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At least 19 recordsLinked to original sources

PubMed1988

The role of indium-111 white blood cells in inflammatory bowel disease.

Inflammatory bowel disease in patients may be difficult to diagnose because of the complex problems associated with this disease. Radionuclides are able to provide a rapid and effective method of imaging the bowel in patients with active inflammatory bowel disease. In the past, clinical work-ups have included barium x-ray studies and endoscopy. Scarring and fistula formation have made it difficult to determine between the active disease and abscesses that may occur. Gallium-67 (67Ga) has been very useful in imaging patients with inflammatory bowel disease, but the multiple-day imaging procedure has been a limitation for the clinicians when achieving a diagnosis. Recent results with Indium-111 (111In)--labeled WBCs have provided excellent correlation between clinical symptoms and colonoscopy findings in patients with inflammatory bowel disease. This technique has also allowed the differentiation between reoccurring inflammatory bowel disease and abscesses that accompany the disease within a 24-hour time period. The use of intravenous (IV) glucagon has increased the clarity of the images in the small bowel. Technetium 99m (99mTc) diethylenetriaminepentaacetic acid (DTPA) has been used in patients with inflammatory bowel disease demonstrating promising results. Investigators feel labelling 99mTc with WBCs will be improved, therefore yielding a greater efficiency, which will have a major impact on imaging patients with inflammatory bowel disease. Imaging patients with inflammatory bowel disease using radionuclides has yielded promising results. This is a significant advancement over barium radiography and endoscopy exams.

Humans↗

PubMed1989

Interleukin-1 in the pathogenesis of and protection from inflammatory bowel disease.

Inflammatory bowel disease affects millions of people, some with fatal consequences. Little is known about the factors which contribute to its pathogenesis particularly regarding cytokine production and action. In this paper we summarize our recent findings using the rabbit model for immune complex-generated experimental colitis, a model which is similar to ulcerative colitis in humans. Recombinant human IL-1 was perfused through rabbit colons and we observed elevated levels of PGE2, TxB2 and 6-keto-PGF1 alpha, the stable metabolite of PGI2. Using radioimmunoassays specific for rabbit IL-1 alpha and IL-1 beta, we induced immune complex colitis and measured the generation of these IL-1's in various tissues. Markedly elevated levels of IL-1 were detected only in inflamed tissues. The levels of IL-1 correlated with the degree of inflammation as judged by a blinded assessment of pathological changes. Similar to other disease models in which small doses of the agonist can afford protection or result in a state of "desensitization" when administered prior to the onset of the disease, we accordingly injected rabbits with a single, small (300 ng/kg) dose of IL-1 and observed a significant reduction in the inflammatory index and necrosis of immune complex colitis. However, unlike other models of IL-1-induced protection, in this model cyclooxygenase products were required since we prevented the IL-1-induced protection with a single dose of ibuprofen given at the same time as the IL-1. This correlated with the reduction in IL-1-induced PGE2. These results demonstrate that IL-1 plays a key role in the pathogenesis of inflammatory bowel disease in the rabbit and that the protection afforded by a low dose of IL-1 24 hours before the onset of the colitis requires IL-1-induced cyclooxygenase products.

Animals↗

PubMed1991

Activation of monocytes during inflammatory bowel disease.

Inflammatory bowel diseases lead to a systemic acute-phase response. Monocyte activation plays a central role during systemic acute-phase response via secretion of inflammatory cytokines. We determined the activation of peripheral-blood monocytes in patients with inflammatory bowel diseases by measuring their interleukin-6 (IL-6) secretion. Blood was obtained from patients with active Crohn's disease before treatment [mean Crohn's disease activity index (CDAI) = 332 +/- 34] and from patients after treatment with prednisolone (mean CDAI index = 139 +/- 20). The mean serum IL-6 levels measured by a hybridoma growth assay (B9) were 23 +/- 4 U/ml before therapy and fell to 16 +/- 3 U/ml after treatment with prednisolone. Healthy persons and patients with inactive Crohn's disease usually had serum IL-6 levels below the detection limit of 4 U/ml. An ex vivo whole-blood system was used to measure IL-6 secretion by peripheral-blood monocytes with and without stimulation. Spontaneous IL-6 secretion in this system was about 9 U/ml in patients with Crohn's disease and below the detection limit of 4 U/ml in healthy controls. Moderate stimulation of blood cells [100 pg/ml lipopolysaccharide (LPS)] from patients with active Crohn's disease before and after treatment led to mean IL-6 concentrations of 1,160 +/- 514 and 131 +/- 54 U/ml, respectively. Maximal stimulation of peripheral blood before and after therapy by LPS (100 ng/ml) led to mean IL-6 concentrations of 5,570 +/- 1,660 and 6,220 +/- 1,630 U/ml, respectively. Thus, administration of glucocorticoids led to a rapid down-regulation of IL-6 synthesis by peripheral-blood monocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute-Phase Proteins↗

PubMed1989

Medical management of inflammatory bowel disease.

Inflammatory bowel disease is a serious ailment that afflicts nearly one million people in the U.S. alone. The medical management of this disorder currently includes salicylates, corticosteroids, immunosuppressive therapy, and symptomatic treatment with antidiarrheal agents, although several promising new drugs have been developed. The epidemiology, etiology, pathogenesis, and medical management of the disease are discussed in this article.

Humans↗

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↗

PubMed1991

Evaluation of a psychological treatment for inflammatory bowel disease.

Inflammatory bowel disease (IBD) encompasses two related gastrointestinal-tract diseases, ulcerative colitis (UC) and Crohn's Disease (CD). This study, a randomized controlled trial, compared the effectiveness of a multi-component behavioral treatment package (n = 11), which included IBD education, progressive muscle relaxation, thermal biofeedback, and training in use of cognitive coping strategies, to the effectiveness of symptom-monitoring (n = 10) as a control condition; 8 controls subsequently completed treatment. At posttreatment, the treatment group showed mean reductions on 5 symptoms, while the symptom monitoring controls showed mean reductions on all 8 symptoms. On a measure of Total Symptomatic change, the controls showed more improvement than the treated group; the treated controls at posttreatment, showed increases on all 8 symptoms. However, treated subjects perceived themselves as coping better with IBD, as feeling less IBD-related stress, and as experiencing less depression and anxiety. It is hypothesized that inherent differences may have existed between CD and UC subjects which could have led to the differences seen in treatment responses.

Adaptation, Psychological↗

PubMed1986

Circulating interferon-like activity in inflammatory bowel disease.

Inflammatory bowel diseases (IBD) has been characterized as having an autoimmune background. We studied the presence of immune interferon in the sera of a small number of patients with IBD. Antiviral activity was detectable in the sera of our patients with well-controlled IBD but it was mainly weak-positive (50% inhibition of virus CPE in a dilution of 1:10 per 0.2 ml of serum). The antiviral activity varied according to the sensitivity of the cell line used. The human amnion cells Wish (81%) and the human embryonic Intestine-407 (73%) were more sensitive.

Antiviral Agents↗

PubMed1977

Emotional factors in inflammatory bowel disease.

Inflammatory bowel diseases are not caused by emotional conflicts, but emotional factors influence both the pathogenesis and the course of the illness. Establishing a trusting physician-patient relationship is important in helping the patient to (1) avoid denial of illness or chronic illness behavior, (2) understand symptoms and diagnostic and treatment procedures, and (3) cope with loss of a key person or the threat of lessened self-control.

Adolescent↗

PubMed1988

Association and linkage studies of immunoglobulin heavy chain allotypes in inflammatory bowel disease.

Inflammatory bowel disease is a familial disorder of unknown etiology, characterized by a variety of immunological abnormalities for which there are no proven genetic markers. Studies of immunoglobulin heavy chain and light chain allotypes were undertaken in 89 patients with Crohn's disease and in 18 families with ulcerative colitis or Crohn's disease in at least two first-degree relatives, to search for association and/or linkage between a postulated disease susceptibility locus and an immunoglobulin allotype locus. No evidence of association or linkage with a specific immunoglobulin allotype was found.

Adolescent↗

PubMed1986

Cutaneous changes associated with inflammatory bowel disease.

Inflammatory bowel disease often begins during adolescence, but may affect younger children. Associated skin lesions are not uncommon. Occasionally, cutaneous alterations may precede the onset of signs or symptoms of the gastrointestinal disorder. Erythema nodosum and pyoderma gangrenosum are the most common associated specific skin changes, but numerous others may be found. Although the skin condition often responds to treatment of the bowel, it may require additional therapy.

Child↗

PubMed1991

[Epidemiology and genetics of inflammatory bowel diseases].

Inflammatory bowel diseases (IBDs) have been reported throughout the world, but their frequency is highest in Northern Europe and the USA. The mean incidence of ulcerative colitis (UC) is 6/10(5) inhabitants, and that of Crohn's disease (CD) is 4/10(5) inhabitants. IBDs occur in young adults, especially Crohn's disease which reaches a peak of incidence between the ages of 20 and 30 years. Among possible factors influencing their incidence, only tobacco smoking has been shown to facilitate the acute episodes and relapses of CD and to diminish those of UC. The frequency of familial IBDs, which mainly affects first degree relatives, varies from 6.1 to 35.8%. A genetic component is present and probably more important for CD than for UC, although no genetic marker has yet been identified.

Adult↗

PubMed1988

Autoreactivity and altered immune responses in inflammatory bowel disease.

Inflammatory bowel disease (IBD) is a poorly understood condition that is associated with a wide variety of immunologic alterations. Because its pathogenesis is unknown, these immunologic alterations have been investigated with an eye toward unraveling the complex mechanism of injury in the bowels of these patients. There are several lines of evidence suggesting that IBD is related to immunologic events. The histopathology of active disease resembles the Arthus reaction, whereas the presence of antiepithelial cell antibodies is reminiscent of Goodpasture's disease. Antibodies against many microorganisms and autoantibodies to mucosal components are commonly found in these patients. Further, there is a marked increase in plasma cells in the lamina propria of patients with active IBD. It is important to keep these findings in perspective. No studies to date have been able to determine whether the features are entirely primary events, that is, related to the initial damage to the intestinal mucosa. If the surface mucosa is injured by an as-yet-unidentified agent, the immunologic findings in IBD may be secondary events. Nonetheless, the similarity in histopathology of the experimental immunologic models of IBD to the human disease encourages investigators to pursue the etiology of this complex disease.

Animals↗

PubMed1978

Ankylosing spondylitis and inflammatory bowel disease. I. Prevalence of inflammatory bowel disease in patients suffering from ankylosing spondylitis.

To establish the prevalence of inflammatory bowel disease in ankylosing spondylitis (AS), 79 AS patients underwent detailed medical screening, including sigmoidoscopic and roentgenological examination, 48 had gastrointestinal symptoms and the others did not. In 3 patients a diagnosis of Crohn's disease was made which was previously established. In all other patients inflammatory bowel disease could be excluded. The prevalence of inflammatory bowel disease in this series of patients with AS therefore was 3.8%.

Enteritis↗

PubMed1990

Histamine release from gut mast cells from patients with inflammatory bowel diseases.

Inflammatory mediators from intestinal mast cells may serve as initiators of acute and delayed inflammation. Mast cell histamine release was measured in 19 patients with inflammatory bowel diseases using gut mast cells from enzymatically dispersed endoscopic forceps biopsy specimens of macroscopically inflamed and normal tissue. Mast cells and corresponding basophils were challenged with anti-IgE, anti-IgG, subclass anti-IgG4, and formyl-methionyl-leucyl-phenylalanine (FMLP) and results were compared with those from nine patient control subjects. The mast cell count in patients with ulcerative colitis was increased compared with that in control subjects and patients with Crohn's disease, and the mast cell count obtained from inflamed tissue was greater than that of normal tissue. The study also shows the heterogeneity of the responsiveness of the histamine releasing cells to various secretagogues. Thus, mast cells released 0.4 (0.0-2.0) (median (range)) ng histamine per sample at anti-IgE challenge, and basophils were also anti-IgE responsive. In contrast, mast cells did not respond to FMLP but the corresponding basophils did. Gut mast cells released 0.3 (0.0-1.0) (median (range)) ng histamine per sample at anti-IgG4 challenge; however, the corresponding basophils did not respond to anti-IgG4. In addition, the anti-IgG4 mediated histamine release was primarily confined to patients with inflammatory bowel disease. This study substantiates previous histopathological findings that mast cells may play a functional role in the inflammatory process of inflammatory bowel diseases and provides evidence for a possible role of subclass IgG4 as a reaginic antibody.

Adolescent↗

PubMed1992

Technetium-99m hexamethyl propylene amine oxine leucocytes in the assessment of disease activity in inflammatory bowel disease.

The inflammatory activity in 108 bowel segments of 40 patients with suspected or known inflammatory bowel disease was assessed macroscopically by endoscopy, histology and technetium-99m hexamethyl propylene amine oxine (99mTc-HMPAO) leucocytes using a numerical grading system (scores 0-3). A 4-h series of scintigrams showed a significant correlation with both histological and macroscopical assessment of disease activity (rho = 0.850, P less than 0.001 and rho = 0.773, P less than 0.001, respectively). Sensitivity, specificity and accuracy of scintigraphy in detecting active inflammatory segments were 85%, 92% and 89%, respectively. A normal scintigram did not completely exclude mild inflammatory activity, especially in the rectosigmoid area. 99mTc-HMPAO leucocytes offer an accurate and non-invasive alternative for the assessment of disease activity in ulcerative colitis and Crohn's disease.

Adult↗

PubMedDate not supplied

Scavenging effect of 5-aminosalicylic acid on neutrophil-derived oxidants. Possible contribution to the mechanism of action in inflammatory bowel disease.

Inflammatory phagocytic leukocytes produce superoxide and hydrogen peroxide and secrete myeloperoxidase (MPO) into the extracellular medium. MPO catalyzes the oxidation of Cl- by H2O2 to yield chlorinated oxidants (e.g. HOCl and NH2Cl), which have been shown to induce pathologic changes in mucosal function. We examined the ability of 5-aminosalicylic acid (5-ASA), a drug used to treat inflammatory bowel disease (IBD), to inhibit oxidation of L-cysteine by NH2Cl, HOCl and H2O2. NH2Cl and HOCl were especially strong oxidants against L-cysteine. 5-ASA prevented L-cysteine oxidation by NH2Cl and HOCl; an interaction associated with the formation of characteristic absorption spectra due to the oxidation of 5-ASA was observed. NH2Cl and HOCl evoked characteristic increases in short-circuit current (Isc), indicative of net electrolyte transport, when added to the serosal side of stripped rat colon mounted in Ussing chambers. Premixing of NH2Cl with 5-ASA 10 min before addition to the tissue markedly reduced the secretory response to NH2Cl. In contrast, 5-ASA immediately reduced the response to HOCl. The reduction in the functional response to NH2Cl and HOCl by 5-ASA may contribute to its mechanism of action in the treatment of the symptoms of IBD.

Aminosalicylic Acids↗

PubMed1991

Inflammatory bowel disease: primary health care management of ulcerative colitis and Crohn's disease.

Inflammatory bowel disease encompasses both ulcerative colitis and Crohn's disease, two conditions so alike clinically that they are frequently indistinguishable from one another. Inflammatory bowel disease occurs at a rate of approximately five per 100,000 people. It tends to cluster in families and is seen four to five times more often in Jewish Caucasians than in other Caucasians. The etiology is unknown. Increasing attention is being paid to autoimmune factors, genetic factors and food allergies, and the notion that inflammatory bowel disease has its roots in a psychological disorder continues to pale for want of empirically sound evidence. Disease pattern is one of remission and exacerbation. The aim of therapy is to maintain an optimal lifestyle in remission through an individually tailored protocol of medications. Sulfasalazine remains the medication of choice; corticosteroids have short-term utility in exacerbation; and immunosuppressants, though controversial, are thought to have some steroid-sparing benefits during acute flare-ups. Indications for surgery vary, depending on whether or not a clear differential diagnosis has been made between ulcerative colitis and Crohn's disease. There is no cure for inflammatory bowel disease except for total colectomy in clearly diagnosed ulcerative colitis. Current research endeavors seek a cause or causes for inflammatory bowel disease, but the literature does not solidly support any one possibility above other rival etiologies.

Colitis, Ulcerative↗

PubMed1986

Chronic inflammatory bowel disease.

Chronic inflammatory bowel disease in children includes Crohn's disease, ulcerative colitis, indeterminate colitis and Behçet's colitis. The reported incidence of Crohn's disease has increased in the last 30 years. The clinical features of Crohn's disease are most commonly abdominal pain and poor weight gain, whereas those of ulcerative colitis are diarrhoea and rectal bleeding. Treatment is with drugs (sulphasalazine, local or systemic steroids, azathioprine), elemental diet or surgery. The prognosis of chronic inflammatory bowel disease in childhood is good.

Child↗