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PubMed1997

Review article: platelets in inflammatory bowel disease--pathogenetic role and therapeutic implications.

An elevated platelet count is well recognized as a marker of inflammatory bowel disease activity. There is an increased incidence of systemic thromboembolism in this disease. Recent work indicates that platelets exhibit several proinflammatory properties including release of inflammatory mediators, and recruitment, chemotaxis and modulation of the activity of other inflammatory cells. Furthermore there is evidence that microvascular thrombosis and a procoagulant state may play a role in the pathogenesis of inflammatory bowel disease. These observations prompted recent studies of platelet activity in inflammatory bowel disease, which indicate enhanced platelet aggregation in vivo and in vitro, and increased platelet activation as measured by increased release of intracellular proteins into plasma and expression of platelet surface markers, including P-selectin and GP53. These abnormalities could contribute to the pathogenesis of inflammatory bowel disease by enhancing inflammation and promoting microinfarction. Aminosalicylates reduce platelet activity although they also have many other additional properties to explain their efficacy in inflammatory bowel disease. There are however several specific antiplatelet drugs now available which may provide new therapeutic possibilities in the management of this disease.

Animals↗
PubMed2002

Role of mucins in inflammatory bowel disease: important lessons from experimental models.

Inflammatory bowel disease (IBD) is characterized by a chronically inflamed mucosa of the gastrointestinal tract, caused by an underlying immune imbalance and triggered by luminal substances, including bacteria. Mucus forms a gel layer covering the gastrointestinal tract, acting as a semi-permeable barrier between the lumen and the epithelium. Mucins, the building blocks of the mucus gel, determine the thickness and properties of mucus. In IBD in humans, alterations in both membrane-bound and secretory mucins have been described involving genetic mutations in mucin genes, changes in mucin mRNA and protein levels, degree of glycosylation, sulphation, and degradation of mucins. As mucins are strategically positioned between the vulnerable mucosa and the bacterial contents of the bowel, changes in mucin structure and/or quantity probably influence their protective functions and therefore constitute possible aetiological factors in the pathogenesis of IBD. This hypothesis, however, is difficult to prove in humans. Animal models for IBD permit detailed analysis of those aspects of mucins necessary for protection against disease. These models revealed pertinent data as for how changes in mucins, in particular in MUC2, imposed by immunological or microbial factors, may contribute to the development and/or perpetuation of chronic IBD, and shed some light on possible strategies to counteract disease.

Animals↗
PubMed1982

Defective autologous mixed-lymphocyte reaction and suppressor cell generation in patients with inflammatory bowel disease.

Impaired regulation of immune function may contribute to the abnormal immune responses associated with idiopathic inflammatory bowel disease. We examined the autologous mixed-lymphocyte culture in inflammatory bowel disease patients because this reaction may reflect self regulation of immune responses in vivo and results in activation of suppressor T cells in vitro. We also examined suppressor T-cell generation in two separate assays. In contrast to healthy and disease controls who had normal values, the autologous mixed-lymphocyte culture response was diminished in 44 of 51 (86%) patients with inflammatory bowel disease, independent of disease type, activity, or steroid therapy. Fourteen of 17 inflammatory bowel disease patients (83%) had decreased suppressor T-cell generation. These results show a distinct abnormality in autologous mixed-lymphocyte culture reactivity and in generation of suppressor cells in inflammatory bowel disease. Such impaired immune regulation may be partly responsible for the immunologic aberrations observed in patients with inflammatory bowel disease.

Adolescent↗
PubMed1999

An investigation of the association of the factor V Leiden mutation and inflammatory bowel disease.

BACKGROUND: A thrombotic aetiology for inflammatory bowel disease (IBD) has been proposed as a result of its association with thrombo-embolic complications, smoking, the oral contraceptive pill and the response of ulcerative colitis (UC) patients to heparin. The factor V Leiden (FVL) mutation is the commonest inherited risk factor for thrombo-embolism. AIM: The aim of the study was to investigate the hypothesis that the pro-thrombotic state associated with the FVL mutation is involved in the aetiology of IBD. PATIENTS AND METHODS: A prospective cohort study of patients attending the Bristol Royal Infirmary IBD outpatient clinic was performed. Fifty-four patients with IBD (30 with Crohn's disease (CD) and 24 with UC) and 55 historical controls were screened for the presence of FVL using the activated protein C (APC) ratio. Abnormal APC ratios were confirmed to be due to FVL using a heteroduplex-based polymerase chain reaction (PCR) technique. RESULTS: Five patients had the FVL mutation, compared to two controls. One of the patients was homozygous. Two of the patients had CD and three UC. The differences between controls and IBD patients was significant when the allelic frequency of the FVL mutation in patients with UC was compared with controls, with a risk ratio of 2.27, but with limited data. CONCLUSION: There appears to be a weak association between FVL and UC. This association is not strong enough to imply a causal relationship, but may be responsible for some of the thrombo-embolic complications.

Activated Protein C Resistance↗
PubMed2003

Distinct elevation of levels of anti-Caenorhabditis elegans antibody in sera of patients with inflammatory bowel disease.

Dysregulation of immune responses to intestinal exogenous antigens contributes to the pathogenesis of inflammatory bowel disease, but the specific antigen responsible for the pathogenesis of inflammatory bowel disease is unknown. We measured serum antibody titers against Caenorhabditis elegans antigens. Immunoglobulin G (IgG) and IgG subclass anti-C. elegans antibodies in serum samples from 29 patients with ulcerative colitis, 30 patients with Crohn's disease, 7 patients with intestinal Behçet's disease, and 11 healthy controls were measured by enzyme-linked immunosorbent assay. Serum IgG and IgG2 antibody titers against C. elegans were significantly higher in patients with inflammatory bowel disease than in controls. Antibody levels were not affected by age, gender, disease activity, extent of disease, or small bowel involvement. The anti-C. elegans antibody titer was significantly lower in patients with Crohn's disease taking mesalazine or sulfasalazine than in patients not taking these drugs. The increased immune responses to C. elegans found in patients with inflammatory bowel disease reflect dysregulated immune responses to enteric antigens, which might play a role in the pathogenesis of inflammatory bowel disease.

Adult↗
PubMed2002

[Extraintestinal manifestations in chronic inflammatory bowel diseases].

60-80% of patients with inflammatory bowel diseases (IBD) develop extraintestinal manifestations. These complications are mostly the result of the underlying disease, deficiencies, or drug therapy and can significantly reduce the quality of life of patients with IBD. The most evident manifestations affect the perianal region, joints, skin, and eyes. Regular check-ups and early substitution in addition to a consistent therapy of the chronic intestinal inflammation usually lead to a significant reduction of the extraintestinal symptoms.

Diagnosis, Differential↗
PubMed1983

Pregnancy and inflammatory bowel disease: a review of the literature.

This review encompasses fertility with inflammatory bowel disease, risk of inheritance, effects of inflammatory bowel disease on pregnancy, effects of pregnancy on inflammatory bowel disease, effects of treatment on the mother and child, and pregnancy after proctocolectomy with ileostomy. Fertility is minimally, if at all, compromised. The fetus is likely to survive despite disease activity. Inactive disease favors a normal pregnancy. Active disease may worsen during the first trimester or the puerperium. Close medical supervision allows therapy to be instituted promptly. Patients with Crohn's disease who have medically induced remissions may fare less well than those who have undergone a successful operation. Previous surgery does not preclude vaginal delivery. Sulfasalazine and corticosteroids may be used. Patients with extensive fistulas may require cesarean section. There are few reasons to consider therapeutic abortion.

Colitis, Ulcerative↗
PubMed2004

Quality of life in patients with established inflammatory bowel disease: a UK general practice survey.

BACKGROUND: The current understanding of quality of life impairment in inflammatory bowel disease has largely been derived from selected populations and may not reflect the experience of patients in the community, where fewer than half are likely to be under specialist care. AIM: To describe the health-related quality of life in a community-based sample of patients with established inflammatory bowel disease and explore its association with the type and extent of disease, gender, age, material deprivation and other factors. METHODS: Adults with established inflammatory bowel disease were identified systematically from the records of 23 family practices in north-east England. The health-related quality of life was assessed by self-completion of the UK Inflammatory Bowel Disease Questionnaire. RESULTS: Five hundred and fifty-six patients were sent the questionnaire and 409 (74%) gave usable replies. Lower scores (worse quality of life) were significantly associated with female gender, Crohn's disease, more extensive disease (ulcerative colitis) and being under specialist care. The mean health-related quality of life score was significantly lower in patients resident in more deprived districts, independent of the type and extent of disease. CONCLUSIONS: Most patients with established inflammatory bowel disease showed only minor impairment of their health-related quality of life. On average, women and those with Crohn's disease were relatively more affected. Clinicians responsible for the care of patients with inflammatory bowel disease should be aware of these more vulnerable groups.

Adolescent↗
PubMedDate not supplied

Serum interleukin-8 in inflammatory bowel disease.

To investigate the relationship between serum concentrations of interleukin-8 (IL-8) and disease activity in inflammatory bowel disease, serum IL-8 concentrations were measured by enzyme-linked immunosorbent assay (ELISA) in 93 patients. Interleukin-8 levels were compared with plasma interleukin-6 (IL-6) levels in 80 of these patients. Interleukin-8 levels were also measured in ten patients with active Crohn's disease, before and after treatment with a defined formula polymeric diet. Of these patients, 70 out of 93 IL-8 concentrations were below the detection limit of the assay. Levels were higher in patients with active ulcerative colitis (median < 20 pg/mL, 75th centile value = 190) compared with inactive disease (median and 75th centile value < 20; P < 0.05). Interleukin-8 concentrations correlated with a combined score for disease severity and extent (P = 0.01). Thirty-eight per cent (8/20) of patients with active Crohn's disease also had high levels of IL-8 but there was no significant difference between active and inactive disease. There was no correlation between serum IL-8 and plasma IL-6; on the contrary, very few patients had raised blood levels of both cytokines. In the diet treated group, serum IL-8 fell significantly after treatment (median = 37 pg/mL, range < 20-4615 before treatment, median < 20, range < 20-104 after treatment; P = 0.03). The results suggest that although IL-8 may be involved in the inflammatory process in inflammatory bowel disease, it is a poor marker of disease activity.

Colitis, Ulcerative↗
PubMed1992

Extension of indications of immunosuppression in inflammatory bowel disease.

Treatment of the two chronic inflammatory bowel diseases (IBD), Crohn's disease (CD) and ulcerative colitis (UC) is still hampered, because we do not understand the pathophysiological processes behind them. Are they caused by a normal inflammatory response reacting towards a foreign agent, or are they caused by an abnormal inflammatory response against a common or even universal agent? Our only choices at present are symptomatic treatments, including immunosuppressive drugs. To make the necessary controlled testing of new immunosuppressive drugs ethically acceptable, we have to choose carefully between different designs: comparing a new drug against placebo in overall treatment failures, to add the new drug or placebo to ongoing treatment (addition design), or to apply a classical group comparison between test drug and placebo in moderately active cases. There exists a strong need for extension of indications for immunosuppressive and anti-inflammatory treatments: to be able to treat long-term instead of short-term, to do without extensive surgery in some UC cases, to treat severe UC cases with isolated distal involvement, to treat CD patients with short bowel syndrome, and to treat CD patients with fistulae and severe extra-intestinal manifestations. Future drug treatment of IBD will probably still be based on immunosuppressive and anti-inflammatory drugs, while waiting for a pathophysiological breakthrough in these two diseases.

Colitis, Ulcerative↗
PubMed2000

Surrogate markers of intestinal inflammation are predictive of relapse in patients with inflammatory bowel disease.

BACKGROUND & AIMS: Prediction of relapse of inflammatory bowel disease has important implications for therapeutic strategies. We assessed whether measurement of intestinal permeability and inflammation could predict relapse of inflammatory bowel disease (IBD). METHODS: Forty-three patients with Crohn's disease (CD) and 37 with ulcerative colitis (UC) in clinical remission provided a stool sample to be assayed for calprotectin (a neutrophil-specific marker), and patients with CD additionally underwent a small intestinal permeability test. Relapse was defined using clinical disease activity indices. RESULTS: Twenty-five (58%) patients with CD and 19 (51%) with UC had a relapse over the 12-month period. Median calprotectin levels in the relapse groups (122 mg/L for CD, 123 mg/L for UC; normal <10 mg/L) differed significantly (P<0.0001) from those of the nonrelapse groups (41.5 mg/L for CD, 29.0 mg/L for UC). At 50 mg/L, the sensitivity and specificity of calprotectin for predicting relapse in all patients with IBD were 90% and 83%, respectively. Permeability in the CD patients who relapsed (median, 0.075; normal <0.04) differed significantly (P = 0. 004) from that in the nonrelapse group (median, 0.038). At the level of 0.05, the sensitivity and specificity of permeability in predicting relapse were 84% and 61%, respectively. CONCLUSIONS: Fecal calprotectin predicts clinical relapse of disease activity in patients with CD and UC, whereas small intestinal permeability is a useful predictor of relapse in patients with small intestinal CD.

Adolescent↗
PubMed1999

Acute major gastrointestinal hemorrhage in inflammatory bowel disease.

BACKGROUND: Acute major gastrointestinal hemorrhage is uncommon in inflammatory bowel disease. METHODS: We characterized the clinical features and course of such hemorrhage in patients at our institution from 1989 to 1996. RESULTS: Thirty-one patients had acute lower gastrointestinal bleeding from inflammatory bowel disease and one had upper gastrointestinal bleeding from duodenal Crohn's disease. Three patients had ulcerative colitis and 28 had Crohn's disease, representing 0.1% of admissions for ulcerative colitis and 1.2% for Crohn's disease. In addition, another patient bled from an ileal J-pouch. In patients with Crohn's disease, the site of bleeding was duodenal in 1, small intestinal in 9, ileocolonic in 8, and colonic in 10. All ulcerative colitis patients had pancolitis. Medical therapy was initiated in 27 patients, including endoscopic therapy in 3. Five patients underwent surgery immediately, and 7 medically treated patients eventually required surgery for ongoing or recurrent bleeding. CONCLUSIONS: Acute major gastrointestinal bleeding is uncommon in inflammatory bowel disease. Most cases are due to Crohn's disease, without a predilection for site of involvement. The presence of an endoscopically treatable lesion is uncommon, and surgery is required in less than half of cases during the initial hospitalization. Recurrent hemorrhage is not rare, and for these cases surgery may be the most appropriate treatment.

Acute Disease↗
PubMed2004

Prevalence and pathogenesis of osteoporosis in patients with inflammatory bowel disease.

Decreased bone mineral density is a frequent finding in patients with inflammatory bowel disease. Factors contributing to this are: 1) malabsorption of vitamin D, calcium and possibly vitamin K and other nutrients, 2) treatment with corticosteroids, 3) inflammatory cytokines in inflammatory bowel disease, and 4) hypogonadism induced by the inflammatory bowel disease. Among patients with Crohn's disease from 32% to 38% have osteopenia (Z-scores <-1), and among patients with ulcerative colitis 23% to 25% have osteopenia. The mean deficit was 0.44+/-0.08 Z-scores in the spine in Crohn's disease and 0.34+/-0.08 in ulcerative colitis. A similar deficit was seen in the hip in both conditions. From these deficits, an increase in overall fracture risk of 1.1-1.3 should be expected. The observed excess fracture risk was limited compared to the general population in both Crohn's disease (RR=1.2, 95% CI: 0.9-1.6 for any fracture and 2.2, 95% CI: 1.2-4.0 for spine fractures) and ulcerative colitis (RR=1.1, 95% CI: 1-1.2 for any fracture, and 1.5, 95% CI: 0.9-2.5 for spine fractures). The observed excess fracture risk was close to that expected from the changes in BMD. Despite the limited excess fracture risk, a relatively large percentage of all fractures may be attributable to corticosteroid use among users of corticosteroids.

Bone Density↗
PubMed1995

Traumatic rupture of the intestine in patients with inflammatory bowel disease.

Three young patients suffering from inflammatory bowel disease were admitted to our hospital during the past year for extensive intestinal rupture caused by disproportionately minor trauma. There was almost no concomitant intra-abdominal injury. We believe that a minimal direct or acceleration/deceleration trauma to a preexisting diseased intestine might have caused extensive damage that was not apparent on admission. It was concluded that these patients should be carefully monitored and that their relative intestinal vulnerability should be borne in mind during diagnosis of and therapeutic planning for their condition.

Adult↗
PubMed2006

Advances in the pathogenesis of inflammatory bowel disease.

Most people do not develop inflammatory bowel disease (IBD) in spite of the density of the commensal flora. In the past few years, several areas of gut mucosal immunology have emerged that will permit advances in the management of IBD at the bedside. The commensal flora is only beginning to be fully appreciated as another metabolic organ in the body. Innate immunity as it relates to the gut has complemented our understanding of the adaptive immune response. The most important susceptibility gene described for Crohn's disease, the NOD2 gene, participates in the innate immune response to pathogens. Patients carrying NOD2 mutations have an increased adaptive immune response to commensal organisms as measured by higher titers of antimicrobial antibodies, such as anti-CBir and anti-Saccharomyces cerevisiae antibodies. Toll-like receptors expressed by antigen-presenting cells (APCs) in the gut and intestinal epithelial cells also play a role in recognition of intestinal flora. Within the APC category, dendritic cells link the innate and adaptive immune systems and shape the nature of the adaptive immune response to commensal bacteria. With respect to adaptive immunity, a new signaling pathway involving a distinct helper CD4 T-cell subset producing interleukin-17 may become a target for the treatment of chronic inflammatory diseases. This review focuses on developments likely to culminate in advances in patient care.

Animals↗
PubMed1985

111Indium autologous granulocytes in the detection of inflammatory bowel disease.

Indium leucocyte scanning and measurement of faecal Indium leucocyte excretion are techniques which have recently been introduced for assessing patients with inflammatory bowel disease. The methodology has recently been made more specific for acute inflammation by labelling pure granulocytes rather than the mixed leucocyte preparation. To determine the accuracy of this modified technique in detecting inflammatory bowel disease, we have prospectively compared Indium granulocyte scanning and faecal In granulocyte excretion with rectal histology and contrast bowel radiology as screening procedures in 100 patients with suspected inflammatory bowel disease. Thirty three patients were shown to have inflammatory bowel disease - 24 with Crohn's disease and nine with ulcerative colitis or indeterminate colitis. Overall the respective sensitivities for detecting inflammatory bowel disease were 97% for faecal Indium granulocyte excretion, 94% for Indium granulocyte scanning, 79% for radiology and 70% for rectal histology. The superiority of In granulocytes over radiology and rectal histology in detecting inflammatory bowel disease was, in the main, due to the difficulty in diagnosing Crohn's with conventional techniques. Although three of the patients with ulcerative colitis and indeterminate colitis had normal sigmoidoscopic appearances - all had abnormal rectal histology. No patient with a non-inflammatory bowel disorder had a positive In granulocyte scan or a raised faecal excretion. These results show that investigations using In granulocytes are accurate in identifying inflammatory bowel disease and offer important advantages over conventional procedures for detecting Crohn's disease.

Colitis, Ulcerative↗
PubMed2002

The role of endoscopic ultrasound in inflammatory bowel disease.

Ultrasonography has been applied to the diagnosis and management of inflammatory bowel disease for over 20 years. The combination of endoscopy with ultrasound has resulted in the application of intraluminal sonographic imaging to multiple diseases, including inflammatory bowel disease. Initial efforts were focused on the sonographic assessment of disease severity as based on bowel wall thickness, but this has been inconsistently demonstrated. Furthermore, disease severity is a clinical assessment that is based on both clinical and imaging studies. Recognizing that Crohn's disease tends to be transmural and ulcerative colitis a superficial mucosal inflammatory process, hopes were raised that endosonography would be effective in discriminating cases of otherwise indeterminate colitis. Efforts to demonstrate this, however, have been largely disappointing, and EUS plays a limited role in discriminating ulcerative colitis from Crohn's disease. On a more positive note, EUS evaluation of perirectal and perianal complications of Crohn's disease has been demonstrated to be superior to fistulography, CT, and equal to or superior to MRI. Because accurate anatomic information is required to guide surgical therapy of these lesions, EUS has the potential to emerge as a powerful imaging tool in the management of perianorectal Crohn's disease.

Abscess↗
PubMed1990

Chlamydia trachomatis and inflammatory bowel disease--a coincidence?

Serological tests of 35 patients suffering from inflammatory bowel disease were compared to those of 35 healthy controls. The tests were performed using the indirect immunoperoxidase assay. Ninety-three per cent of 15 patients with Crohn's disease had IgG antibodies against Chlamydia, compared to 26% in the control group. In the 20 patients with ulcerative colitis, 45% had IgG antibodies against Chlamydia, compared to 10% in the control group. High serum titres of IgG antibodies were found in most of the patients with inflammatory bowel disease, mainly with Crohn's disease, while weak reactions appeared in most of the controls in which antibodies were detected. These results suggest a high incidence of Chlamydia infection in the studied patients with inflammatory bowel disease, especially in those with Crohn's disease. The possible association between Chlamydia trachomatis and inflammatory bowel disease is discussed.

Antibodies, Bacterial↗