within the month] − baseline prednisone dose). The calculation was expressed as mg/day and negative values indicated that the average dose for a particular month decreased relative to baseline levels. The mixed model was fitted with random coefficient terms and included a treatment-by-time interaction effect, allowing evaluation of the rate of change in the average dose over the 6 months. A statistical test was performed to evaluate treatment arm differences in these rates of change estimates. Predicted mean values of change from baseline doses at each month then were calculated for each treatment arm based on parameter estimates from the model. Differences in these predicted values provided estimates of treatment effect. The study center had a negligible effect on model efficiency and was removed from the final analysis. Analysis assumptions were not always satisfied when the mixed model was applied to the other disease-related medication data that were continued during the study (eg, small number of patients treated with a specific medication), and a limited number of post hoc analyses subsequently were performed to assess whether any gross differences existed between the treatment arms. Two-sample Wilcoxon rank-sum tests were applied to assess treatment arm differences for the DAI total score, modified Baron’s score, and total histology index score (sum of the acute and chronic scores). To help account for the variable early drop-out rates occurring between the treatment arms, end point scores were used for the analyses, selecting the last available postbaseline value as the data point of interest. Robustness of using last available scores was assessed by performing additional analyses based on the last observation carried forward algorithm (including baseline scores). Results from this imputation strategy did not differ grossly from those obtained using the actual last available score, and therefore was omitted from further presentation. Analysis of the remaining data was assessed for treatment arm differences by use of the 2-sample Wilcoxon rank-sum test (continuous variables) and the χ2 test (discrete variable). Descriptive statistics were computed for all variables and data listings were prepared to aid the interpretation of safety issues (eg, detection of extreme laboratory values). The 5 centers participating in the trial randomized a total of 121 patients. Patients were recruited into the study and were followed-up from September 1994 through December 1997. On review of eligibility criteria, 86 patients were deemed completers. A patient was deemed to have completed the study if all components of the initial assessment were performed, a minimum of 3 months of dietary supplementation with one of the study formulas was consumed, and all clinical and laboratory assessments were performed at 3 and 6 months. Baseline demographic and disease characteristics of the 2 study groups for completed and intent-to-treat patients are shown in Table 2. The 2 groups were well matched for age, sex, extent of disease, smoking status, and use of disease-related drugs. There were no significant differences between the groups for all patient characteristics with the exception of a higher mean DAI score in the UCNS group as compared with the placebo group and a lower proportion of patients who used sulfasalazine in the UCNS group vs. the placebo group. More than half of the study population were men, nearly all were Caucasian, the extent of disease was left-sided in two thirds and extensive in one third of the patients, and nearly half of the patients had stopped smoking before the onset of their illness.Table 2Baseline Patient Demographic and Disease CharacteristicsIntent-to-treat patientsCompleted patientsUCNS (n = 59)Placebo (n = 62)P valueUCNS (n = 36)Placebo (n = 50)P valueAge (y)aValues are means ± SD.42.6 ± 13.341.3 ± 11.9.7445.5 ± 13.842.7 ± 11.8.44Height (cm)aValues are means ± SD.169.4 ± 21.1172.3 ± 10.4.95172.3 ± 11.1171.6 ± 10.2.39Weight (kg)aValues are means ± SD.79.8 ± 17.177.2 ± 18.3.4181.7 ± 16.078.8 ± 17.9.46Sex, n (%)Male35 (59.3)37 (59.7).9224 (66.7)30 (60.0).53Female24 (40.7)25 (40.3)12 (33.3)20 (40.0)Race, n (%)Caucasian53 (89.8)50 (80.7).3233 (91.7)40 (80.0).10African American3 (5.1)8 (12.9)0 (.0)6 (12.0)Other3 (5.1)4 (6.4)3 (8.3)4 (8.0)Primary diagnosis, n (%)Left-sided colitis37 (62.7)38 (61.3).9020 (55.6)31 (62.0).55Pancolitis22 (37.3)24 (38.7)16 (44.4)19 (38.0)Smoking, n (%)Never smoked27 (45.8)29 (46.8)1.0014 (38.9)24 (48.0).69Stopped smoking28 (47.4)29 (46.8)20 (55.5)24 (48.0)Active smoker4 (6.8)4 (6.4)2 (5.6)2 (4.0)Use of disease-related drugs, n (%)Prednisone29 (49.2)30 (48.4)1.0023 (63.9)27 (54.0).36Sulfasalazine6 (10.2)19 (30.7).0075 (13.9)16 (32.0).054Oral mesalamine31 (52.2)27 (43.6).3725 (69.4)25 (50.0).07Rectal mesalamine6 (10.2)5 (8.1).765 (13.9)5 (10.0).58DAI total scoreaV" @default.
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• W2020473612 title "An oral supplement enriched with fish oil, soluble fiber, and antioxidants for corticosteroid sparing in ulcerative colitis: A randomized, controlled trial" @default.
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