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At least 703 records · Page 39Linked to original sources
PubMed1999

Colonoscopy and technetium-99m white cell scan in children with suspected inflammatory bowel disease.

OBJECTIVES: To determine the utility of the technetium-labeled autologous white cell scintigraphy (Tc-WCS) for detecting intestinal inflammation in children with suspected inflammatory bowel disease (IBD). Tc-WCS was compared with colonoscopy and histologic examination. STUDY DESIGN: Forty-eight children (26 boys; median age, 10 years; range, 2-17 years) with symptoms and signs suggesting IBD had colonoscopy with exploration of terminal ileum and mucosal biopsies. The scans were judged to be abnormal if activity was seen in the gut within the first hour. RESULTS: Twenty-one patients had a diagnosis of IBD (Crohn's disease, 13; ulcerative colitis, 5; indeterminate colitis, 3); results of scintigraphy were positive in 16 and negative in 5 (sensitivity, 76.2%); the latter had a moderate degree of intestinal inflammation. In 27 patients, IBD was ruled out. Results of scintigraphy were negative in children with non-specific colitis and in those with lymphoid hyperplasia of the terminal ileum, whereas results were positive in 6 of 12 patients with spondyloarthropathy. In children with IBD, there was a significant correlation between results of scintigraphy and endoscopy for the intensity of inflammation (r = 0.70); however, there was a poor correlation regarding the number of involved segments (r = 0.30) because in 16 patients, endoscopy revealed additional diseased segments as compared with scintigraphy. CONCLUSIONS: A positive Tc-WCS result indicates the presence of an inflammatory process of the gut, whereas a negative test result does not rule out intestinal inflammation, especially when the latter is of moderate degree. Colonoscopy and biopsy are the investigations of choice to establish the diagnosis of IBD and are superior to Tc-WCS in assessing topographic extension of IBD.

Adolescent↗
PubMed2001

Colorectal cancer rates among first-degree relatives of patients with inflammatory bowel disease: a population-based cohort study.

BACKGROUND: Inflammatory bowel disease (IBD) and colorectal cancer might share a common cause and, therefore, relatives of patients with IBD could be at increased risk of this malignant disease. We aimed to assess cancer rates among first-degree relatives of patients with IBD to try to determine whether an association between the two diseases exists. METHODS: In a population-based study, we identified 114,102 first-degree relatives by registry linkage and followed them up for cancer occurrence. We used standardised incidence ratio (SIR) of cancer as relative risk. FINDINGS: 560 colorectal cancers were identified among relatives. First-degree relatives of patients with Crohn's disease or ulcerative colitis were not at increased risk of cancer (SIR 0.90, 95% CI 0.82-0.97). The relative risk was 0.96 (0.87-1.06, n=379) for colon cancer and 0.78 (0.68-0.91, 181) for rectal cancer. The SIRs were not affected by age, relation to patient, or type or extent of IBD in the patient. Relatives of patients with both IBD and colorectal cancer had an 80% increased risk of colorectal cancer. INTERPRETATION: Our results do not endorse a common cause of IBD and colorectal cancer. The slightly decreased relative risk for colorectal cancer among relatives could indicate the proportion of all colorectal cancer cases attributable to IBD.

Adult↗
PubMed2005

[Inflammatory bowel disease and pregnancy: report of 76 cases and review of the literature].

OBJECTIVE: Obstetrical prognosis for women suffering from Crohn's disease and from ulcerative colitis, and consequences of pregnancy on inflammatory bowel diseases (IBD). PATIENTS AND METHODS: Retrospective study, of 76 pregnancies, after the diagnosis of IBD among 77 women (33 ulcerative colitis, 44 Crohn's disease). RESULTS: Pregnancy did not modify the evolutive profile of IBD. No particular gravity of IBD revealed during pregnancy or post-partum was noticed. The outcome of the 54 pregnancies associated with quiescent IBD was the same as in the general population. Five of ten pregnancies started during an active period of Crohn's disease or ulcerative colitis ended in fetal loss (3 spontaneous abortions, 2 medical terminations). In women with a first acute episode or IBD reactivation during pregnancy (n=12), one-third of the newborns were low weight for gestational age, one-third were born preterm and only one-third were term babies with normal weight. Vaginal delivery did not trigger development or exacerbation of perianal Crohn's disease (n=20). Cesarean section was performed in 2 with an ileal pouch-anal anastomosis (n=4) and 1 patient with an ileo-rectal anastomosis (n=3) to avoid injury to the anal sphincter. Ileostomy (n=2) did not contraindicate delivery. CONCLUSION: Control of IBD is the main obstetrical factor for prognosis. Starting pregnancy can be advised if the disease is quiescent, with rapid and efficient management of possible flare-ups. Delivery route must be determined on a case-by-case basis, each considering pregestational anal continence and the clinical presentation of the perineum.

Chronic Disease↗
PubMedDate not supplied

[Environmental risk factors in Crohn's disease and ulcerative colitis (excluding tobacco and appendicectomy)].

A rapid increase in the incidence of Crohn's disease and ulcerative colitis in developed countries, the occurrence of Crohn's disease in spouses, and a lack of complete concordance in monozygotic twins are strong arguments for the role of environmental factors in inflammatory bowel disease (IBD). Research in the field of environmental factors in IBD is based upon epidemiological (geographical and case-control), clinical and experimental studies. The role of two environmental factors has clearly been established in IBD. Smoking is a risk factor for Crohn's disease and a protective factor for ulcerative colitis; appendectomy is a protective factor for ulcerative colitis. Many other environmental factors for IBD have been investigated, including infectious agents, diet, drugs, stress and social status. They are detailed in the present review. Among them, atypical Mycobacteria, oral contraceptives and antibiotics could play a role in Crohn's disease. To date, three hypotheses associate environmental factors with the pathophysiology of IBD (loss of tolerance of intestinal immune system towards commensal bacterial flora): the hygiene, infection and cold chain hypotheses. Much work remains to be done to identify risk factors for IBD. Research identifying environmental factors that might cause a predisposition to IBD is useful. It may lead to disease prevention in subjects who are genetically predisposed and disease improvement in patients.

Adolescent↗
PubMed2000

Psychosocial aspects of inflammatory bowel disease.

Crohn's disease (CD) and ulcerative colitis (UC) are known as inflammatory bowel disease (IBD), chronic and potentially disabling diseases, affecting about 90 to 300 per 100,000 people in the general population. Although significant gains have been made in our understanding of these diseases, particularly with respect to pathophysiology and treatment, its etiology is still unknown. IBD is a significant disease that can severely impact one's psychological and social well-being. This article reviews the literature on the psychosocial aspects of IBD. We also address the importance of conceptualizing IBD from a biopsychosocial perspective, considering psychosocial factors along with disease activity. The biopsychosocial approach offers a broadened perspective that reflects the many factors that may contribute to the expression and maintenance of IBD symptoms. Issues of concerns for patients with IBD are also discussed. Finally, we highlight the importance of establishing a collaborative therapeutic relationship between patients and their physicians, facilitating open and honest discussions acknowledging patients' fears and concerns. In doing so, much of these IBD-related issues of concerns may be ameliorated, potentially improving one's coping abilities, and lead to an improved quality of life for individuals with inflammatory bowel disease.

Humans↗
PubMed2000

Deficient iNOS in inflammatory bowel disease intestinal microvascular endothelial cells results in increased leukocyte adhesion.

Microvascular endothelial cells play a key role in inflammation by undergoing activation and recruiting circulating immune cells into tissues and foci of inflammation, an early and rate-limiting step in the inflammatory process. We have previously [Binion et al., Gastroenterology112:1898-1907, 1997] shown that human intestinal microvascular endothelial cells (HIMEC) isolated from surgically resected inflammatory bowel disease (IBD) patient tissue demonstrate significantly increased leukocyte binding in vitro compared to normal HIMEC. Our studies [Binion et al., Am. J. Physiol.275 (Gastrointest. Liver Physiol. 38):G592-G603, 1998] have also demonstrated that nitric oxide (NO) production by inducible nitric oxide synthase (iNOS) normally plays a key role in downregulating HIMEC activation and leukocyte adhesion. Using primary cultures of HIMEC derived from normal and IBD patient tissues, we sought to determine whether alterations in iNOS-derived NO production underlies leukocyte hyperadhesion in IBD. Both nonselective (N(G)-monomethyl-L-arginine) and specific (N-Iminoethyl-L-lysine) inhibitors of iNOS significantly increased leukocyte binding by normal HIMEC activated with cytokines and lipopolysaccharide (LPS), but had no effect on leukocyte adhesion by similarly activated IBD HIMEC. When compared to normal HIMEC, IBD endothelial cells had significantly decreased levels of iNOS mRNA, protein, and NO production following activation. Addition of exogenous NO by co-culture with normal HIMEC or by pharmacologic delivery with the long-acting NO donor detaNONOate restored a normal leukocyte binding pattern in the IBD HIMEC. These data suggest that loss of iNOS expression is a feature of chronically inflamed microvascular endothelial cells, which leads to enhanced leukocyte binding, potentially contributing to chronic, destructive inflammation in IBD.

Cell Adhesion↗
PubMed2002

The probability that similar haplotypes are identical by descent.

The logic of gene mapping in highly penetrant diseases is to find the minimal overlap of haplotypes that are identical by descent (IBD). If the pedigree is unknown, identity by descent of haplotype overlap cannot be established with certainty. In many cases, it is intuitively clear that similar haplotypes are indeed IBD. The logical and statistical evaluation of haplotype overlap requires that probabilities of IBD are substantial. It is, therefore, important to estimate these probabilities. In this paper, we derive a recursive formula for the probability of IBD. Simulations are used to validate the expected values and to study the variability around the expected value. We demonstrate that for populations 1000 generations of age - without bottlenecks - haplotypes of 1 cM consisting of at least five microsatellite markers have a significant probability to be IBD. Likewise, SNP haplotypes of 1 cM should consist of at least nine identical SNP alleles for a similar probability of IBD. Without considering bottlenecks, haplotypes consisting of as few as three SNPs spanning a region of less than 0.01 cM are likely IBD in populations that are 10000 generations of age.

Chromosome Mapping↗
PubMed2000

Inflammatory bowel diseases are not associated with major hereditary conditions predisposing to thrombosis.

Patients with inflammatory bowel diseases (IBD) are at increased risk for thromboembolic complications. Our aim was to evaluate whether the increased risk for thrombosis in IBD could be due to a genetic association of IBD with hereditary prothrombotic conditions. In all, 102 IBD patients (51 with ulcerative colitis and 51 with Crohn's disease) with no history of thrombosis and 204 matched normal subjects were enrolled. DNA specimens were evaluated by PCR and restriction fragment length polymorphism for factor V Leiden, methylene tetrahydrofolate reductase (MTHFR) and prothrombin gene mutations. In IBD patients and matched controls the observed allele frequencies were similar, being 1.5% and 1.2% for factor V Leiden gene mutation, 1.1% and 0.7% for prothrombin gene mutation, and 45.1% and 47.4% for MTHFR gene mutation, respectively. These rates also were not significantly different when patients were analyzed according to age and sex distribution, diagnosis, and extension and clinical type of disease. In conclusion, our study shows no association between IBD and the most frequent hereditary prothrombotic conditions. Other factors should be evaluated in order to understand the mechanisms underlying the thrombotic risk of IBD.

Adult↗
PubMed1998

Risk of colorectal cancer in relatives of patients with inflammatory bowel disease (Denmark)

OBJECTIVES: It has been suggested that inflammatory bowel disease (IBD) and colon cancer are associated because they have genetic susceptibility in common, rather than IBD causing cancer. We examined the risk of colorectal cancer in first-degree relatives of patients with IBD in order to evaluate if they share the same genetic susceptibility. METHODS: We identified patients with IBD in the Danish Hospital Discharge Registry. A cohort of all first-degree relatives to these patients were linked to the Danish Cancer Registry. Colorectal cancers observed were compared with expected values based on age, gender, and calendar-specific incidence rates in the general population. RESULTS: Among 4,496 patients with IBD, a total of 19,645 relatives were identified. For parents of patients with Crohn's disease, we observed 19 cases of colorectal cancer compared with 20 expected (standardized incidence ratio [SIR] = 1.0, 95 percent confidence interval [CI] = 0.6-1.5). For parents of patients with ulcerative colitis, 55 cases were observed compared with 51 expected (SIR = 1.1, CI = 0.8-1.4). CONCLUSIONS: The study did not corroborate the hypothesis that the same genetic factors play a significant role in the etiology of colorectal cancer and IBD, but more information is needed to disregard the possible link between IBD and colon cancer.

Adult↗
PubMed2006

Epithelial myosin light chain kinase expression and activity are upregulated in inflammatory bowel disease.

The intestinal epithelial barrier is frequently disrupted in inflammatory bowel disease (IBD) and this has been proposed to play a role in disease pathogenesis and reactivation. In vitro studies show that cytokine-induced epithelial barrier dysfunction can be mediated by increased myosin light chain kinase (MLCK) expression and subsequent myosin II regulatory light chain (MLC) phosphorylation. However, this has never been examined in human disease. The aim of these studies, therefore, was to determine whether MLCK is upregulated in the intestinal epithelium of IBD patients. MLCK expression and MLC phosphorylation in human intestinal resection and biopsy specimens were determined by quantitative immunofluorescence microscopy and correlated with clinical and histopathological data. The data show that ileal epithelial MLCK expression was mildly upregulated in inactive IBD. Expression increased further in active disease, with progressive increases in MLCK expression correlating positively with histological disease activity. This correlation between activity and MLCK expression was also seen in individual patients where areas of differing disease activity were analyzed. Colonic epithelial MLCK expression was similarly increased in active IBD and these increases also correlated positively with disease activity, both in individual patients and the overall study group. To evaluate MLCK enzymatic activity, MLC phosphorylation was assessed in snap-frozen colon biopsies. MLC phosphorylation was significantly increased in biopsies with active, but not inactive, IBD. Therefore, these data show that MLCK expression and enzymatic activity are increased in IBD. Moreover, the correlation with disease activity suggests that MLCK upregulation may contribute to barrier dysfunction and IBD pathogenesis.

Adult↗
PubMed2000

Comprehensive nutritional status in recently diagnosed patients with inflammatory bowel disease compared with population controls.

OBJECTIVE: Malnutrition is observed frequently in patients with inflammatory bowel disease (IBD). Knowledge of the nutritional status in patients with recently diagnosed IBD is limited. The aim of this study was to establish a comprehensive picture of the nutritional status in recently diagnosed IBD patients. SUBJECTS: Sixty-nine IBD patients (23 Crohn's disease (CD) and 46 with ulcerative colitis (UC)) within 6 months of diagnosis and 69 age- and sex-matched population controls were included in the study. METHODS: The nutritional status was assessed by: (1) body composition (anthropometry and dual-energy X-ray absorptiometry); (2) dietary intake (dietary history); (3) biochemical indexes of nutrition; and (4) muscle strength (isokinetic dynamometer). RESULTS: Body weight and body mass index were significantly lower in UC patients compared with controls. The mean daily intake of carbohydrates was significantly higher in CD patients and the intakes of protein, calcium, phosphorus, and riboflavin were significantly lower in UC patients compared with controls, respectively. Serum concentrations of several nutrients (beta-carotene, magnesium, selenium and zinc) were significantly lower in UC patients compared with controls. Serum vitamin B12 concentration was significantly lower in CD patients. Muscle strength did not significantly differ between IBD patients and controls. CONCLUSIONS: This study showed that the nutritional status of IBD patients was already affected negatively at time of diagnosis. It needs to be elucidated whether nutritional supplementation in recently diagnosed IBD patients may improve the clinical course of the disease.

Adult↗
PubMed2003

Genome-wide search in Finnish families with inflammatory bowel disease provides evidence for novel susceptibility loci.

Epidemiological and genetic linkage studies have indicated a strong genetic basis for development of inflammatory bowel disease (IBD) which was recently supported by discovery of the Crohn's disease (CD) susceptibility gene termed NOD2/CARD15. We carried out a genome-wide linkage study in Finnish IBD families, providing a particular advantage to map susceptibility genes for ulcerative colitis (UC) within a genetic isolate. Initially, 92 IBD families with 138 affected sib-pairs (ASPs), were genotyped for 429 markers spaced at approximately 10 cM intervals. Next, the loci on chromosomes 2p13-11, 11p12-q13, and 12p13-12 were high-density mapped in the extended family cohort of 130 families with 173 ASPs. In this study, the most significant lod scores were observed for the UC families on chromosome 2p11 (D2S2333), in the vicinity of the REG gene cluster which is strikingly overexpressed in the IBD mucosa. The maximum two-point lod score was 3.34 (dominant model), and the corresponding NPL score 2.61. For UC, the second highest two-point NPL score of 2.00 was observed at proximal 12p13, where also some evidence for linkage disequilibrium emerged (P=0.07 and P=0.007 for the basic and extended IBD cohorts, respectively). The highest two-point NPL score for the CD families was 2.34 at D12S78 (12q23) with significant evidence for linkage disequilibrium (P=0.004), and for the mixed (MX) families 2.07 at D4S406 near the linkage peak reported previously. This study confirmed several of the IBD loci that have previously been reported and gives evidence for new IBD loci on chromosomes 2p11, 11p12-q13, 12p13-12, 12q23, and 19q13.

Female↗
PubMed2002

Interleukin-1 receptor antagonist VNTR-polymorphism in inflammatory bowel disease.

Both genetic and environmental factors have been implicated in the etiology of inflammatory bowel diseases (IBD) i.e., Crohn's disease (CD) and ulcerative colitis (UC). Polymorphisms in cytokine genes are likely to influence an individual's predisposition to IBD. In intron 2 of the interleukin-1 receptor antagonist (IL-1ra) gene, a variable number of an 86-bp tandem repeat (VNTR) polymorphism leads to the existence of five different alleles. In order to analyze the association between certain IL-1ra VNTR-alleles and IBD, we investigated the IL-1ra genotype and allele frequencies in 342 unrelated IBD patients and in 401 healthy control individuals. CD patients were also genotyped for the three main associated variants in the NOD2/CARD15 gene. In the IBD group, a significant decrease in the frequency of IL-1ra allele 1 (P=0.048) compared to controls was observed. The frequency of IL-1ra genotype 1/1 was significantly lower in the IBD population vs the control group (P=0.018). Analysis of the CD population without NOD2 homozygotes and compound heterozygotes revealed a more significant decrease in IL-1ra genotype 1/1 compared to controls (P=0.038). These results support the hypothesis that the IL-1ra VNTR-polymorphism could be among the genetic factors that are of importance in IBD susceptibility.

Adolescent↗
PubMed1997

Association between myelodysplastic syndromes and inflammatory bowel diseases. Report of seven new cases and review of the literature.

We report seven patients with both myelodysplastic syndrome (MDS) and inflammatory bowel disease (IBD): Crohn's disease in six cases, ulcerative colitis in one case. We describe their characteristics, and those of 10 previously published similar cases are presented here. Median age at diagnosis of IBD (61 years) was high, as compared to the usual age at diagnosis of IBD. IBD was diagnosed first in nine cases, MDS first in one patient, and both diseases were diagnosed simultaneously in seven cases. Concerning IBD, there was a strong predominance of Crohn's disease (15/17 cases), with an unusually high frequency of colonic involvement (11/15 cases). MDS, in 12/17 cases, showed no excess of marrow blasts. Cytogenetic analysis was abnormal in five of the 13 evaluable cases. These observations suggest that the association between MDS and IBD may not be fortuitous in some cases, and that, in particular, patients with IBD and anemia of nonobvious origin should be evaluated for MDS. The pathogenesis of those associations, however, remains unclear.

Adult↗
PubMed1996

Immunoregulatory properties of IL-13 in patients with inflammatory bowel disease; comparison with IL-4 and IL-10.

Activated monocytes with increased expression of proinflammatory cytokines play a major role in inflammatory bowel disease (IBD). Immunoregulatory cytokines such as IL-4 and IL-10 can effectively suppress the proinflammatory response of activated monocytes. IL-13 is a recently described antiinflammatory agent in vitro. The aim of our study was to determine the in vitro immunosuppressive capacity of IL-13, IL-4 and IL-10 in patients with IBD. Peripheral blood monocytes were isolated from 27 patients with ulcerative colitis (UC), 27 patients with Crohn's disease (CD) and 16 healthy controls. Cells were stimulated with pokeweed mitogen (PWM) after treatment with IL-13, IL-4 and IL-10, and secretion of IL-1beta, tumour necrosis factor-alpha (TNF-alpha) and IL-6 was assessed using sandwich ELISA systems. Peripheral blood monocytes secreted significantly increased amounts of TNF-alpha and IL-6 under stimulation with PWM in patients with CD, while UC patients showed significantly elevated levels of IL-1beta. The antiinflammatory cytokines IL-13, IL-4 and IL-10 were all capable of inhibiting monocyte secretion of IL-1beta in a dose-dependent manner. With regard to IL-13 and IL-4, there was no significant suppression of TNF-alpha and IL-6 in patients with active IBD. By contrast, IL-10 was able to down-regulate all proinflammatory cytokines in active IBD as well as in controls. Proinflammatory cytokines from patients with inactive IBD could be significantly down-regulated by all three immunoregulatory cytokines. The inhibitory effect of IL-13 on TNF-alpha and IL-6 production in differentiated macrophages was diminished in IBD patients, as well as in controls. In disease controls we also observed a reduced inhibition of TNF-alpha and IL-6 after treatment with IL-13. In conclusion, the antiinflammatory activity of IL-13 is partially reduced in patients with active IBD. The hyporesponsiveness of activated and differentiated monocytes to IL-13 and IL-4 does not seem to be a disease-specific phenomenon.

Adolescent↗
PubMed2002

IgA autoreactivity: a feature common to inflammatory bowel and connective tissue diseases.

The immunopathogenic mechanisms in inflammatory bowel disease (IBD) are not yet fully established. The aim of this study was to determine the profile and magnitude of IgA and IgG autoantibodies in IBD patients. The autoantigen profile defined by IgA and IgG antibodies from 24 IBD (14 Crohn's disease CD], 10 ulcerative colitis UC]), three coeliac, 12 connective tissue disease (CTD) patients and 10 healthy individuals was studied in human cellular extracts by Western blotting. The magnitude of the IgA and IgG1-4 subclass responses was measured by ELISA. IBD patients could not be distinguished from healthy individuals on the basis of IgG autoantibodies to Western blotted proteins. IgG subclass analysis indicated no clear bias towards Th1 or Th2 immune responses in IBD or CTD. In accordance with previous work, we found that IgA autoreactivity was strongest in coeliac disease patients. Unexpectedly, IBD as well as CTD patients exhibited strong IgA autoantibody reactivities to components of similar molecular weights (16-80 kD) in intestinal and non-intestinal epithelial cell lines. Our data indicate immunopathogenic similarities between IBD and CTD.

Adult↗
PubMed2002

An insight into the experiences of parents with inflammatory bowel disease.

AIMS AND OBJECTIVES: To identify parents' views, both positive and negative on: how inflammatory bowel disease (IBD) affects people in their parenting role; effects parents with IBD have noticed in their children; ways of dealing with any difficulties in parenting; and support needed by parents with IBD. DESIGN: This was a small-scale exploratory study, adopting a qualitative research design. A purposive sample of 19 mothers and five fathers with IBD was recruited through two hospitals and a voluntary group in the north of England. RESEARCH METHODS: Data were collected through a combination of focus groups and interviews, and analysed using the 'framework approach'. FINDINGS: The main positive effect for parents was developing a closer relationship with their children. When parents were experiencing symptoms there were difficulties in caring for young children; problems taking children to and from school, and attending school events; restrictions in social life; irritability and reduced tolerance of children. When in hospital, it was sometimes difficult to arrange for care of young children. These difficulties caused worry and guilt for parents, and a few spoke of periods of depression. Parents noticed that their children seemed caring and understanding of illness, but were also anxious when the parent was ill or in hospital, and reacted with anger or frustration to restrictions in social activities. Strategies commonly used to deal with difficulties were turning to family for support and trying to control symptoms. Support from health professionals was variable. Parents wanted more practical assistance, information for families on the effects of IBD, and support in coping with the condition. Awareness-raising about IBD was considered important within health, social services, education and housing departments. CONCLUSIONS: As a group in regular contact with parents with IBD, health professionals have an important role to play in providing support. Staff should be particularly vigilant towards parents with severe symptoms, mothers of younger children, and those receiving limited help from their families.

Adaptation, Psychological↗
PubMed2002

Inflammatory bowel disease.

Although inflammatory bowel disease (IBD) usually presents in adolescents and young adults, both ulcerative colitis and Crohn's disease can also present in older adults. The diagnosis of IBD in the elderly is often difficult and can easily be confused with diverticulitis or ischaemic colitis. The symptoms and complications of IBD in the elderly are similar to those found in younger patients. However, when IBD presents later in life the disease is often less extensive and milder. Older IBD patients are treated with the same medications as younger patients, although the risk for drug toxicity is greater, especially with corticosteroid therapy. Comorbid illness in older patients often has a significant impact on the outcome of medical and surgical therapy for IBD but, in the absence of significant co-morbid disease, most elderly IBD patients can expect a good response to therapy.

Aged↗