Displaying publications 1 - 20 of 77 in total

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  1. Imawana RA, Smith DR, Goodson ML
    Ann Gastroenterol, 2020 06 06;33(5):485-494.
    PMID: 32879595 DOI: 10.20524/aog.2020.0507
    Background: The current literature suggests a protective benefit of Helicobacter pylori (H. pylori) infection against inflammatory bowel disease (IBD). Here we assessed whether this effect varied by IBD subtype-Crohn's disease (CD) or ulcerative colitis (UC)-and geographic region: East Asia, Europe (non-Mediterranean) or Mediterranean region.

    Methods: A database search was performed up to July 2019 inclusive for all studies that compared H. pylori infection in IBD patients vs. non-IBD controls. The relative risk (RR) was used to quantify the association between IBD and H. pylori, and the effects were combined across studies using a mixed-effects meta-regression model, which included IBD subtype and geographic region as categorical moderator variables.

    Results: Our meta-regression model exhibited moderate heterogeneity (I2=48.74%). Pooled RR depended on both region (P=0.02) and subtype (P<0.001). Pooled RRs were <1 for all subtype and region combinations, indicative of a protective effect of H. pylori against IBD. The pooled RR was 28% (9%, 50%; P=0.001) greater for UC vs. CD and 43% (4%, 96%; P=0.02) greater for Mediterranean countries vs. East Asia. The pooled RR was 18% (-13%, 60%; P=0.48) greater for Europe vs. East Asia and 21% (-13%, 68%; P=0.42) greater for Mediterranean vs. Europe, though these differences were not statistically significant.

    Conclusions: The protective effect of H. pylori on IBD varied by both subtype (more protection against CD vs. UC) and region (East Asia more protected than Mediterranean regions). Variation due to these effects could provide insight into IBD etiology.

    Matched MeSH terms: Colitis, Ulcerative
  2. Pandurangan AK, Esa NM
    Asian Pac J Cancer Prev, 2014;15(2):551-60.
    PMID: 24568457
    Colorectal cancer (CRC) is the third most common malignancy and fourth most common cause of cancer mortality worldwide. Untreated chronic inflammation in the intestine ranks among the top three high-risk conditions for colitis-associated colorectal cancer (CAC). Signal Transducer and Activator of Transcription 3 (STAT3) protein is a member of the STAT family of transcription factors often deregulated in CRC. In this review, we try to emphasize the critical role of STAT3 in CAC as well as the crosstalk of STAT3 with inflammatory cytokines, nuclear factor (NF)- κB, PI3K/Akt, Mammalian Target of Rapamycin (mTOR), Notch, Wnt/β-catenin and microRNA (MiR) pathways. STAT3 is considered as a primary drug target to treat CAC in humans and rodents. Also we updated the findings for inhibitors of STAT3 with regard to effeects on tumorigenesis. This review will hopefully provide insights on the use of STAT3 as a therapeutic target in CAC.
    Matched MeSH terms: Colitis/complications*
  3. Naidu J, Wong Zh, Palaniappan Sh, Ngiu ChS, Yaacob NY, Abdul Hamid H, et al.
    Asian Pac J Cancer Prev, 2017 04 01;18(4):933-939.
    PMID: 28545190
    Background and Aims: Patients with inflammatory bowel disease (IBD) are subjected to a large amount of ionizing
    radiation during the course of their illness. This may increase their risk of malignancy to a greater level than that due
    to the disease itself. In Caucasian patients with Crohn’s disease, this has been well documented and recommendations
    are in place to avoid high radiation imaging protocols. However, there are limited data available on radiation exposure
    in Asian IBD patients.We therefore sought to identify total radiation exposure and any differences between ethnically
    diverse ulcerative colitis (UC) and Crohn’s disease (CD) patients at our centre along with determining factors that may
    contribute to any variation. Methods: The cumulative effective dose (CED) was calculated retrospectively from 2000
    to 2014 using data from our online radiology database and patients’ medical records. Total CED in the IBD population
    was measured. High exposure was defined as a radiation dose of greater than 0.2mSv (equivalent to slightly less than
    ½ a year of background radiation). Results: A total of 112 cases of IBD (36 CD and 76 UC) were reviewed. Our CD
    patients were diagnosed at an earlier age than our UC cases (mean age 26.1 vs 45.7). The total CED in our IBD population
    was 8.53 (95% CI: 4.53-12.52). Patients with CD were exposed to significantly higher radiation compared to those
    with UC. The mean CED was 18.6 (7.30-29.87) and 3.65 (1.74-5.56, p=0.01) for CD and UC patients respectively. 2
    patients were diagnosed as having a malignancy during follow up with respective CED values of 1.76mSv and 10mSv.
    Conclusions: CD patients, particularly those with complicated disease, received a higher frequency of diagnostic
    imaging over a shorter period when compared to UC patients. Usage of low radiation imaging protocols should be
    encouraged in IBD patients to reduce their risk of consequent malignancy.
    Matched MeSH terms: Colitis, Ulcerative
  4. Hilmi I, Hartono JL, Pailoor J, Mahadeva S, Goh KL
    BMC Gastroenterol, 2013;13:80.
    PMID: 23651739 DOI: 10.1186/1471-230X-13-80
    There is increasing evidence for the role of microscopic inflammation in patients with IBS. We aimed to examine the prevalence of microscopic colitis and inflammation in Malaysian IBS patients with diarrhoea (IBS-D).
    Matched MeSH terms: Colitis, Collagenous/complications; Colitis, Collagenous/pathology*; Colitis, Lymphocytic/complications; Colitis, Lymphocytic/pathology*
  5. Mokhtar NM, Nawawi KNM, Verasingam J, Zhiqin W, Sagap I, Azman ZAM, et al.
    BMC Public Health, 2019 Jun 13;19(Suppl 4):550.
    PMID: 31196184 DOI: 10.1186/s12889-019-6858-2
    BACKGROUND: Inflammatory bowel disease (IBD) was once considered as a Western disease. However, recent epidemiological data showed an emerging trend of IBD cases in the Eastern Asia countries. Clinico-epidemiological data of IBD in Malaysia is scarce. This study aimed to address this issue.

    METHODS: Retrospective analysis of ulcerative colitis (UC) and Crohn's disease (CD), diagnosed from January 1980 till June 2018 was conducted at our centre.

    RESULTS: A total of 413 IBD patients (281 UC, 132 CD) were identified. Mean crude incidence of IBD has increased steadily over the first three decades: 0.36 (1980-1989), 0.48 (1990-1999) and 0.63 per 100,000 person-years (2000-2009). In the 2010 to 2018 period, the mean crude incidence has doubled to 1.46 per 100,000 person-years. There was a significant rise in the incidence of CD, as depicted by reducing UC:CD ratio: 5:1 (1980-1989), 5:1 (1990-1999), 1.9:1 (2000-2009) and 1.7:1 (2010-2018). The prevalence rate of IBD, UC and CD, respectively were 23.0, 15.67 and 7.36 per 100,000 persons. Of all IBD patients, 61.5% (n = 254) were males. When stratified according to ethnic group, the highest prevalence of IBD was among the Indians: 73.4 per 100,000 persons, followed by Malays: 24.8 per 100,000 persons and Chinese: 14.6 per 100,000 persons. The mean age of diagnosis was 41.2 years for UC and 27.4 years for CD. Majority were non-smokers (UC: 76.9%, CD: 70.5%). The diseases were classified as follows: UC; proctitis (9.2%), left-sided colitis (50.2%) and extensive colitis (40.6%), CD; isolated ileal (22.7%), colonic (28.8%), ileocolonic (47.7%) and upper gastrointestinal (0.8%). 12.9% of CD patients had concurrent perianal disease. Extra intestinal manifestations were observed more in CD (53.8%) as compared to UC (12%). Dysplasia and malignancy, on the other hand, occurred more in UC (4.3%, n = 12) than in CD (0.8%, n = 1). Over one quarter (27.3%) of CD patients and 3.6% of UC patients received biologic therapy.

    CONCLUSION: The incidence of IBD is rising in Malaysia, especially in the last one decade. This might be associated with the urbanization and changing diets. Public and clinicians' awareness of this emerging disease in Malaysia is important for the timely detection and management.

    Matched MeSH terms: Colitis, Ulcerative/epidemiology*
  6. Narula N, Wong ECL, Dehghan M, Mente A, Rangarajan S, Lanas F, et al.
    BMJ, 2021 07 14;374:n1554.
    PMID: 34261638 DOI: 10.1136/bmj.n1554
    OBJECTIVE: To evaluate the relation between intake of ultra-processed food and risk of inflammatory bowel disease (IBD).

    DESIGN: Prospective cohort study.

    SETTING: 21 low, middle, and high income countries across seven geographical regions (Europe and North America, South America, Africa, Middle East, south Asia, South East Asia, and China).

    PARTICIPANTS: 116 087 adults aged 35-70 years with at least one cycle of follow-up and complete baseline food frequency questionnaire (FFQ) data (country specific validated FFQs were used to document baseline dietary intake). Participants were followed prospectively at least every three years.

    MAIN OUTCOME MEASURES: The main outcome was development of IBD, including Crohn's disease or ulcerative colitis. Associations between ultra-processed food intake and risk of IBD were assessed using Cox proportional hazard multivariable models. Results are presented as hazard ratios with 95% confidence intervals.

    RESULTS: Participants were enrolled in the study between 2003 and 2016. During the median follow-up of 9.7 years (interquartile range 8.9-11.2 years), 467 participants developed incident IBD (90 with Crohn's disease and 377 with ulcerative colitis). After adjustment for potential confounding factors, higher intake of ultra-processed food was associated with a higher risk of incident IBD (hazard ratio 1.82, 95% confidence interval 1.22 to 2.72 for ≥5 servings/day and 1.67, 1.18 to 2.37 for 1-4 servings/day compared with <1 serving/day, P=0.006 for trend). Different subgroups of ultra-processed food, including soft drinks, refined sweetened foods, salty snacks, and processed meat, each were associated with higher hazard ratios for IBD. Results were consistent for Crohn's disease and ulcerative colitis with low heterogeneity. Intakes of white meat, red meat, dairy, starch, and fruit, vegetables, and legumes were not associated with incident IBD.

    CONCLUSIONS: Higher intake of ultra-processed food was positively associated with risk of IBD. Further studies are needed to identify the contributory factors within ultra-processed foods.

    STUDY REGISTRATION: ClinicalTrials.gov NCT03225586.

    Matched MeSH terms: Colitis, Ulcerative/epidemiology*
  7. Ong SCL, Mohaidin N
    BMJ Case Rep, 2018 Sep 30;2018.
    PMID: 30275028 DOI: 10.1136/bcr-2018-227121
    Matched MeSH terms: Colitis, Ulcerative/diagnosis
  8. Pandurangan AK, Saadatdoust Z, Esa NM, Hamzah H, Ismail A
    Biofactors, 2015 Jan-Feb;41(1):1-14.
    PMID: 25545372 DOI: 10.1002/biof.1195
    Colorectal cancer (CRC) is the third most common malignancy in males and the second most common cancer worldwide. Chronic colonic inflammation is a known risk factor for CRC. Cocoa contains many polyphenolic compounds that have beneficial effects in humans. The objective of this study is to explore the antioxidant properties of cocoa in the mouse model of azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced colitis-associated cancer, focusing on the activation of Nrf2 signaling. Mice were treated with AOM/DSS and randomized to receive either a control diet or a 5 and 10% cocoa diet during the study period. On day 62 of the experiment, the entire colon was processed for biochemical and histopathological examination and further evaluations. Increased levels of malondialdehyde (MDA) were observed in AOM/DSS-induced mice; however, subsequent administration of cocoa decreased the MDA. Enzymatic and nonenzymatic antioxidants, such as superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase, were decreased in the AOM/DSS mice. Cocoa treatment increases the activities/levels of enzymatic and nonenzymatic antioxidants. Inflammatory mediators, such as inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2, were elevated during AOM/DSS-induction, and treatment with 5 and 10% cocoa effectively decreases the expression of iNOS and COX-2. The NF-E2-related factor 2 and its downstream targets, such as NQO1 and UDP-GT, were increased by cocoa treatment. The results of our study suggest that cocoa may merit further clinical investigation as a chemopreventive agent that helps prevent CAC.
    Matched MeSH terms: Colitis/chemically induced; Colitis/diet therapy; Colitis/genetics; Colitis/prevention & control*
  9. Pandurangan AK, Mohebali N, Hasanpourghadi M, Looi CY, Mustafa MR, Mohd Esa N
    Biofactors, 2016 May;42(3):247-58.
    PMID: 26891685 DOI: 10.1002/biof.1267
    Ulcerative colitis (UC) is a nonspecific inflammatory disorder characterized by oxidative and nitrosative stress, leucocyte infiltration, and upregulation of inflammatory mediators. Boldine is an alkaloid compound found in Boldo tree, with multiple pharmacological actions, mainly anti-inflammatory, antioxidant, antitumor, and immunomodulatory activities. Hence, the effect of boldine for its anti-inflammatory properties against dextran sulfate sodium (DSS)-induced UC in BALB/c mice was studied. Administration of boldine to DSS-induced mice protects colon damage by reduced disease activity index, spleen weight, and increased colon length. Also administration of boldine showed a reduction in the activity of myeloperoxidase (MPO) and CD 68+ expression. Boldine reduced the colon damage, with significant reductions in both the extent and the severity of the inflammation as well as in crypt damage and leukocyte infiltration in the mucosa. Analysis in vivo showed clear decrease in the production of tumor necrosis factor (TNF)-α, Interleukin (IL)-6, IL-17, and signal transducer and activator of transcription-(p-STAT3)(Y705) with nuclear factor (p65-NF-κB) production being reduced significantly. Moreover, p65-NF-κB activation was reduced in mouse macrophage RAW 264.7 cells in vitro. The data demonstrated that boldine may be beneficial in colitis through selective immunomodulatory effects, which may be mediated, at least in part, by inhibition of p65-NF-κB and STAT3 signaling pathways. © 2016 BioFactors, 42(3):247-258, 2016.
    Matched MeSH terms: Colitis/chemically induced; Colitis/drug therapy*; Colitis/genetics
  10. Yuan F, Hung RJ, Walsh N, Zhang H, Platz EA, Wheeler W, et al.
    Cancer Res, 2020 Sep 15;80(18):4004-4013.
    PMID: 32641412 DOI: 10.1158/0008-5472.CAN-20-0447
    Registry-based epidemiologic studies suggest associations between chronic inflammatory intestinal diseases and pancreatic ductal adenocarcinoma (PDAC). As genetic susceptibility contributes to a large proportion of chronic inflammatory intestinal diseases, we hypothesize that the genomic regions surrounding established genome-wide associated variants for these chronic inflammatory diseases are associated with PDAC. We examined the association between PDAC and genomic regions (±500 kb) surrounding established common susceptibility variants for ulcerative colitis, Crohn's disease, inflammatory bowel disease, celiac disease, chronic pancreatitis, and primary sclerosing cholangitis. We analyzed summary statistics from genome-wide association studies data for 8,384 cases and 11,955 controls of European descent from two large consortium studies using the summary data-based adaptive rank truncated product method to examine the overall association of combined genomic regions for each inflammatory disease group. Combined genomic susceptibility regions for ulcerative colitis, Crohn disease, inflammatory bowel disease, and chronic pancreatitis were associated with PDAC at P values < 0.05 (0.0040, 0.0057, 0.011, and 3.4 × 10-6, respectively). After excluding the 20 PDAC susceptibility regions (±500 kb) previously identified by GWAS, the genomic regions for ulcerative colitis, Crohn disease, and inflammatory bowel disease remained associated with PDAC (P = 0.0029, 0.0057, and 0.0098, respectively). Genomic regions for celiac disease (P = 0.22) and primary sclerosing cholangitis (P = 0.078) were not associated with PDAC. Our results support the hypothesis that genomic regions surrounding variants associated with inflammatory intestinal diseases, particularly, ulcerative colitis, Crohn disease, inflammatory bowel disease, and chronic pancreatitis are associated with PDAC. SIGNIFICANCE: The joint effects of common variants in genomic regions containing susceptibility loci for inflammatory bowel disease and chronic pancreatitis are associated with PDAC and may provide insights to understanding pancreatic cancer etiology.
    Matched MeSH terms: Colitis, Ulcerative/genetics
  11. Corrie L, Gulati M, Awasthi A, Vishwas S, Kaur J, Khursheed R, et al.
    Chem Biol Interact, 2022 Dec 01;368:110238.
    PMID: 36306865 DOI: 10.1016/j.cbi.2022.110238
    Polysaccharides (PS) represent a broad class of polymer-based compounds that have been extensively researched as therapeutics and excipients for drug delivery. As pharmaceutical carriers, PS have mostly found their use as adsorbents, suspending agents, as well as cross-linking agents for various formulations such as liposomes, nanoparticles, nanoemulsions, nano lipid carriers, microspheres etc. This is due to inherent properties of PS such as porosity, steric stability and swellability, insolubility in pH. There have been emerging reports on the use of PS as therapeutic agent due to its anti-inflammatory and anti-oxidative properties for various diseases. In particular, for Crohn's disease, ulcerative colitis and inflammatory bowel disease. However, determining the dosage, treatment duration and effective technology transfer of these therapeutic moieties have not occurred. This is due to the fact that PS are still at a nascent stage of development to a full proof therapy for a particular disease. Recently, a combination of polysaccharide which act as a prebiotic and a probiotic have been used as a combination to treat various intestinal and colorectal (CRC) related diseases. This has proven to be beneficial, has shown good in vivo correlation and is well reported. The present review entails a detailed description on the role of PS used as a therapeutic agent and as a formulation pertaining to gastrointestinal diseases.
    Matched MeSH terms: Colitis, Ulcerative*
  12. Abdalla LF, Chaudhry Ehsanullah R, Karim F, Oyewande AA, Khan S
    Cureus, 2020 May 22;12(5):e8240.
    PMID: 32582499 DOI: 10.7759/cureus.8240
    The process of inflammation occurs due to inflammatory mediators, including prostaglandins, cytokines, and tumor necrosis factor (TNF). All these mediators activate the process of tumorigenesis and dysplasia, leading to colitis-associated cancer. Several drugs used to decrease these mediators will help in the treatment of acute attacks and also help in prolonged remissions of the disease by using nonsteroidal anti-inflammatory drugs (NSAIDs), steroids, and biological factors. Reducing these inflammatory mediators also have a role in chemoprevention and prevent progression to colorectal carcinoma. The most researched drugs in this process of chemoprevention are NSAIDs as it has both cyclooxygenase-2 (COX-2) inhibitory and non-inhibitory effects. These drugs should be taken for a long time and in large doses to reach this effect, which puts the patient at risk for various side effects. Researchers will need to do more research in the future to find the lowest effective dose that can reach the chemopreventive effect. We used database Pubmed as the main source for data search and extracted articles exploring the relationship between NSAIDs and their role in chemoprevention of colorectal carcinoma in inflammatory bowel disease (IBD) patients. We chose 23 studies which included seven review articles. We found that inflammatory mediators have a key role in colitis-associated cancer.
    Matched MeSH terms: Colitis
  13. Opstelten JL, Beelen RMJ, Leenders M, Hoek G, Brunekreef B, van Schaik FDM, et al.
    Dig Dis Sci, 2016 Oct;61(10):2963-2971.
    PMID: 27461060 DOI: 10.1007/s10620-016-4249-4
    BACKGROUND: Industrialization has been linked to the etiology of inflammatory bowel disease (IBD).

    AIM: We investigated the association between air pollution exposure and IBD.

    METHODS: The European Prospective Investigation into Cancer and Nutrition cohort was used to identify cases with Crohn's disease (CD) (n = 38) and ulcerative colitis (UC) (n = 104) and controls (n = 568) from Denmark, France, the Netherlands, and the UK, matched for center, gender, age, and date of recruitment. Air pollution data were obtained from the European Study of Cohorts for Air Pollution Effects. Residential exposure was assessed with land-use regression models for particulate matter with diameters of <10 μm (PM10), <2.5 μm (PM2.5), and between 2.5 and 10 μm (PMcoarse), soot (PM2.5 absorbance), nitrogen oxides, and two traffic indicators. Conditional logistic regression analyses were performed to calculate odds ratios (ORs) with 95 % confidence intervals (CIs).

    RESULTS: Although air pollution was not significantly associated with CD or UC separately, the associations were mostly similar. Individuals with IBD were less likely to have higher exposure levels of PM2.5 and PM10, with ORs of 0.24 (95 % CI 0.07-0.81) per 5 μg/m(3) and 0.25 (95 % CI 0.08-0.78) per 10 μg/m(3), respectively. There was an inverse but nonsignificant association for PMcoarse. A higher nearby traffic load was positively associated with IBD [OR 1.60 (95 % CI 1.04-2.46) per 4,000,000 motor vehicles × m per day]. Other air pollutants were positively but not significantly associated with IBD.

    CONCLUSION: Exposure to air pollution was not found to be consistently associated with IBD.

    Matched MeSH terms: Colitis, Ulcerative/epidemiology*
  14. Sohail M, Mudassir, Minhas MU, Khan S, Hussain Z, de Matas M, et al.
    Drug Deliv Transl Res, 2019 04;9(2):595-614.
    PMID: 29611113 DOI: 10.1007/s13346-018-0512-x
    Ulcerative colitis (UC) is an inflammatory disease of the colon that severely affects the quality of life of patients and usually responds well to anti-inflammatory agents for symptomatic relief; however, many patients need colectomy, a surgical procedure to remove whole or part of the colon. Though various types of pharmacological agents have been employed for the management of UC, the lack of effectiveness is usually predisposed to various reasons including lack of target-specific delivery of drugs and insufficient drug accumulation at the target site. To overcome these glitches, many researchers have designed and characterized various types of versatile polymeric biomaterials to achieve target-specific delivery of drugs via oral route to optimize their targeting efficiency to the colon, to improve drug accumulation at the target site, as well as to ameliorate off-target effects of chemotherapy. Therefore, the aim of this review was to summarize and critically discuss the pharmaceutical significance and therapeutic feasibility of a wide range of natural and synthetic biomaterials for efficient drug targeting to colon and rationalized treatment of UC. Among various types of biomaterials, natural and synthetic polymer-based hydrogels have shown promising targeting potential due to their innate pH responsiveness, sustained and controlled release characteristics, and microbial degradation in the colon to release the encapsulated drug moieties. These characteristic features make natural and synthetic polymer-based hydrogels superior to conventional pharmacological strategies for the management of UC.
    Matched MeSH terms: Colitis, Ulcerative/drug therapy*
  15. Pandurangan AK, Mohebali N, Norhaizan ME, Looi CY
    Drug Des Devel Ther, 2015;9:3923-34.
    PMID: 26251571 DOI: 10.2147/DDDT.S86345
    Gallic acid (GA) is a polyhydroxy phenolic compound that has been detected in various natural products, such as green tea, strawberries, grapes, bananas, and many other fruits. In inflammatory bowel disease, inflammation is promoted by oxidative stress. GA is a strong antioxidant; thus, we evaluated the cytoprotective and anti-inflammatory role of GA in a dextran sulfate sodium (DSS)-induced mouse colitis model. Experimental acute colitis was induced in male BALB/c mice by administering 2.5% DSS in the drinking water for 7 days. The disease activity index; colon weight/length ratio; histopathological analysis; mRNA expressions of IL-21 and IL-23; and protein expression of nuclear erythroid 2-related factor 2 (Nrf2) were compared between the control and experimental mice. The colonic content of malondialdehyde and the activities of superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase activity were examined as parameters of the redox state. We determined that GA significantly attenuated the disease activity index and colon shortening, and reduced the histopathological evidence of injury. GA also significantly (P<0.05) reduced the expressions of IL-21 and IL-23. Furthermore, GA activates/upregulates the expression of Nrf2 and its downstream targets, including UDP-GT and NQO1, in DSS-induced mice. The findings of this study demonstrate the protective effect of GA on experimental colitis, which is probably due to an antioxidant nature of GA.
    Matched MeSH terms: Colitis/chemically induced; Colitis/genetics; Colitis/metabolism; Colitis/pathology; Colitis/prevention & control*
  16. Tsiountsioura M, Wong JE, Upton J, McIntyre K, Dimakou D, Buchanan E, et al.
    Eur J Clin Nutr, 2014 Jun;68(6):700-6.
    PMID: 24424079 DOI: 10.1038/ejcn.2013.286
    BACKGROUND/OBJECTIVES: In the era of modern multidisciplinary clinical management, very little is known about the prevalence and presentation of malnutrition in children with gastrointestinal disorders (GastroD) particularly employing composite, global measures of nutritional status.
    SUBJECTS/METHODS: Anthropometry, body composition, dietary intake, eating habits and grip strength were assessed with bedside methods in 168 patients from outpatient gastroenterology clinics (n, median (IQR) years; Crohn's disease (CD): n=53, 14.2 (11.6:15.4); ulcerative colitis (UC): n=27, 12.2 (10.7:14.2); coeliac disease: n=31, 9.3 (7.5:13.6); other GastroD: n=57, 9.8 (7.2:13.8)) and compared with 62 contemporary healthy controls (n, median (IQR): 9.8 (6.9:13.8)) and the results of the recent UK, National Diet and Nutritional Survey (NDNS).
    RESULTS: Children with CD had lower BMI z-scores than controls (median (IQR): -0.3 (-0.9:0.4) vs 0.3 (-0.6:1.4); P=0.02) but only 2% were classified as thin (BMI z-score
    Matched MeSH terms: Colitis, Ulcerative/complications
  17. Bergmann MM, Hernandez V, Bernigau W, Boeing H, Chan SS, Luben R, et al.
    Eur J Clin Nutr, 2017 04;71(4):512-518.
    PMID: 28120853 DOI: 10.1038/ejcn.2016.271
    BACKGROUND/OBJECTIVES: The role of long-term alcohol consumption for the risk of developing ulcerative colitis (UC) and Crohn's disease (CD) is unclear. For the first time, to prospectively assess the role of pre-disease alcohol consumption on the risk of developing UC or CD.

    SUBJECTS/METHODS: Nested within the European Prospective Investigation into Cancer and Nutrition (EPIC-IBD), incident UC and CD cases and matched controls where included. At recruitment, participants completed validated food frequency and lifestyle questionnaires. Alcohol consumption was classified as either: non-use, former, light (⩽0.5 and 1 drink per week), below the recommended limits (BRL) (⩽1 and 2 drinks per day), moderate (⩽2.5 and 5 drinks per day), or heavy use (>2.5 and >5 drinks per day) for women and men, respectively; and was expressed as consumption at enrolment and during lifetime. Conditional logistic regression was applied adjusting for smoking and education, taking light users as the reference.

    RESULTS: Out of 262 451 participants in six countries, 198 UC incident cases/792 controls and 84 CD cases/336 controls were included. At enrolment, 8%/27%/32%/23%/11% UC cases and 7%/29%/40%/19%/5% CD cases were: non-users, light, BRL, moderate and heavy users, respectively. The corresponding figures for lifetime non-use, former, light, BRL, moderate and heavy use were: 3%/5%/23%/44%/19%/6% and 5%/2%/25%/44%/23%/1% for UC and CD cases, respectively. There were no associations between any categories of alcohol consumption and risk of UC or CD in the unadjusted and adjusted odds ratios.

    CONCLUSION: There was no evidence of associations between alcohol use and the odds of developing either UC or CD.

    Matched MeSH terms: Colitis, Ulcerative/etiology*; Colitis, Ulcerative/epidemiology
  18. Munchar J, Rahman HA, Zawawi MM
    Eur J Gastroenterol Hepatol, 2001 Nov;13(11):1385-7.
    PMID: 11692068
    Localized giant pseudopolyposis is an interesting but unusual manifestation of both ulcerative colitis and Crohn's disease. The purpose of this report is to present a case of localized giant pseudopolyposis complicating an ulcerative colitis, and review other cases reported in the literature. The clinical and pathological findings are described. The authors also discuss the possible aspect of proper management in this type of lesion.
    Matched MeSH terms: Colitis, Ulcerative/complications*
  19. Lean QY, Gueven N, Eri RD, Bhatia R, Sohal SS, Stewart N, et al.
    Expert Rev Clin Pharmacol, 2015;8(6):795-811.
    PMID: 26308504 DOI: 10.1586/17512433.2015.1082425
    Current drug therapies for ulcerative colitis (UC) are not completely effective in managing moderate-to-severe UC and approximately 20% of patients with severe UC require surgical interventions. Heparins, polydisperse mixtures of non-anticoagulant and anticoagulant oligosaccharides, are widely used as anticoagulants. However, heparins are also reported to have anti-inflammatory properties. Unfractionated heparin was initially used in patients with UC for the treatment of rectal microthrombi. Surprisingly, it was found to be effective in reducing UC-associated symptoms. Since then, several pre-clinical and clinical studies have reported promising outcomes of heparins in UC. In contrast, some controlled clinical trials demonstrated no or only limited benefits, thus the potential of heparins for the treatment of UC remains uncertain. This review discusses potential mechanisms of action of heparins, as well as proposed reasons for their contradictory clinical effectiveness in the treatment of UC.
    Matched MeSH terms: Colitis, Ulcerative/drug therapy*; Colitis, Ulcerative/physiopathology
  20. Lee YY, Gangireddy V, Khurana S, Rao SS
    Gastroenterology, 2014 Aug;147(2):544.
    PMID: 24976027 DOI: 10.1053/j.gastro.2014.03.053
    Matched MeSH terms: Colitis, Ulcerative/drug therapy*
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