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PubMed1990

Management of children and adolescents with inflammatory bowel disease.

The management of children and adolescents with inflammatory bowel disease requires all the skills offered by the health care team. This article reviews the principles of therapy, the specifics of therapy, and the attitudes of the authors relating to long-term management of these patients. Specific recommendations relating to nutritional support for patients are also made. A pertinent updated bibliography is also given.

Adolescent↗
PubMed2025

Deciphering microbial and metabolic influences in gastrointestinal diseases-unveiling their roles in gastric cancer, colorectal cancer, and inflammatory bowel disease.

INTRODUCTION: Gastrointestinal disorders (GIDs) affect nearly 40% of the global population, with gut microbiome-metabolome interactions playing a crucial role in gastric cancer (GC), colorectal cancer (CRC), and inflammatory bowel disease (IBD). This study aims to investigate how microbial and metabolic alterations contribute to disease development and assess whether biomarkers identified in one disease could potentially be used to predict another, highlighting cross-disease applicability. METHODS: Microbiome and metabolome datasets from Erawijantari et al. (GC: n = 42, Healthy: n = 54), Franzosa et al. (IBD: n = 164, Healthy: n = 56), and Yachida et al. (CRC: n = 150, Healthy: n = 127) were subjected to three machine learning algorithms, eXtreme gradient boosting (XGBoost), Random Forest, and Least Absolute Shrinkage and Selection Operator (LASSO). Feature selection identified microbial and metabolite biomarkers unique to each disease and shared across conditions. A microbial community (MICOM) model simulated gut microbial growth and metabolite fluxes, revealing metabolic differences between healthy and diseased states. Finally, network analysis uncovered metabolite clusters associated with disease traits. RESULTS: Combined machine learning models demonstrated strong predictive performance, with Random Forest achieving the highest Area Under the Curve(AUC) scores for GC(0.94[0.83-1.00]), CRC (0.75[0.62-0.86]), and IBD (0.93[0.86-0.98]). These models were then employed for cross-disease analysis, revealing that models trained on GC data successfully predicted IBD biomarkers, while CRC models predicted GC biomarkers with optimal performance scores. CONCLUSION: These findings emphasize the potential of microbial and metabolic profiling in cross-disease characterization particularly for GIDs, advancing biomarker discovery for improved diagnostics and targeted therapies.

Humans↗
PubMed1997

A case series of transplant recipients who despite immunosuppression developed inflammatory bowel disease.

OBJECTIVES: We describe 14 patients who developed inflammatory bowel disease (IBD) after transplantation despite immunosuppression. METHODS: Using an electronic medical archival retrieval system, records of 6800 liver and kidney transplant patients were searched for evidence of IBD. The pathology was reviewed, and infectious etiologies were excluded. RESULTS: Fourteen patients developed IBD after transplantation. Twelve patients had undergone liver transplantation, and two kidney transplantation. Four had transplantation for autoimmune hepatitis; four for non-A, non-B, non-C hepatitis; two for primary sclerosing cholangitis; one for giant cell hepatitis; one for biliary atresia; one for polycystic kidney disease; and one for obstructive uropathy. Mean age at development of IBD was 38 yr. Mean time to development of IBD after transplantation was 4 yr. Endoscopically there were two cases limited to the left side, eight of pancolitis, of which one had terminal ileal disease, and four of patchy colitis. Histology was consistent with ulcerative colitis in nine patients and Crohn's disease in five. Patients with ulcerative colitis either responded and remained in remission on maintenance therapy (seven of nine) or were refractory and required a colectomy (two of nine). Patients with Crohn's disease continued to have flares despite treatment (five of five). CONCLUSION: 1) New onset IBD can develop after solid organ transplantation, despite use of immunosuppressive therapy. 2) A full spectrum of IBD can be seen after transplantation. 3) Study of these patients could shed light on why immunosuppression is not uniformly effective for IBD and provide clues to the inflammatory determinants of IBD.

Adolescent↗
PubMed1990

Acquired protein C and S deficiency, inflammatory bowel disease and cerebral arterial thrombosis.

Thromboembolic complications may occur in inflammatory bowel disease. Recently, we had the opportunity to observe a case of a cerebral arterial thrombosis in a young patient with active ulcerative colitis. Investigation of blood coagulation revealed a temporary Protein C, Protein S and Factor II deficiency. To our knowledge, this is the first reported case of a temporary Protein C and S deficiency in a patient with thrombosis and inflammatory bowel disease.

Adult↗
PubMed1999

Nutrition and inflammatory bowel disease.

This article reviews the nutritional aspects of inflammatory bowel disease (IBD) including the mechanisms and manifestations of malnutrition and the efficacy of nutritional therapies. Nutrient deficiencies in patients with IBD occur via several mechanisms and may complicate the course of the disease. Nutritional status is assessed by clinical examination and the use of nutritional indices such as the Subjective Global Assessment of nutritional status. Nutritional intervention may improve outcome in certain individuals; however, because of the costs and complications of such therapy, careful selection is warranted, especially in patients presumed to need parenteral nutrition.

Anti-Inflammatory Agents↗
PubMed1993

Comparison of simultaneous 99mTc-HMPAO and 111In oxine labelled white cell scans in the assessment of inflammatory bowel disease.

Forty-seven patients, 29 with chronic inflammatory bowel disease (IBD) and 18 with presumed irritable bowel syndrome, including one with uncomplicated diverticular disease, were studied with simultaneous technetium-99m hexamethylpropylene amine oxime and indium-111 oxine labelled leucocyte scans performed at 1, 3 and 24 h. Twenty-seven patients with IBD had active disease as judged by clinical and laboratory criteria and all of these had positive scans with both agents. No false positive studies were obtained. The 1-h 99mTc-HMPAO WBC scans showed the same distribution to disease as the 3-h 111-In WBC scans, with no difference in intensity (P < 0.92); they showed more extensive disease (P < 0.02) and more intense uptake (P < 0.001) than did the 1-h 111-In scans. The 3-h 99mTc-HMPAO WBC scans showed more extensive disease (P < 0.002), with greater intensity (P < 0.0005), than did the 3-h 111In WBC scans. Physiological bowel activity on 3-h 99mTc-HMPAO WBC scans was present in 12 patients but was faint and did not interfere with assessment of disease extent and activity. It is concluded that in terms of isotope availability, radiation dosimetry and image quality, 99mTc-HMPAO is the agent of choice in detecting active IBD, with localization of disease possible at 1-h after re-injection and optimal resolution and definition of disease extent at 3 h. A negative scan reliably excludes active disease.

Adult↗
PubMed1989

Hepatobiliary abnormalities in inflammatory bowel disease.

Hepatobiliary abnormalities are among the most frequent extraintestinal manifestations of inflammatory bowel disease. Hepatic amyloidosis and granulomas may be found in patients with Crohn's ileitis. Clinical problems are generally absent. This also applies to fatty infiltration of the liver. The prevalence of gallstones is increased in patients with extensive ileitis. Primary sclerosing cholangitis occurs in about 5% of patients with ulcerative and Crohn's colitis. Serious complications such as bacterial cholangitis and bile duct carcinoma may develop. Because of increased awareness of primary sclerosing cholangitis complicating inflammatory bowel disease and widespread availability of endoscopic cholangiography, asymptomatic patients are now often detected Although controversial, the prognosis of these patients may be better than previously thought. Therefore, endoscopic cholangiography should probably be deferred until symptoms develop in order to avoid the risk of procedure-related cholangitis. Although a liver biopsy is not as diagnostic as cholangiography, it may have prognostic relevance. Recent preliminary results of immunosuppressive and anti-fibrogenic therapies and treatment with urodeoxycholic acid for primary sclerosing cholangitis are promising, but should be confirmed in prospective controlled trials.

Bile Duct Diseases↗
PubMed1990

Endoscopy in inflammatory bowel disease: indications and differential diagnosis.

Colonoscopy with multiple biopsies adds a considerable amount of information to the overall clinical approach to the patient with inflammatory bowel disease. Because colonoscopy is an invasive procedure requiring a vigorous bowel clean-out, it is not a first-line investigative procedure for patients with inflammatory bowel disease. However, in certain indicated circumstances, colonoscopy can assist greatly in the management and diagnosis of patients with inflammatory bowel disease.

Colitis↗
PubMed2000

Familial and sporadic inflammatory bowel disease: different entities?

The strongest risk factor for developing inflammatory bowel disease (IBD) is having a relative with the disease. Familial IBD may be one homogeneous subgroup, phenotypically different from sporadic IBD. Several observations support a role for familiarity in disease site and behavior, particularly in Crohn's disease (CD), but published findings do not all concur. Early disease onset is often found in children with IBD who have a parent with the disease. Genetic anticipation may explain this finding but other explanations and/or observational biasis are more likely. Location and type may differ between familial and sporadic CD cases: family studies report many cases involving both small bowel and colon, and few cases of colonic disease alone, although such features may be secondary to early age at onset. Most studies found no effect of positive family history on severity and course of CD. In ulcerative colitis (UC), phenotypic differences between familial and sporadic cases appear to be limited, but little data are available for analysis. No difference has been found between familial and sporadic IBD as far as disease markers such as pANCA, ASCA, or intestinal permeability are concerned. In conclusion, the only message available for clinical practice is that the relative risk of IBD in first-degree relatives is increased by a factor of 10-15 compared with the general population. Families should not receive genetic counseling/information about age at onset and disease severity.

Genetic Predisposition to Disease↗
PubMed1993

Diarrhoeal disease: current concepts and future challenges. Intestinal cytokines in inflammatory bowel disease and invasive diarrhoea.

In the intestine large numbers of bacteria and their products are separated by a single epithelial layer from resident inflammatory cells (macrophages and lymphocytes). Many of these bacterial products, such as lipopolysaccharides and peptidoglycans, are potent stimulators of free radical and inflammatory cytokine production by macrophages. This can occur in vivo in response to mucosal invasion by enteropathogenic bacteria or because of inappropriate activation of these cells, as in chronic inflammatory bowel disease. In this review we present evidence for production of cytokines in normal intestine and in intestinal inflammatory conditions. The adverse effects of cytokine production upon intestinal homeostasis, in particular disruption of epithelial integrity and prothrombotic changes in the vascular endothelium, are also discussed.

Cytokines↗
PubMed1991

Do life events or depression exacerbate inflammatory bowel disease? A prospective study.

OBJECTIVE: To determine whether depressed mood or life events are associated with an exacerbation of inflammatory bowel disease. DESIGN: A prospective study of a consecutive sample of patients with relapsing inflammatory bowel disease, followed by monthly questionnaires and periodic office visits. SETTING: A referral-based gastroenterology clinic at a medical school. PATIENTS: A consecutive sample of 32 patients with inflammatory bowel disease who had had at least one relapse in a 2-year period after entry into the study. MEASUREMENTS AND MAIN RESULTS: The Social Readjustment Rating Scale (measuring life events), the Beck Depression Inventory (a visual analog scale for depressed mood) and an inventory of intestinal symptoms were completed monthly by each subject with a 78% rate of compliance. A mean of 2.2 exacerbations was seen per subject during the study period. Life events were not temporally associated with changes in intestinal symptoms. Significant associations were found between intestinal symptoms and the two mood scales (P less than 0.05 for each), but no directionality in symptom occurrence could be detected in a time-lagged analysis. The results were similar when the months preceding exacerbations of inflammatory bowel disease were analyzed separately. CONCLUSIONS: Although these findings suggest that mood changed concurrently with exacerbation of inflammatory bowel disease, no evidence indicated that stressful life events or depressed mood precipitated exacerbations in this study group.

Colitis, Ulcerative↗
PubMed2002

Fundamental mechanisms of growth failure in inflammatory bowel disease.

Growth failure is common in children with inflammatory bowel disease (IBD) and has been attributed chiefly to undernutrition. Liquid enteral feeding can reverse the calorie deficit and increase growth velocity. The inflammatory process per se may also directly inhibit linear growth. After institution of enteral nutrition, significant changes in serum growth factors and inflammatory indices have been observed before any changes in nutritional parameters [Bannerjee et al., Gastroenterology 2000;118:A526]. In rats with trinitrobenzenesulphonic acid (TNBS)-induced colitis, about 60% of the final growth impairment can be attributed to undernutrition, inflammation accounting for the remaining growth deficit. Young patients with Crohn's disease and growth failure have normal stimulated and spontaneous growth hormone (GH) secretion and reduced plasma concentrations of insulin-like growth factor-1 (IGF-I), suggesting a degree of GH resistance. Rats with TNBS colitis also have normal plasma GH and reduced IGF-I concentrations, mediated by a combination of undernutrition and active inflammation. Immunoneutralization of interleukin-6 (IL-6) increases hepatic IGF-I mRNA expression, plasma concentrations of IGF-I and linear growth. In contrast, administration of anti-tumour necrosis factor-alpha antibodies (TNF-ab) had no effect on IGF-I in this model. TNFab did, however, increase linear growth, suggesting inhibitory effects of TNF-alpha on the growth axis by mechanisms other than reduction in IGF-I. Preliminary data suggests that TNF-alpha inhibits maturation of growth plate chondrocytes. We have identified IL-6 receptors on growth plate chondrocytes but to date have not identified the effect, if any, of IL-6 directly at the growth plate.

Animals↗
PubMedDate not supplied

Patients' diets and preferences in a pediatric population with inflammatory bowel disease.

PURPOSE: To determine the dietary practices of the pediatric inflammatory bowel disease population at the Children's Hospital of the Hamilton Health Sciences Corporation and the reported effectiveness of those diets. PATIENTS AND METHODS: A questionnaire mailed to 153 pediatric patients was returned by 125 patients (76 Crohn's disease [CD] and 49 ulcerative colitis [UC] patients)--an 82% response rate. RESULTS: The median age of respondents was 13 years, and 62% were male. Ninety per cent and 71% of CD and UC patients, respectively, had changed their diets since diagnosis. Caloric supplements (eg, BOOST [Mead Johnson Nutritionals]), sole source nutrition, low fibre and lactose-free diets were used by more than 15% of CD patients, whereas lactose-free, nonspicy, low acid, additive-free, caloric supplement and low fibre diets were used by more than 15% of UC patients. A diet supplement was more commonly used in CD patients (P < 0.05) and an additive-free diet in UC patients. Corn and corn products, nuts, milk and bran were avoided by more than 20% of CD and UC patients; however, more CD than UC patients avoided corn and corn products. In addition, UC patients (more than 20%) also avoided tomato, other dairy (nonfluid milk-based products and foods containing milk products), chocolate, cheese, wheat, tomato sauces and fruit juice. A benefit was reported for 103 of 141 reported diets, with the most commonly alleviated symptoms being abdominal pain, diarrhea and flatulence. CONCLUSION: Many children with inflammatory bowel disease have altered their diets to manage their disease and have attributed symptomatic relief to these diets.

Adolescent↗
PubMed2003

Differential mucosal expression of three superoxide dismutase isoforms in inflammatory bowel disease.

Mucosal tissue damage and dysfunction in chronic inflammatory bowel disease (IBD) are partly caused by an enduring exposure to excessive amounts of reactive oxygen metabolites (ROMs). Although the three human isoforms of superoxide dismutase (SOD), copper/zinc (Cu/Zn)-SOD, manganese (Mn)-SOD, and extracellular (EC)-SOD, form the primary endogenous defence against ROMs, their expression levels and cellular localization in IBD mucosa are largely unknown. The present study used enzyme-linked immunosorbent assays (ELISAs), spectrophotometric activity assays, and immunohistochemistry to evaluate the protein concentration, enzymatic activity, and distribution of Cu/Zn-, Mn-, and EC-SOD in paired inflamed and non-inflamed mucosal resection specimens of patients with Crohn's disease (CD) or ulcerative colitis (UC) and compared these with the levels obtained in normal control mucosa. Gut mucosal SOD isoform expression was found to be differentially affected in IBD patients, without major differences between CD and UC. A marked step-wise increase in Mn-SOD protein levels was observed in non-inflamed and inflamed IBD mucosae, whereas the Cu/Zn-SOD content decreased with inflammation. EC-SOD was only found in low amounts, which tended to be decreased in IBD patients. Immunohistochemical evaluation confirmed these observations. Mn-SOD and Cu/Zn-SOD were both predominantly expressed in intestinal epithelial cells and the percentage of epithelial cells positive for Mn-SOD was considerably increased in IBD, whereas epithelial Cu/Zn-SOD expression was much less affected. Within the lamina propria, SOD expression was much lower. Cu/Zn-SOD and Mn-SOD were prominently present in neutrophils and macrophages, and EC-SOD was mainly localized in small vessels, stromal cells, and neutrophils. The percentage of lamina propria cells positive for Cu/Zn-, Mn-, or EC-SOD was not affected by inflammation. Enzyme activity measurements showed consistent results for Cu/Zn-SOD and EC-SOD, but the activity of Mn-SOD did not concordantly increase with the immunological assessments, which may indicate that a proportion of the Mn-SOD in IBD is present in an enzymatically inactive form. This study reveals remarkable changes in the expression levels of the three SOD isoforms in IBD, particularly in the epithelium. Disturbances in the carefully orchestrated mucosal antioxidant cascade may contribute to the induction and perpetuation of intestinal inflammation in IBD, and may have important implications for the development of antioxidant treatment of IBD patients.

Adult↗
PubMed1997

[Nutrition in the etiopathogenesis of chronic inflammatory bowel diseases].

It is currently held that the pathogenesis of inflammatory bowel disease (IBD) involves a complex interaction of host responses, some immunologic and genetically determined, and external influences including microbial and dietary factors. Nutritional surveys and studies testing stepwise exclusion dietary compounds have suggested that dietary factors might be linked to the occurrence of IBD. Food allergy was suggested early as a possible trigger for the inflammatory response; however, no firm evidence has been gathered over the years to substantiate this possibility. The possibility that patients with Crohn's disease may have an unusual premorbid pattern of dietary intake has also been examined since the early seventies. Several groups of investigators report a high intake of refined sugars (i.e. sucrose), recycled cooking oil, a more frequent consumption of fast foods in patients with Crohn's disease and ulcerative colitis respectively. However, a critical comparison of incidence and prevalence studies published from 1976 until 1994 clearly showed no pre-existing nutritional abnormality that has been identified consistently in patients who develop inflammatory bowel disease.

Adolescent↗
PubMed1994

Peristomal pyoderma gangrenosum and inflammatory bowel disease.

Pyoderma gangrenosum (PG) is a debilitating skin disease most often associated with inflammatory bowel disease and is a reportedly rare cause of peristomal ulceration. The lesions of PG rapidly evolve from small, erythematous pustules to deep, painful, pyogenic ulcers within hours to days of onset. Although the behavior and the appearance of the lesions of peristomal PG are diagnostic, a lack of familiarity with PG often leads to misdiagnosis and inappropriate therapy. This study reports four cases of peristomal PG and discusses the 20 previously reported cases in patients with inflammatory bowel disease. Seventy-five percent of patients were female and 67% had Crohn's disease. All patients had colitis, including all of the patients with Crohn's disease, 82% of whom had additional perineal complications. The diagnosis of peristomal PG was based on clinical appearance alone in 83% of cases. The onset of peristomal PG ranged from 2 weeks to 3 years following ostomy. The response to medical therapy was variable. All cases (17 of 17) treated with high-dose corticosteroids and local wound care responded, but five cases required additional therapy. No patient was successfully treated with stoma revision. Risk factors for the development of peristomal PG include Crohn's colitis, female gender, and perineal disease. While most patients respond well to systemic steroids and local wound care, up to one third of patients require long-term medical management.

Adolescent↗
PubMed1994

Periodicity of hospital admissions for inflammatory bowel disease.

OBJECTIVES: It has been speculated that exacerbations of inflammatory bowel disease are influenced by seasonal variations. METHODS: This hypothesis was tested in a large data base of the Health Care Financing Administration (HCFA), consisting of all hospitalized US Medicare beneficiaries from four consecutive years. RESULTS: The total of hospital admissions (for all diagnoses) was characterized by a marked seasonal variation occurring similarly in each consecutive year. It was high during winter and low during summer. Peak and trough of admission rate varied by 10%. In striking contrast to this general pattern, both Crohn's disease and ulcerative colitis showed an annual pattern of variability without any clear-cut seasonality. However, the time trends of both diseases showed a striking parallelism concerning their short-term changes (affecting 1-3 consecutive months) and long-term changes (affecting 4-8 consecutive months). The parallelism of the temporal changes affected different age and sex groups alike. CONCLUSIONS: The parallel monthly variations suggest that exacerbations in the activity of inflammatory bowel disease may be modulated by exogenous factors, and that Crohn's disease and ulcerative colitis may be influenced by identical modulators of disease activity.

Aged↗
PubMed1999

[Immunology in medical practice. XXVI. Immunogenetics of chronic inflammatory bowel diseases].

Epidemiological and family studies have shown that the inflammatory bowel diseases (IBD), encompassing ulcerative colitis and Crohn's disease, are in large part genetically determined. This genetic susceptibility is complex and does not follow Mendelian inheritance patterns. The search for susceptibility genes is further complicated by genetic and clinical heterogeneity. Recent developments in molecular biology have enabled the identification of chromosomal regions and genes underlying IBD. Genetic association studies have established a role of HLA genes and cytokine gene polymorphisms in the pathogenesis of IBD. Whole genome linkage analysis studies using microsatellite markers and affected sib-pair analysis have identified two chromosomal locations (IBD1 on chromosome 16 and IBD2 on chromosome 12) associated with IBD. Recent investigations have shown that some chromosomal regions play a role in several autoimmune disorders. This suggests the presence of two types of genes in these diseases: genes that encode proteins that play a key role in the immune response and predisposing for autoimmune diseases in general, and disease-specific genes that are responsible for the phenotype and the severity of the disease.

Chromosomes, Human, Pair 12↗