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PubMed2004

Ocular manifestations of inflammatory bowel disease.

Extraintestinal manifestations of inflammatory bowel disease (IBD) occur in one third of patients. Ocular complications are infrequent, occurring in less than 10% of cases, but can be associated with significant morbidity, including blindness. Ocular complaints are often nonspecific; clinical relevance may not be appreciated by patient or physician and, thus, be misdiagnosed. Evaluation of the eye should be a routine component in the care of patients with IBD. Clinicians must be aware of the spectrum of ocular symptoms and know that these complaints may precede a diagnosis of ulcerative colitis (UC) or Crohn's disease (CD). We review ocular pathology in IBD to alert clinicians to the diverse, at times confusing, spectrum of eye disorders associated with these diseases. Clinical manifestations include blurred vision, teary, burning or itchy eyes, ocular pain, photophobia, conjunctival or scleral hyperemia, loss of visual acuity, and possible blindness. Many patients are unaware that IBD has a risk of eye complications and, therefore, patient education is vital.

Colitis, Ulcerative↗
PubMed2002

Assessing disease activity and disease activity indices for inflammatory bowel disease.

A crucial step in the development of clinical trials to determine the efficacy of various therapies for inflammatory bowel disease (IBD) has been the creation of activity indices. This article reviews the major components and operating characteristics of clinical activity indices commonly used in randomized, controlled trials of IBD therapy. In addition, the paper provides a brief overview of the developmental requirements for any new index.

Colitis, Ulcerative↗
PubMed2000

Transfer of interleukin-4 and interleukin-10 in patients with severe inflammatory bowel disease of the rectum.

Inflammatory bowel disease (IBD) comprises the two disorders ulcerative colitis (UC) and Crohn's disease (CD). Although the etiology is still unclear, initiation and aggravation of the inflammatory processes seem to be due to a massive local mucosal immune response. An increased number of greatly activated macrophages seems to contribute to the onset of IBD by expressing upregulated costimulatory molecules (e.g., CD80/CD86) and a cytokine profile favouring a type I proinflammatory response. The release of interleukin 2 (IL-2) and Interferon-gamma (IFN-gamma) by naive T lymphocytes predominantly stimulates cytotoxic T lymphocytes, macrophages, and natural killer (NK) cells and increases the antigen-presenting potential of all these cell types. Opposite this proinflammatory immune reaction a compensatory type II antiinflammatory response has been suggested in the inflamed mucosa, involving mainly interleukin 4 and interleukin 10. Both cytokines are able to down-regulate inflammatory mediators including tumor necrosis factor-alpha (TNF-alpha) and interleukin 1 and favor a humoral immune response. The main goal of this clinical trial is the local liposome-mediated gene transfer of these two antiinflammatory cytokines, interleukin 4 and interleukin 10, in patients with severe IBD of the rectum. This local administration of antiinflammatory cytokines will avoid toxic systemic side effects, prevents blocking of the beneficial effects of proinflammatory cytokines, e.g., TNF-alpha in other tissue compartments and increases the local concentration of interleukin 4 and interleukin 10 over a prolonged period of time. The combined effects of IL-4 and IL-10 have been shown to shift the Th1/Th2 cell activation in favor of a Th2 immune response which seems to be essential for fighting against the inflammation and ultimative healing.

Clinical Trials as Topic↗
PubMed2003

CARD4/NOD1 is not involved in inflammatory bowel disease.

BACKGROUND AND AIMS: Inflammatory bowel diseases (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), are complex genetic disorders. CARD15/NOD2, a member of the Ced4 superfamily which includes Apaf-1 and CARD4/NOD1, has recently been associated with genetic predisposition to CD but additional genetic factors remain to be identified. Because CARD4/NOD1 shares many structural and functional similarities with CARD15, we tested its putative role in IBD. PATIENTS AND METHODS: The 11 exons of CARD4 were screened for the presence of variants in 63 unrelated IBD patients. The only non-private genetic variation encoding for a substitution in the peptidic chain was genotyped in 381 IBD families (235 CD, 58 UC, 81 mixed, and seven indeterminate colitis families) using a polymerase chain reaction-restriction fragment length polymorphism procedure. Genotyping data were analysed by the transmission disequilibrium test. RESULTS: Five of nine sequence variations identified in the coding sequence of the gene encoded for non-conservative changes (E266K, D372N, R705Q, T787M, and T787K). Four were present in only one family. The remaining variant (E266K), which exhibited an allele frequency of 0.28, was not associated with CD, UC, or IBD. Furthermore, IBD patients carrying sequence variations in their CARD4 gene had a similar phenotype to those with a normal sequence. CONCLUSION: Our results suggest that CARD4 does not play a major role in genetic susceptibility to IBD.

Adaptor Proteins, Signal Transducing↗
PubMed2004

Assessment of the influence of disease activity on the quality of life of patients with inflammatory bowel disease using a short questionnaire.

OBJECTIVES: Inflammatory bowel disease impairs health-related quality of life. Therefore, it is very important to develop adequate instruments to measure the disease impact, but these instruments need to be practical as well as accurate. Our aim was to determine whether a short questionnaire obtained from the reduction of the 36-item version of the inflammatory bowel disease questionnaire (IBDQ-36) accurately reflects the impact of clinical and endoscopic activity on health-related quality of life. METHODS: To this purpose the original IBDQ-36 and a reduced version, composed of only 9 items (IBDQ-9), were administered to 68 patients with inflammatory bowel disease. Disease activity was established by standard clinical activity indices (Rachmilewitz for ulcerative colitis (UC) and Harvey-Bradshaw for Crohn's disease (CD)) and by information gathered at colonoscopy. RESULTS: In UC patients the Spearman's correlation coefficients between IBDQ-9 and clinical and colonoscopic indices were statistically significant (-0.67 and -0.70, respectively, p < 0.01) and similar to those obtained with IBDQ-36 (-0.61 and -0.67). In CD patients IBDQ-9 also correlated well with the clinical index (-0.59, p < 0.05) but less with the colonoscopic index (-0.30, p= 0.1). In CD patients, the correlation of the IBDQ-36 with clinical and colonoscopic indices gave similar results to the IBDQ-9 (-0.58 and -0.21, respectively). The IBDQ-9 power to discriminate between clinical relapse and remission was statistically significant (p < 0.01) both for UC (55 (48-57) vs 69 (63-75) and CD (58 (51-63) vs 69 (64-83)) patients. Similar results were obtained for conoloscopic indices of endoscopic relapse and remission (56 (52-65) vs 70 (66-77) in UC and 58 (52-63) vs 68 (62-73) in CD). CONCLUSIONS: Quality of life impairment produced by relapses of inflammatory bowel disease can be reliably assessed with a short questionnaire, with considerable savings in time and expense.

Adult↗
PubMed2000

Filiform polyposis of the colon in chronic inflammatory bowel disease (so-called giant inflammatory polyps).

On the basis of 3 of our own cases, we describe unusually intense forms of filiform polyposis and local giant polyposis as a consequence of chronic inflammatory bowel disease. The patients are: A 52-year-old woman who for 7 years has been known to have Crohn's disease (CD); a 55-year-old man who for 14 years has been known to have chronic inflammatory bowel disease, which was first thought to have been ulcerative colitis, but, as a result of the findings on the subtotal colectomy specimen, had to be classified as Crohn's disease or colitis indeterminate; and a 53-year-old woman known to have had ulcerative colitis for 37 years. From the literature on the subject, we drew up a chronological list of a total of 43 cases with similar or completely identical findings. The clinical significance of the findings in their particularly massive intensity results from their necessary differentiation--in the context of differential diagnosis--from a malignant tumor, in particular from a carcinoma in association with chronic inflammatory bowel disease, or from a villous adenoma. The indication of a need to operate results from the impossibility of being able definitely to rule out a malignant degeneration by means of clinical methods. Also, experience shows that with massive findings of the kind described a spontaneous disappearance cannot be expected. Finally, too, the clinical symptoms and the patients subjective complaints necessitate balanced surgical treatment, taking into consideration the site and the extent of the lesion.

Colectomy↗
PubMed2002

Prevalence of factor V G1691A (Leiden), prothrombin G20210A, and methylene tetrahydrofolate reductase C677T thrombophilic mutations in children with inflammatory bowel disease.

BACKGROUND: Patients with inflammatory bowel disease (IBD) have an increased incidence of thromboembolic events. This risk may be caused by an increased frequency of thrombophilic mutations such as factor V Leiden G1691A (FVL), prothrombin G20210A (PT), or methylene tetrahydrofolate reductase C667T (MTHFR). Prevalence rates of heterozygous mutations in FVL, PT, and MTHFR are reported for whites (1.8%, 1.3%, 26.6%, respectively), blacks (0.8%, 0.3%, and 12.4%, respectively), and Hispanics (1.2%, 2.4%, and 41.5%, respectively). We sought to determine the prevalence of these thrombophilic mutations in a large cohort of children with IBD. METHODS: Children aged 21 years or younger with IBD were genotyped for FVL, PT, and MTHFR mutations by polymerase chain reaction amplification and restriction enzyme digestion. Prevalence rates were compared with established rates in the respective populations. RESULTS: Of 92 patients enrolled, 89 (62 with Crohn disease, 24 with ulcerative colitis, and 3 with indeterminate colitis) had genotype results available. The mean age was 13.3 +/- 4.2 years (range, 2-21 years). Statistical analysis was performed on 89 FVL, PT, and MTHFR allele pairs. Polymerase chain reaction genotyping identified 5 patients with heterozygous FVL mutations, 3 patients heterozygous for the PT mutation, and 36 patients heterozygous and 4 patients homozygous for the MTHFR mutation. The thrombophilic allele mutation frequencies in our sample were not significantly different from predicted weighted average values: FVL, 2.8% versus 1.5%; PT, 1.7% versus 1.1%; and MTHFR, 24.7% versus 24.4%. In 24 patients with a family history of thrombosis, 1 was heterozygous for FVL and for MTHFR, 1 was heterozygous for FVL and homozygous for MTHFR, 2 were heterozygous for PT, and 9 were heterozygous MTHFR. There was no significant correlation between family history of thrombosis and presence of a thrombophilic mutation. The four patients with homozygous mutations for MTHFR, two of whom also were heterozygous for FVL, did not have either a personal history of thrombosis or a family history of thrombotic events. Two patients had thrombotic events without mutations in these genotypes: one had protein S deficiency and the other had no identifiable cause. CONCLUSIONS: The presence of genetic mutations that predispose to hypercoagulable states does not appear to correlate with the prevalence of IBD or to thromboembolic events in patients with IBD. There was no statistical difference between the proportions of the mutated allele frequency in our study patients and the general population.

Adolescent↗
PubMed1996

Increased hepatic urea synthesis in patients with active inflammatory bowel disease.

BACKGROUND/METHODS: Patients with active inflammatory bowel disease are often reported to be in negative nitrogen balance. Therefore, we examined basal and amino acid stimulated urea synthesis in 11 patients with active inflammatory bowel disease (six with Crohn's disease and five with ulcerative colitis) and in 10 patients with non-active disease (six with Crohn's disease and four with ulcerative colitis). A primed continuous infusion of an amino acid mixture was given from t = 1 h to t = 5 h; during the first and the last 2 h no amino acid infusion was given. Urea nitrogen synthesis rate was calculated in hourly intervals for 7 consecutive hours. Urea nitrogen synthesis rate was quantified independent of changes in blood amino acid concentration by means of the functional hepatic nitrogen clearance, i.e. the linear slope of the regression of urea nitrogen synthesis rate of blood amino acid concentration. RESULTS: Basal urea nitrogen synthesis rate was 24.5 +/- 2.9 mmol/h in the patients with no disease activity and 43.8 +/- 2.2 mmol/h in patients with active disease (p < 0.01). During amino acid infusion urea nitrogen synthesis rate was elevated two-fold in the patients with active disease. Functional hepatic nitrogen clearance was 28.2 +/- 1.5 1/h in patients with no disease activity and 56.1 +/- 4.1 1/h in patients with active disease (p < 0.01). No differences between the two groups were observed as regards basal or stimulated plasma glucagon and cortisol and serum levels of interleukin-1 alpha, interleukin-1 beta, tumor necrosis factor alpha and interleukin-6. CONCLUSIONS: The results show that the liver function related to conversion of amino-nitrogen to urea is increased in patients with active inflammatory bowel disease. No differences among known and possible regulators of urea synthesis were found between the two groups. The accelerated hepatic amino-nitrogen conversion contributes to the less efficient nitrogen economy in patients with active inflammatory bowel disease.

Adolescent↗
PubMed1992

Antineutrophil cytoplasmic autoantibodies in inflammatory bowel diseases.

Antineutrophil cytoplasmic autoantibodies have been recently reported in sera from patients with inflammatory bowel disease. We report our experience based on 90 patients with ulcerative colitis, 148 patients with Crohn's disease, and 60 controls. Determination of antineutrophil cytoplasmic autoantibodies was performed by the indirect immunofluorescence technique on ethanol fixed leucocytes. The specificities for proteinase 3, myeloperoxidase, and lactoferrin were tested by enzyme-linked immunosorbent assay. Forty-three out of 90 (48%) patients with ulcerative colitis, 10 out of 148 (7%) patients with Crohn's disease, and none of controls were positive by indirect immunofluorescence technique. All patients but two with positive immunofluorescence exhibited a perinuclear staining pattern. Among patients with ulcerative colitis, there was no relationship between the presence of perinuclear antineutrophil cytoplasmic autoantibodies and disease location or activity. Seven out of 20 (35%) patients with ulcerative colitis who had a previous colectomy (including 1 with ileoanal anastomosis) had perinuclear antineutrophil cytoplasmic autoantibodies. Antineutrophil cytoplasmic autoantibody specificity was not directed against myeloperoxidase, proteinase 3 or lactoferrin in sera from patients with inflammatory bowel diseases. Inflammatory bowel diseases are associated with a new subset of antineutrophil cytoplasmic autoantibodies. Among patients with Crohn's disease and ulcerative colitis, the sensitivity and specificity of the presence of perinuclear antineutrophil cytoplasmic autoantibodies for ulcerative colitis was 46% and 93%, respectively. Their presence reinforces the likelihood of underlying immunologic dysregulation in ulcerative colitis. Identification of the autoantigen(s) to which these antibodies are directed might facilitate the understanding of inflammatory bowel disease pathophysiology.

Adolescent↗
PubMed1996

Cigarette smoking and quality of life in patients with inflammatory bowel disease. South Limburg IBD Study Group.

OBJECTIVE: Smoking has been reported as influencing disease activity in inflammatory bowel disease. The aim of our study was to elucidate the relationship between smoking and aspects of disease-specific quality of life in inflammatory bowel disease. DESIGN: Cross-sectional study. METHODS: In 1105 prevalent patients with inflammatory bowel disease, diagnosed according to the criteria of Lennard-Jones and Truelove and Witts, disease-specific quality of life was investigated using the Inflammatory Bowel Disease Questionnaire (IBDQ). RESULTS: In Crohn's disease, smoking females reported a lower quality of life than non-smoking females (all four dimensions of the IBDQ). Using an explanatory model of relationships between the four dimensions for the analysis, it became evident that smoking is associated with more bowel symptoms in young Crohn's disease females, with more emotional dysfunction in all Crohn's disease females, and with more systemic symptoms in all three diagnostic groups with marked bowel symptoms. Moderately smoking male ulcerative colitis patients reported fewer bowel complaints compared with non-smoking male ulcerative colitis patients. CONCLUSION: There is a relationship between smoking and disease-specific quality of life in both ulcerative colitis and Crohn's disease. The hypothesis is presented that a part of the observed differences in the studied quality of life dimensions with respect to age, sex and disease group are related to concomitant oral contraceptive use.

Adolescent↗
PubMed2001

Transcription factor-targeted therapies in inflammatory bowel disease.

Although the causes of inflammatory bowel disease currently are not fully understood, increasing evidence implicates cytokines as key factors in the development of this disorder. The rationale for cytokine-targeted therapy for inflammatory bowel disease has been refined significantly, and clinical studies have been initiated. Recent investigations have focused on transcription factors that regulate production and activation of cytokines, including the nuclear factor-kappa B, the p38 mitogen-activated protein kinase, the peroxisome proliferator-activated receptor-gamma, and the Janus kinases/signal transducers and activator of transcription pathways. Although their exact role in inflammatory bowel disease is still unknown, further studies may lead to identification of additional possible targets for therapeutic intervention that could improve management of the disease.

Cytokines↗
PubMed2003

Modern therapy for inflammatory bowel disease.

Modern therapy for inflammatory bowel disease implies that therapy should be disease modifying rather than merely symptomatic. To achieve this goal, induction and maintenance of bowel healing are mandatory. Long-term bowel healing results in fewer hospitalizations and less surgery. Only immunosuppression therapy and biological approaches, or a combination of both, result in long-term healing of the bowel mucosa. Unsolved issues are when these drugs should be initiated and whether we should aim at eradicating the bowel inflammation from the onset of therapeutic intervention immediately following diagnosis. Identification of genetic and serologic parameters which allow prediction of the course of the disease would be useful for identifying patients who need aggressive treatment early in the disease. Once total control of the disease is achieved, long-term maintenance of a healed bowel is important. We hypothesize that changing the gut flora, e.g. using probiotics, may allow maintenance of bowel healing after induction with biologicals and immunosuppression.

Algorithms↗
PubMed1999

Risk of ulcerative colitis and Crohn's disease among offspring of patients with chronic inflammatory bowel disease.

OBJECTIVE: The incidence of inflammatory bowel disease (IBD) varies among and within countries, but several studies have indicated that genetic factors may play an important role in the etiology of IBD. A Danish regional study has observed an almost 10-fold increased risk for ulcerative colitis (UC) and Crohn's disease (CD) among first-degree relatives of patients with these diseases. To give more precise risk estimates we conducted a nationwide study using population-based data from the Danish National Registry of Patients (NRP). METHODS: All patients from the entire Danish population (5.2 million), who were discharged between 1977 and 1992 with a diagnosis of either UC or CD were extracted from the NRP. The offspring of these patients born in 1958 or later were identified in the Civil Registration System and subsequently linked to the NRP by means of the civil registration number. All Danish citizens alive or born on April 1, 1968 or later are registered in the Civil Registration System by a unique registration number, which includes the data of birth and links the offspring to their parents. The prevalence proportion ratio (PPR) was estimated by dividing the observed number of offspring with UC or CD, respectively, with the expected number of cases from the general population. RESULTS: The PPRs of CD and UC among offspring of patients with UC were 2.6 and 5.1, respectively, and the PPRs of CD and UC among offspring of patients with CD were 12.8 and 4.0, respectively. All ratios were significantly increased. CONCLUSION: The risk for UC and CD among offspring of patients with IBD is 2-13 times higher than the risk within the general population.

Child↗
PubMed2006

Role of the IBD5 susceptibility locus in the inflammatory bowel diseases.

The field of inflammatory bowel disease genetics plays a leading role in the genetics of complex traits. One of the first genetic loci for a complex trait to be identified by genome-wide linkage scans and confirmed by multiple studies was IBD1 for Crohn's disease. Shortly after this initial success, a second susceptibility locus, the IBD5 risk haplotype, was discovered and unequivocally replicated. In this review, we examine the genetics and potential functional implications of the IBD5 locus on disease susceptibility, prognosis, classification, and treatment. In addition, we discuss the challenges faced when the region identified by association contains multiple genes that are not easily separated by recombination-the primary tool of the human geneticist.

Chromosomes, Human, Pair 5↗
PubMedDate not supplied

The overlap of inflammatory bowel disease and diverticular disease.

An overlap of inflammatory bowel disease and diverticular disease has long been recognized. Crohn's disease and diverticulitis share clinical and radiologic features but usually differ in histopathologic findings. There is a suggestion, however, that even the characteristic pathology of Crohn's disease can be a secondary reaction to diverticulitis. It is possible, moreover, that the presence of Crohn's disease in association with diverticulosis predisposes to the development of diverticulitis. Finally, an apparently distinct form of segmental colitis associated with sigmoid diverticula has been described further contributing to the overlap of inflammatory bowel disease and diverticular disease.

Anti-Bacterial Agents↗
PubMed1999

[Education of patients with inflammatory bowel diseases].

Patients with chronic inflammatory bowel disease were interviewed about their degree of satisfaction with the medical information provided by the professional staff and the reasons for their satisfaction. 30 patients, suffering from ulcerative colitis or Crohn's disease, underwent semistandardized interviews with the result that professional education about their disease was provided either in a single concluding session or in several consecutive sessions. The patients were informed about the diagnosis, the assumed etiology and medical treatment, yet much less frequently were they told about the course of their disease or its possible consequences. On the average the clarifying sessions did not take more than 10 to 15 minutes. Only 50% of the patients were able to fully understand the information they received. 40% were dissatisfied. Greater patient satisfaction was related to more time, more detailed explanation, and emotional support by the physician. These facts should be seriously considered during medical training.

Adult↗