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PubMed2003

Intestinal oxidative damage in inflammatory bowel disease: semi-quantification, localization, and association with mucosal antioxidants.

Intestinal inflammation is accompanied by excessive production of reactive oxygen and nitrogen metabolites. In order to counteract their harmful effects, the intestinal mucosa contains an extensive system of antioxidants. It has previously been shown that the levels of and the balance between the most important antioxidants are seriously impaired within the intestinal mucosa from inflammatory bowel disease (IBD) patients compared with normal mucosa. The present study investigated the consequences of this antioxidative imbalance by evaluating parameters of oxidative stress-related mucosal damage in the same tissue samples. The extent of apoptosis, peroxynitrite-mediated protein nitration (3-NT), and lipid peroxidation were assessed in relation to the expression of nitric oxide synthase (NOS) and the superoxide-producing enzyme xanthine oxidase (XO). In addition, bi- and multi-variate regression analyses were performed to associate these parameters with the levels of the antioxidants assessed previously. Apoptotic cell death was visualized by TUNEL staining in luminal epithelium of normal controls, and in IBD additionally in the inflammatory infiltrate and in deeper parts of the crypts, but its frequency was unrelated to the severity of inflammation. In Crohn's disease (CD), epithelial apoptosis levels were strongly associated with the expression of XO, implying a role for this enzyme in the regulation of epithelial cell homeostasis, although its levels were unaffected by intestinal inflammation and were comparable to those in normal control mucosa. 3-NT immunoreactivity was substantially increased in luminal crypt cells, neutrophils, and mononuclear cells in the inflamed mucosa of ulcerative colitis (UC) patients. The inflamed IBD luminal epithelium, but not the inflammatory cells, also contained increased amounts of NOS. The immunoreactivity of both 3-NT and NOS was significantly higher in UC than in CD. Unexpectedly, the increased 3-NT expression in UC was associated with neutrophilic myeloperoxidase and not with NOS, which suggests that 3-NT is formed in areas with a dense neutrophilic infiltrate via a peroxynitrite-independent oxidation pathway. Lipid peroxidation, as estimated by the malondialdehyde (MDA) concentration, was elevated in both the inflamed CD and the inflamed UC mucosa, and was identified in the luminal epithelium using a histochemical technique. In CD, lipid peroxidation was independently associated with the concentration of metallothionein and with Mn-superoxide dismutase activity, suggesting the involvement of hydroxyl radicals and superoxide anions. In UC, however, the amount of MDA was associated with epithelial catalase expression and neutrophilic myeloperoxidase activity, suggesting a hydrogen peroxide- and/or hypochlorous acid-mediated mechanism. The present study underlines the importance of oxidative stress in the pathogenesis of IBD and provides clues regarding the (anti)oxidants involved which indicate that this process evolves through diverging pathways in CD and UC.

Adult↗
PubMed2001

Distribution and activation of eosinophils in inflammatory bowel disease using an improved immunohistochemical technique.

Eosinophils are a recognized feature of inflammatory bowel disease (IBD), but their tissue distribution and functional importance in Crohn's disease (CD) and ulcerative colitis (UC) remain obscure. This study describes an improved immunohistochemical protocol to identify eosinophils in full thickness bowel wall specimens of IBD (n=40) and their in situ relationships with the chemoattractants eotaxin and RANTES. Eosinophils were identified using immunohistochemistry with a combination of monoclonal antibodies (EG1+EG2+MBP), an ultrasensitive technique superior to other methodologies, and their tissue distributions were related to those for eotaxin, RANTES, mast cells and neutrophils. Increased numbers of eosinophils (up to 400 cells/mm(2)) were observed in active, fulminant inflammation in both CD and UC, this being related to the severity of inflammation and not the diagnosis of the two disorders. The chemoattractants eotaxin (CCL11) and RANTES (CCL5) were upregulated in IBD tissues showing eosinophilia. Neutrophils and mast cells were commonly associated with eosinophil accumulations. Eosinophil numbers and their in situ activation are increased in active rather than chronic IBD. The observations strongly suggest a pivotal role for the eosinophil and its potent mediators in many pathophysiological symptoms of CD and UC, where it represents the major proportion of all granulocytic cells in active inflammatory bowel disease.

Adult↗
PubMed2004

Thiopurine drug adverse effects in a population of New Zealand patients with inflammatory bowel disease.

PURPOSE: The thiopurine drugs, azathioprine and 6-mercaptopurine are effective in the treatment of inflammatory bowel disease (IBD). However, their use is limited by serious adverse effects that can lead to cessation of therapy. The incidence of these adverse effects has been reported to be approximately 9% but in Christchurch it was felt that the incidence was higher. METHODS: We searched our letter database to identify all patients with IBD who had received a thiopurine drug between 1996 and 2002. The case notes were then reviewed to identify those patients who had suffered an adverse effect that required cessation of the drug. RESULTS: From a total of 216 patients with IBD taking a thiopurine drug, 56 (25.9%) had an adverse reaction requiring cessation of the drug. Adverse effects included allergic-type (25%), liver test abnormalities (34%), nausea/vomiting (6%), bone marrow suppression (7%), pancreatitis (7%) and other (9%). Males were significantly more likely than females to have an allergic-type reaction (p = 0.003). All adverse effects resolved with cessation of the drug, with a median of 7 days to resolution. Of the patients with liver test abnormalities on azathioprine, most were able to tolerate 6-mercaptopurine, however challenge with 6-mercaptopurine was not successful for most other patients. CONCLUSIONS: In Canterbury, New Zealand, patients with IBD have a high rate of therapy-limiting adverse effects to thiopurine drugs. There is a significant gender bias for allergic-type adverse effects. Mechanisms for both these observations are not clear.

Adolescent↗
PubMed2000

Endothelial cell autoantibodies are a marker of disease susceptibility in inflammatory bowel disease but apparently not linked to persistent measles virus infection.

Intestinal vasculitis caused by persistent measles virus infection of intestinal endothelial cells was described in Crohn's disease. Furthermore, endothelial cell autoantibodies have been demonstrated in inflammatory bowel disease (IBD). Autoantibodies against intestinal endothelial cells were visualized by indirect immunofluorescence in patients with IBD, in their healthy first-degree relatives, in patients with infectious enterocolitis, and in healthy, unrelated controls. In intestinal tissue specimens of 22 antibody-positive IBD patients a search for the measles virus genome was performed. Endothelial cell autoantibodies were significantly more frequent in patients with IBD, in both groups of first-degree relatives, and in patients with infectious enterocolitis than in the healthy controls (P = 0.0002 or less). The measles virus genome was found in none of the intestinal biopsies. Endothelial cell autoantibodies are not a genetic but rather an epigenetic (infectious) marker of disease susceptibility. The expression of these autoantibodies is unlikely to be triggered by a persistent measles virus infection.

Adolescent↗
PubMed2006

Cytokines, NF-kappaB, microenvironment, intestinal inflammation and cancer.

Inflammation and cancer have been viewed as closely linked for many years. This link is not merely a loose association but causative. In colorectal cancer (CRC), chronic inflammation as observed in inflammatory bowel (IBD) disease is a key predisposing factor and IBD-associated CRC comprises five percent of all CRCs. Although the molecular mechanisms linking IBD with CRC are not well understood, recent results obtained in preclinical models point to the transcription factor NF-kappaB as a central player. On the one hand, NF-kappaB regulates the expression of various cytokines and modulates the inflammatory processes in IBD. On the other, NF-kappaB stimulates the proliferation of tumor cells and enhances their survival through the regulation of anti-apoptotic genes. Furthermore, it has been clearly established that most carcinogens and tumor promoters activate NF-kappaB, while chemopreventive agents generally suppress this transcription factor. Actually, several lines of evidence suggest that activation of NF-kappaB may cause cancer. These include the finding that NF-kappaB genes can be oncogenes, and that this transcription factor controls apoptosis, cell-cycle progression and proliferation, and possibly also cell differentiation.

Apoptosis↗
PubMed2006

Multiparameter analysis of immunogenetic mechanisms in clinical diagnosis and management of inflammatory bowel disease.

The integrity of the intestinal mucosa depends on a functional coordination of the epithelium, lumenal microorganisms, and the local immune system. The mammalian immune system is superbly organized for innate and adaptive recognition of microbial antigens, a defensive capacity that must be balanced against the tissue damage produced by immune activity to preserve normal intestinal function. Inflammatory bowel disease (IBD) is generally thought to reflect an impairment in this balance, due to a combination of host genetic traits that shift the balance of immune and epithelial function to commensal microbiota, and perhaps the composition or activity of certain microbial elements as well. There has been much progress defining the fundamental disorders of these host traits, immunologic processes, and microbial targets in inflammatory bowel disease. Other fields of clinical and geologic microbiology are teaching us about the dynamic interaction of commensal bacteria with their host environment. These lines of investigation have revealed not only important insights about inflammatory bowel disease (IBD) pathogenesis, but also defined technologies and tools useful for its diagnosis and clinical management. This review focuses on these advances at the translational interface. We will first consider the innate anti-microbial response, centering on the utility of NOD2 genotyping for predicting disease susceptibility, prognosis, and therapeutic response profile. We will then turn to the adaptive anti-microbial response, focusing on the application of antibodies to fungal and bacterial species and products for Crohn's disease (CD) diagnosis and prognosis, and immunogenetics of T cell immunosuppression management. Finally, we will describe autoimmune mechanisms in IBD, with particular attention to autoantibodies in IBD diagnosis and infliximab responsiveness. We will conclude with the concept of multiparameter analysis of patients, to refine patient characterization and stratification in diagnosis and clinical management.

Animals↗
PubMed1996

Effect of interferon therapy on bile duct inflammation in hepatitis C.

Inflammation of the bile ducts was studied in liver biopsies from patients with chronic hepatitis C to determine whether the frequency of inflamed bile ducts changes with therapy and correlates with other histological variables and expression of class I and II MHC antigens on ductal epithelium. Twenty patients treated at UMMC between 1991 and 1994 underwent needle biopsies of the liver before and after therapy with interferon alpha 2B (IFN). A complete response to therapy was defined as a return to normal serum alanine aminotransferase levels occurring and persisting during therapy. The number of inflamed bile ducts/total ducts (%IBDs), presence of piecemeal necrosis and lymphoid aggregates, and grade of inflammation were assessed in each high-power field in all areas with bile ducts. The frequencies of these variables were compared in cirrhotics and non-cirrhotics and in patients with complete or incomplete responses to IFN. Frozen sections of biopsies from 5 patients were immunostained using antibodies to HLA-DR and B-2 microglobulin, and positive staining was noted on bile ducts. Before therapy, the %IBD was slightly greater in patients with cirrhosis. After IFN, both %IBD and serum alkaline phosphatase levels decreased in non-cirrhotics who responded to IFN. The change in frequency of IBD with IFN paralleled the changes in the other histological features. No correlation was noted between bile duct inflammation and expression of class I and II antigens. The conclusion is that inflammation of the bile ducts occurs frequently in chronic hepatitis C, correlates with other features of inflammation in the triads, and decreases in response to IFN therapy.

Adult↗
PubMed1989

Prothrombotic abnormalities in inflammatory bowel disease.

Inflammatory bowel disease (IBD) is known to be associated with a thrombotic tendency, which is often attributed to thrombocytosis, elevated fibrinogen, or decreased antithrombin III. We prospectively studied eight patients with IBD, seven of whom had little or no disease activity, to determine if they had any laboratory abnormality known to be associated with an increased risk of thrombosis. Abnormalities in fibrinolysis were noted in five patients: four with high plasminogen activator inhibitor levels and one with poor release of tissue plasminogen activator following venous occlusion. Circulating immune complexes were present in the sera of five patients. Fibrinogen was mildly elevated in one patient, and two patients had mild thrombocytosis. Decreased levels of antithrombin III, protein C, or protein S were not observed. There appears to be a high incidence of abnormalities in fibrinolysis in inactive IBD, which may contribute to the high frequency of thrombosis seen in IBD. The presence of circulating immune complexes may contribute to vascular injury and thrombosis.

Adult↗
PubMed1989

Health-related quality of life in inflammatory bowel disease. Functional status and patient worries and concerns.

The assessment of health-related quality of life may be an adjunct to understanding the chronic illness experience and its effects on health outcomes. In this study, we evaluated health-related quality of life of 150 patients with inflammatory bowel disease (63 ulcerative colitis, 87 Crohn's disease). We used a standardized measure, the Sickness Impact Profile, and a questionnaire we developed that elicits and prioritizes the disease-related worries and concerns of patients with IBD. Our preliminary data indicate that: (1) IBD patients experience moderate functional impairment more in the social and psychological than in the physical dimensions; (2) Crohn's disease patients report psychosocial dysfunction to a greater degree than ulcerative colitis patients; (3) IBD patients report greatest concerns about having surgery, degree of energy, and body image issues such as having an ostomy bag; and (4) functional status and patient concerns correlate better with other measures of health status and previous health care utilization than the physician's rating of disease activity. We believe that questionnaires measuring health-related quality of life (HRQOL) can be used in research and patient care to extend the clinical assessment of patients with IBD. Further work is needed to determine the role of HRQOL relative to disease activity and other physician-based assessments in predicting health outcomes.

Adult↗
PubMed1991

Inflammatory mediators in chronic inflammatory bowel diseases.

Crohn's disease and ulcerative colitis are chronic inflammatory bowel diseases (IBD) of unknown etiology. They are characterized by an activation of intestinal mononuclear cells. Cytokines play a crucial role in the regulation of the functions of these cells. An increased synthesis of the cytokines interleukin-1 (IL-1), interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF alpha), which are primarily synthesized by activated monocytes/macrophages has been described in patients with IBD. The synthesis of interleukin-2 (IL-2) and of interferon gamma (IFN gamma), which are produced by lymphocytes, on the other hand, has been found to be decreased. The published data are, however, not quite consistent. In patients with IBD there is not only a stimulation of the local cytokine production in the gut. The blood levels and the synthesis of the cytokines IL-1, IL-6 and TNF alpha by peripheral blood mononuclear cells are also increased, in particular in patients with Crohn's disease. Drugs, which are commonly used for the treatment of IBD impair the synthesis of these cytokines in monocytes/macrophages.

Colitis, Ulcerative↗
PubMed1991

Clinical relevance of oxygen radicals in inflammatory bowel disease--facts and fashion.

Oxygen radicals particularly superoxide and hydroxyl radicals are very reactive species believed to be involved in cell and tissue damage in a variety of diseases including inflammatory bowel disease (IBD). Today there are four major arguments for such a role in IBD: Infiltration of the inflamed intestinal mucosa with myeloperoxidase containing activated neutrophils able to produce superoxide, hydroxyl and hypochlorite, increased chemoluminescence response of peripheral and mucosal phagocytic cells to various stimuli, decreased inflammation following specific scavenger treatment in animal models of colitis and defined radical scavenger and inhibitory properties of drugs, especially aminosalicylates used in the therapy of IBD. In the absence of a specific therapy, radical scavenging and/or inhibition may be an adjunctive modality in IBD.

Aminosalicylic Acids↗
PubMed1987

The immediate and long-term effects of postoperative total parenteral nutrition on body composition.

The short and long-term effects of postoperative total parenteral nutrition (TPN) on body composition were studied in a randomised series of patients undergoing major colorectal surgery. Ninety-two patients (colorectal cancer: 50, ulcerative colitis or Crohn's disease: 42) were grouped according to diagnosis and clinical inflammatory activity. TPN was given for 9.7 +/- 1.1 days. The complication rate was not changed by the TPN. Nitrogen balance was studied during the first week. Body weight, total body potassium, triceps skinfold, serum albumin and body water were measured before and at intervals up to 24 weeks after the operation. Cumulative nitrogen balance in control patients at 7 days after surgery was -47.3 g. Patients given TPN balanced nitrogen intake and output (cancer patients and patients with quiescent inflammatory bowel disease, IBD) or were in positive balance (patients with active IBD). Weight loss at 1 week after surgery was less in TPN patients compared to controls and this difference remained statistically significant up to 6 months after termination of the nutritional treatment. A similar, although not statistically significant, difference was noted in total body potassium and triceps skinfold. Patients with active IBD regained pre-operative body composition earlier than cancer patients and patients with quiescent IBD. It is concluded that TPN after major colorectal surgery reduces postoperative weight loss and that this effect lasts after termination of the nutritional treatment. In the absence of increased body potassium and increased body water, we conclude that the long-term effect of TPN on body weight is most likely due to preservation of fat.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1992

Comparison between double-contrast barium enema and colonoscopy to investigate lower gastrointestinal bleeding.

A retrospective study was performed to compare the diagnostic accuracy of high-quality double-contrast barium enema (DCBE) against gold standard colonoscopy in 288 patients with suspected lower gastrointestinal bleeding who went through both examinations. Colonoscopy detected the potential cause of bleeding in 99 patients (100%); in order of frequency: polyps greater than or equal to 1 cm (N = 47; 48%), carcinoma (N = 21; 21%), inflammatory bowel disease (IBD) (N = 15; 15%), solitary ulcers (N = 6; 6%), other types of colitis (N = 5; 5%), angiodysplasia (N = 3; 3%), and stenosis (N = 2; 2%). DCBE diagnosed 88 cases (89%) and missed 11 consisting of IBD (N = 4), angiodysplasia (N = 3), solitary ulcers (N = 3), and polyps (N = 1). The overall sensitivity and specificity of DCBE was 0.89 and 0.97, respectively. The sensitivity for carcinoma, polyps, and IBD was 1.00, 0.98, and 0.73, respectively. We conclude that DCBE is very effective to diagnose carcinoma and polyps greater than or equal to 1 cm, the most frequent causes of bleeding, but less effective to diagnose IBD and other nonfrequent causes. If a high-quality DCBE does not reveal the cause of bleeding, the contribution of a following colonoscopy will be to diagnose causes of bleeding other than carcinoma and polyps less than 1 cm and to offer therapeutic possibilities.

Adolescent↗
PubMed1991

Inflammatory mediators in cotton-top tamarins (CTT) with acute and chronic colitis.

Spontaneous colitis in CTT's presents cytological characteristics similar to chronic ulcerative colitis in humans, e.g. inflammatory cell infiltrate and crypt abscesses. To better characterize CTT colitis as a potential model for human inflammatory bowel disease (IBD), inflammatory mediators identified in colonic tissue of human IBD patients and/or experimental colitis models were assayed. Inflammatory mediator changes in plasma and colon from tamarins with acute (n = 10) and chronic (n = 10) colitis (by mucosal biopsy) were assayed by RIAs. Similar inflammatory mediators were found in the CTT's with acute colitis. In the plasma, PAF and PGE2 levels were lower in acute colitis CTT's, no LTB4 was detected, and histamine levels were not different from chronic colitic animals. In the colon, myeloperoxidase and interleukin-1 beta were significantly higher in acute colitis, PGE2 and LTB4 were higher but not significantly, and PAF was not different from chronic CTT's. These data suggest that a combination of events are occurring in the pathogenesis of tamarin colitis that involves some of the same mediators that are found in the human disease and in other experimental models. The importance of these findings to human IBD remains for further investigation; however, the spontaneous primate model offers an exciting approximation of the disease development and merits further investigation for understanding the pathogenesis of human IBD as well as to aid in development of targeted therapeutics.

Acute Disease↗
PubMed1992

Distribution and quantification of somatostatin in inflammatory disease.

To study the possible alteration of mucosal-submucosal somatostatin-containing cells in inflammatory bowel diseases (IBD), the total numbers of somatostatin-containing endocrine cells (SCEC) and submucosal ganglion cells (SGC) were counted in Crohn's disease (CD) and ulcerative colitis (UC). Tissue specimens from 25 CD and 25 UC patients were fixed in Hollande's fixative immediately after resection and were investigated by immunohistochemical staining. A single specimen was collected from 25 colorectal cancer patients, the control group. There was a significant difference in the number of SCEC between the tissues taken from the proximal colon (ascending and transverse colon) and the distal colon (descending and sigmoid colon). The distal colon tended to contain more somatostatin-immunoreactive cells than did the proximal colon. In IBD, SCEC were decreased in number compared with the controls. This decrease was related to the degree of inflammation in CD; the higher the grade of inflammation, the lower the number of SCEC. The number of SGC was decreased in IBD: however, a significant decrease was noticed only in CD. The anatomic origin and the degree of inflammation did not affect the number of SGC. In the present study, the decrease of somatostatin-containing cells was noticed in both CD and UC, but there was no significant difference between CD and UC. Therefore, it was assumed that this decrease was secondary to inflammation. However, the decrease of somatostatin, which works as an inhibitory peptide for inflammation, might have some role in the pathogenesis of IBD.

Analysis of Variance↗
PubMed1995

Subtotal colectomy with Hartmann's pouch for inflammatory bowel disease.

PURPOSE: Fulminant or unremitting colitis caused by inflammatory bowel disease (IBD) is effectively managed by subtotal colectomy (STC) and standard ileostomy. However, controversy exists regarding the optimal management of the retained rectum. We reviewed our experience with intraperitoneal Hartmann's closure to determine whether this is an acceptable way to handle the rectal remnant. METHODS: We retrospectively reviewed hospital and office records of 114 consecutive patients with IBD colitis who underwent STC with Hartmann's pouch since 1988. Patient demographic data, operative details, and postoperative complications were recorded. In patients who underwent subsequent surgery, technical difficulty and complications related to rectal dissection were documented. RESULTS: There were three instances of pelvic sepsis secondary to leakage from the Hartmann's pouch, an overall incidence of 2.6 percent. Two of these patients required exploratory surgery. The third patient responded dramatically to antibiotics and transanal catheter decompression of the Hartmann's pouch. Subsequent to this experience, patients undergoing STC and Hartmann's closure for IBD colitis had transanal catheter drainage of the rectal remnant as a routine part of their postoperative care. There were no instances of leakage among the 41 patients who underwent rectal decompression. There were two reports (3 percent) of technical difficulty in locating or mobilizing the intraperitoneal rectal remnant at 60 subsequent surgical procedures. CONCLUSION: Intraperitoneal Hartmann's closure of the rectum is the preferred management in patients with intractable IBD colitis requiring STC.

Adolescent↗
PubMed1996

Increased leukocyte adhesiveness/aggregation in patients with inflammatory bowel disease during remission. Further evidence for subclinical inflammation.

PURPOSE: We have used a novel leukocyte adhesiveness/aggregation test (LAAT) to show that many patients with inflammatory bowel disease (IBD) in clinical remission have a subclinical low grade inflammation. METHODS: Included in the study are 500 controls, 96 patients with IBD in remission, and 106 patients in relapse. RESULTS: The percent of aggregated white blood cells detected in the peripheral blood was 5.9 +/- 3.9, 9.1 +/- 5.9, and 18.8 +/- 9.4, respectively. The difference between each group and any other was significant at P < 0.0001. Similar results were obtained when other acute phase reactants like the erythrocyte sedimentation rate, white blood cell count, differential count, and C-reactive protein level were examined. However, in a linear regression analysis, LAAT was the only significant (P < 0.0006) variable that could classify correctly each subject to the appropriate category of control and IBD in remission or relapse. CONCLUSIONS: Identification of patients with IBD in clinical remission who have ongoing inflammation may be of clinical-therapeutic relevance. The LAAT is a simple, rapid, and convenient test. The present study indicates that it is also very sensitive.

Adolescent↗
PubMed1994

Characterization of circulating interleukin-1 receptor antagonist expression in children with inflammatory bowel disease.

The cytokines IL-1 beta and IL-6 appear to be important in the pathogenesis of inflammatory bowel disease (IBD). Recently, a naturally occurring interleukin-1 receptor antagonist, designated IL-1ra, which inhibits IL-1 beta activity in vitro and in vivo has been described. The purpose of the present study was to assess the circulating levels and relative relationships of IL-1ra, IL-1 beta, and IL-6 in children with IBD of varying severity. Serum/plasma samples were obtained from 32 children with ulcerative colitis, 45 with Crohn's disease, and 24 control patients. Cytokine assays were performed by enzyme-linked immunoassay. IL-1ra levels were significantly elevated in children with ulcerative colitis or Crohn's disease of moderate/severe activity compared to patients with inactive/mild IBD or control subjects (P < 0.001). IL-1 beta was only detectable in the circulation of two subjects with severe colitis (one ulcerative colitis, one Crohn's disease), and both had extremely elevated IL-1ra levels. IL-1ra levels were significantly related to IL-6 levels for patients with IBD (P < 0.00001). Our results suggest that circulating IL-1ra appears in increasing concentrations in children with mounting degrees of disease severity as determined by clinical scoring methods as well as by the level of IL-6. Future work will need to address the clinical and prognostic value of measuring circulating IL-1ra in individuals with inflammatory bowel disease.

Adolescent↗