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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↗
PubMed2003

Association between K469E allele of intercellular adhesion molecule 1 gene and inflammatory bowel disease in a Japanese population.

BACKGROUND AND AIMS: The genetic contribution to inflammatory bowel disease (IBD) is under investigation. Recent evidence indicates a significant linkage between a locus on chromosome 19p13 and IBD. We investigated the association between an intercellular adhesion molecule 1 gene (ICAM-1) polymorphism located on chromosome 19p13 and IBD in a Japanese population. METHODS: We compared 207 Japanese patients who had IBD (79 with Crohn's disease (CD); 128 with ulcerative colitis (UC)) with 103 unrelated Japanese controls. We determined R241G and K469E polymorphisms of the ICAM-1 gene using polymerase chain reaction (PCR) techniques. RESULTS: Both frequency and carriage rate of the K469 allele were significantly higher in IBD patients than in controls (allelic frequency, p(c)=0.0026; carriage rate, p(c)=0.0034; odds ratio 2.59; 95% confidence interval 1.42-4.68). Furthermore, the frequency of the K469 allele was significantly increased in both CD and UC. Subgroup analysis demonstrated that both K469 allelic frequency and K469 carriage rate were significantly higher in patients with the small bowel and colon type of CD and entire colitis compared with healthy controls. CONCLUSIONS: We identified an overall association between IBD and ICAM-1 K469 in a Japanese population. Further studies of this chromosome region are required to elucidate the gene responsible for IBD.

Adolescent↗
PubMed2001

Inflammatory bowel disease is associated with changes of enterocytic junctions.

Changes of the intestinal mucosal barrier are considered to play a role in the pathogenesis of inflammatory bowel disease (IBD). Our experiments were designed to identify dysregulation of epithelial junctional molecules in the IBD intestinum and to address whether altered expression of these molecules is a primary event in IBD or a phenomenon secondary to the inflammatory process. Noninflamed and inactively and actively inflamed mucosal tissues from patients with ulcerative colitis or Crohn's disease as well as tissues from control subjects were analyzed for the expression of junctional molecules by different methods. Marked downregulation of junctional proteins and their respective mRNAs was observed in actively inflamed IBD tissues. In IBD tissues with inactive inflammation, only a few junctional molecules such as E-cadherin and alpha-catenin were affected, whereas expression of desmosomal or tight junction-associated proteins appeared almost unchanged. In noninflamed IBD tissues, junctional protein expression was not different from that seen in normal control subjects. In IBD, downregulation of junctional molecule expression is apparently associated with the inflammatory process and does not likely represent a primary phenomenon.

Adult↗
PubMed2002

Self-reported awareness and use of the International Classification of Diseases coding of inflammatory bowel disease services by Ontario physicians.

RATIONALE: Population and health services research can be performed by linkage analysis of administrative data. However, the robustness of study results is determined by the accuracy of the diagnostic coding. OBJECTIVES: To estimate the awareness, use and accuracy of the International Classification of Diseases, Ninth Revision (ICD-9) coding by physicians providing services for patients with Crohn's disease (CD) and ulcerative colitis (UC). METHODS: All Ontario gastroenterologists and a 10% random sample of internists, pediatricians, pediatric or general surgeons, and family physicians were surveyed by postal questionnaire to estimate the frequency and 95% CI of using codes 555 or 556 when billing for CD- and UC-related services, respectively. c2 tests were used for between-group comparisons. RESULTS: Of the physicians who were surveyed, 67.7% (416 of 614) responded; 258 of 391 (66%) who were still practising in Ontario saw patients with inflammatory bowel disease (IBD), and 54% had more than 10 IBD patients; 86.5% (95% CI 82.4% to 90.6%) were familiar with ICD-9 codes, and 91.4% (95% CI 88.1% to 95.6%) used the codes 555 (CD) or 556 (UC) for billing. Rates of ICD-9 use did not differ by sex but were used more frequently by those graduating after 1981 (P<0.02). Gastroenterologists used ICD-9 IBD codes 555 or 556 significantly more often than all other physicians (P=0.001). Most (more than 75%) Ontario physicians used ICD-9 IBD codes always or frequently when billing for IBD-related services. Few (10%) used these codes to bill for non-IBD-related problems. CONCLUSIONS: These data suggest that there is acceptable use and accuracy of ICD-9 diagnostic coding for CD and UC services - comparable with results from studies of other diseases. Administrative data may thus be used to undertake epidemiological studies in IBD in Ontario.

Awareness↗
PubMed2006

[99mTc-HMPAO-leukocyte-labeled scintigraphy in the detection and follow-up of inflammatory bowel disease].

To assess the clinical value of 99mTc-HMPAO-leukocyte-labeled scintigraphy (LLS) in the detection and follow-up of inflammatory bowel disease (IBD) in the pediatric population, we retrospectively reviewed 33 patients (15 boys; mean age 10.7 +/- 2.2 years) with suspected IBD. A total of 58 examinations were performed: 29 for screening purposes, 23 for follow-up and 6 to detect relapses. LLS was compared with clinical symptoms (PCDAI index), biologic markers of inflammation, barium contrast radiology (BCR; n = 22), sonography (n = 22), colonoscopy (n = 16), and biopsy (n = 13). The final diagnosis was Crohn's disease in 12, ulcerative colitis in 4, and no IBD in 17. In the 17 patients without IBD, LLS was always negative. Among the 16 patients with IBD, LLS showed concordant results with BCR in 7/10 patients, with sonography in 6/11, with colonoscopy in 9/12 and with biopsy in 8/9. The severity of LLS increased with the PCDAI index (p < 0.001), with a positive correlation between the scintigraphic activity index/PCDAI r = 0.76. An increase in the PCDAI index with the severity of LLS (p < 0.001) was also observed in the follow-up, and a weak correlation (r = 0.50) between erythrocyte sedimentation rate/scintigraphic activity index was obtained. In 5 patients with normal biologic markers, LLS detected inflammation. All 6 patients with relapses were symptomatic; 5 had inflammation on LLS and 5 had abnormal biologic markers. In conclusion, LLS can be a useful screening tool in the detection of IBD in children to assess the grade of inflammation and extension of IBD. This technique can detect the presence of inflammation during follow-up and should be performed when relapses are suspected.

Adolescent↗
PubMedDate not supplied

Facilitating adjustment to inflammatory bowel disease: a model of psychosocial intervention in non-psychiatric patients.

BACKGROUND: There is no consensus about the most appropriate psychosocial interventions for people with inflammatory bowel disease (IBD) or the most appropriate criteria by which to select which patients might benefit from the available interventions. Nonetheless the perception that stress and other subjective factors contribute to suffering in IBD is persistent and professionals are often called upon to offer appropriate support. A model of normal psychosocial adjustment to IBD and the interventions which can improve difficulties with adjustment will facilitate rational therapeutic intervention and needed research in this area. METHODS: A model of normal adjustment to IBD is developed from a synthesis of the empirical literature and clinical experience in a tertiary care medical/surgical IBD centre and is used to identify potential points of psychosocial intervention. RESULTS: Normal adjustment to IBD can be understood as a process involving the interaction of a triad of adaptive challenges: illness uncertainty, loss and change, and suffering. Each of these challenges requires different criteria of psychosocial assessment and may lead to different interventions. CONCLUSIONS: Although the interventions available for improving adjustment to IBD have not been exhaustively investigated, the existing data support the value of further study. The model of psychosocial adjustment presented here provides a synthesis of the existing data and a starting point for further research.

Adaptation, Psychological↗
PubMedDate not supplied

Animal models of inflammatory bowel disease: an overview.

Inflammatory bowel disease (IBD) research has been performed in human in vitro studies and in in vivo studies using appropriate animal models. Such animal models allow both the examination of inflammatory processes (both early and late events) as well as the evaluation of new therapeutic modalities. Since the first description of the immune complex colitis in rabbits in 1961, overall 63 models have been described, most of which within the last decade. These IBD animal models can be divided into 5 different categories: (1) antigen-induced colitis and colitis induced by microbials; (2) other inducible forms of colitis (chemical, immunological, and physical); (3) genetic colitis models (transgenic and knock-out models); (4) adoptive transfer models, and (5) spontaneous colitis models. In spite of the high overall number of models, none of them is the 'perfect' model and therefore numerous aspects need to be considered when choosing one model for a particular study. Importantly, most clinical aspects (e.g. extraintestinal manifestations or fistula) have recently been described in one or the other model allowing further studies with relevance for almost all aspects of IBD. So far, IBD animal models have taught us important lessons, e.g. the requirement of T-helper cells in most models, the need of a particular genetic background, and the role of the flora in the initiation of IBD. It is expected that our understanding of IBD will further increase in a number of additional areas using animal models, e.g. exploring the role of the innate immune system in IBD.

Animals↗
PubMed2003

Rationale for probiotic and antibiotic treatment strategies in inflammatory bowel diseases.

Inflammatory bowel diseases (IBD), commonly referred to as Crohn's disease and ulcerative colitis are chronic aggressive disorders which share many similarities concerning pathomechanism and clinical course, but have very distinct features. Both entities are mainly located in areas with high bacterial concentrations, such as the terminal ileum and cecum in Crohn's disease and the rectum in ulcerative colitis. In recent years, overwhelming evidence accumulated, supporting the hypothesis that IBD are characterized by a genetically determined, overly aggressive immune response towards ubiquitous luminal antigens, especially commensal bacteria and their products. Trials in both human IBD and experimental colitis have demonstrated that broad-spectrum antibiotics may influence the course of ulcerative colitis and Crohn's disease and antibiotics with narrow activity against the anaerobic fraction of the flora can prevent relapse in Crohn's disease after surgically induced remission. Since relevant antibiotic strategies can be associated with some side effects, the ongoing research recently focused on alternative methods to modify the intestinal flora in patients with IBD. Clinical observations including few controlled trials, basic research, and animal studies have suggested a potential role for probiotic bacteria within the treatment regimens for IBD. However, the mode of action of these organisms is still largely unclear and in vitro studies are inconclusive. This review summarizes recent in vitro and in vivo data regarding the role of the intestinal microflora in the pathogenesis of chronic intestinal inflammation and possible therapeutic mechanisms of probiotic bacteria relevant to IBD. Furthermore, we will review clinical trials examining the efficacy of antibiotic and probiotic treatment strategies in IBD.

Anti-Bacterial Agents↗
PubMed2005

The insulin-like growth factor system and markers of inflammation in adult patients with inflammatory bowel disease.

BACKGROUND AND OBJECTIVES: Catabolism and growth impairment are well-known complications of inflammatory bowel disease (IBD). Recent studies have demonstrated significant changes in the IGF system in IBD patients. The aim of the present study was to investigate correlations between the IGF system and markers of inflammation in IBD. METHODS: A cross-sectional study comprising 99 IBD patients (Crohn's disease (CD, n = 50) and ulcerative colitis (UC, n = 49)). Correlations between markers of inflammation and IGF-I, IGF-II and IGFBP-3 were examined in CD and UC patients in remission and relapse. The patients were clinically scored using Crohn's Disease Activity Index (CDAI) for CD patients and Activity Index (AI) for UC patients. RESULTS: In the UC group we found correlations between IGF-I and CRP (r(s) = Spearman's rho) (r(s) = -0.40, p < 0.01) and albumin (r(s) = 0.46, p < 0.001), IGFBP-3 and albumin (r(s) = 0.36, p < 0.01) and AI score (r(s) = -0.31, p < 0.05). IGF-II correlated with CRP (r(s) = -0.42, p < 0.01), IL-6 (r(s) = -0.65, p < 0.001), albumin (r(s) = 0.41, p < 0.01), AI score (r(s) = -0.30, p < 0.05) and orosomucoid (r(s) = -0.47, p < 0.001). In the CD group we found correlations between IGF-I and CRP (r(s) = -0.40, p < 0.05), and albumin (r(s) = -0.46, p < 0.01), IGFBP-3 and albumin (r = 0.36, p < 0.01). IGF-II correlated with IL-6 (r(s) = -0.65, p < 0.001), albumin (r(s) = 0.41, p < 0.01), CDAI score (r(s) = -0.30, p < 0.05) and orosomucoid (r(s) = -0.47, p < 0.001). CONCLUSIONS: IGF-I, IGF-II and IGFBP-3 are correlated to albumin and IGF-I and IGF-II are correlated to CRP in IBD patients. Further, IGF-II is correlated to IL-6 in IBD patients. This may suggest a correlation between inflammation and the IGF system with involvement in muscle and bone catabolism in IBD.

Adult↗
PubMed2006

Antidepressants and inflammatory bowel disease: a systematic review.

BACKGROUND: A number of studies have suggested a link between the patient's psyche and the course of inflammatory bowel disease (IBD). Although pharmacotherapy with antidepressants has not been widely explored, some investigators have proposed that treating psychological co-morbidities with antidepressants may help to control disease activity. To date a systematic analysis of the available studies assessing the efficacy of antidepressants for the control of somatic symptoms in IBD patients has not been performed. METHODS: We searched electronic databases, without any language restriction. All relevant papers issued after 1990 were examined. RESULTS: 12 relevant publications were identified. All of them referred to non-randomised studies. Antidepressants reported in these publications included paroxetine, bupropion, amitriptyline, phenelzine, and mirtazapine. In 10 articles, paroxetine, bupropion, and phenelzine were suggested to be effective for treating both psychological and somatic symptoms in patients suffering from IBD. Amitriptyline was found ineffective for treating somatic symptoms of IBD. Mirtazapine was not recommended for IBD patients. CONCLUSION: Although most of reviewed papers suggest a beneficial effect of treatment with antidepressants in patients with IBD, due to the lack of reliable data, it is impossible to judge the efficacy of antidepressants in IBD. Properly designed trials are justified and needed based upon the available uncontrolled data.

Journal Article↗
PubMed2004

Expression of CD45RB functionally distinguishes intestinal T lymphocytes in inflammatory bowel disease.

The importance of CD45RB expression on T cells was already shown in mice where CD45RB(high) expression determines pathogenic potential. In this study, we analyzed the expression of CD45RA, CD45RB, and CD45RO on CD4(+) T lymphocytes in the intestinal mucosa and in the circulation of patients with inflammatory bowel disease (IBD). In addition, we studied the cytokine profile of these cells. In the circulation, virtually all CD4(+)CD45RB(high) T cells expressed the naive marker CD45RA, and circulating CD4(+)CD45RB(low) cells expressed the memory marker CD45RO in IBD patients and a control patient population. In contrast, the intestinal CD4(+) CD45RB(high) T cells are in normal controls for 90% CD45RO(+). However, in IBD, 27.7% [Crohn's disease (CD)] and 49% [ulcerative colitis (UC)] of the intestinal CD4(+) CD45RB(high) T cells are CD45RA(+). This special CD4CD45RA(+) T cell in IBD can be found in the lamina propria as well as in lymphoid follicles (confocal laser-scanning microscopy). The CD4(+)CD45RB(high) T lymphocytes produce significantly less interleukin (IL)-10 and IL-4 and produce more tumor necrosis factor alpha than CD45RB(low) T lymphocytes in control patients. CD4(+)CD45RB(low) T cells from IBD patients produced less IL-10 than CD4(+)CD45RB(low) T lymphocytes of controls, and interferon-gamma production by both T lymphocyte subsets was decreased in IBD. These data indicate that CD and UC are characterized by an influx of CD4(+)CD45RB(high) T lymphocytes. These CD4(+)CD45RB(high) T lymphocytes seem to be important in the pathogenesis of IBD, as they produce more proinflammatory cytokines and less anti-inflammatory cytokines compared with CD4(+)CD45RB(low) T lymphocytes.

Adult↗
PubMed1996

Influence of inflammatory bowel disease on the ability of patients to tolerate systemic fluorouracil-based chemotherapy.

PURPOSE: To evaluate the safety of administering fluorouracil (5FU)-based chemotherapy to cancer patients with inflammatory bowel disease (IBD). PATIENTS AND METHODS: We retrospectively reviewed all patients entered into the Memorial Sloan-Kettering Cancer Center clinical data base from 1985 through 1995 who had a diagnosis of IBD, had a gastrointestinal malignancy, and were treated with systemic 5FU-based chemotherapy. A total of 19 patient charts were identified and reviewed. RESULTS: Fifty-three percent of patients reviewed experienced severe (grade III/IV) diarrhea on treatment. Sixty percent of patients with a history of active IBD and 40% of patients with a history of inactive IBD experienced severe diarrhea on treatment. The incidence of severe diarrhea did not appear to be substantially influenced by age, schedule of 5FU administration, concurrent radiation, or type of IBD. CONCLUSION: While there does appear to be an increased risk of diarrhea exacerbation in IBD patients treated with 5FU, a substantial number of patients tolerate chemotherapy without increased difficulty. The degree of IBD activity or other clinical parameters can not be used to predict accurately the likelihood of toxicity.

Adult↗
PubMed2003

A crucial role for the vitamin D receptor in experimental inflammatory bowel diseases.

The active form of vitamin D (1,25D3) suppressed the development of animal models of human autoimmune diseases including experimental inflammatory bowel disease (IBD). The vitamin D receptor (VDR) is required for all known biologic effects of vitamin D. Here we show that VDR deficiency (knockout, KO) resulted in severe inflammation of the gastrointestinal tract in two different experimental models of IBD. In the CD45RB transfer model of IBD, CD4+/CD45RBhigh T cells from VDR KO mice induced more severe colitis than wild-type CD4+/CD45RBhigh T cells. The second model of IBD used was the spontaneous colitis that develops in IL-10 KO mice. VDR/IL-10 double KO mice developed accelerated IBD and 100% mortality by 8 wk of age. At 8 wk of age, all of the VDR and IL-10 single KO mice were healthy. Rectal bleeding was observed in every VDR/IL-10 KO mouse. Splenocytes from the VDR/IL-10 double KO mice cells transferred IBD symptoms. The severe IBD in VDR/IL-10 double KO mice is a result of the immune system and not a result of altered calcium homeostasis, or gastrointestinal tract function. The data establishes an essential role for VDR signaling in the regulation of inflammation in the gastrointestinal tract.

Animals↗
PubMed2006

Pharmacokinetics of 7-carboxymethyloxy-3',4',5-trimethoxy flavone (DA-6034), a derivative of flavonoid, in mouse and rat models of chemically-induced inflammatory bowel disease.

The pharmacokinetics (including distribution in the gastrointestinal tract) of 7-carboxymethyloxy-3',4',5-trimethoxy flavone (DA-6034) has been investigated in several mouse and rat models of chemically-induced inflammatory bowel disease (IBD). In the female ICR mouse model, IBD was induced by dextran sulfate and the mice administered 30 mg kg(-1) DA-6034 intravenously or orally. In the male SJL mouse model of IBD induced by oxazolone, 30 mg kg(-1) DA-6034 was administered orally. In the male Sprague-Dawley rat model of IBD induced by trinitrobenzene sulfonic acid (TNBS), 10 mg kg(-1) DA-6034 was administered intravenously and orally. After intravenous administration, the total area under the plasma concentration-time curve from time zero to the last measured time, t, in plasma (AUC(0-t)) values were comparable between control and dextran sulfate-induced IBD mice, and between control and TNBS-induced rats. This suggested that the disposition of DA-6034 was not affected considerably by dextran sulfate in mice and TNBS in rats. However, after oral administration in mice and rats with IBD, the AUC(0-t) values were greater compared with the respective controls. This could have been due to an increase (slow) in the gastrointestinal transit time (in IBD mice and rats, the percentages of the oral dose recovered from the rinsing fluid of the small intestine and large intestine as unchanged drug were greater and smaller, respectively), and an increase in intestinal permeability.

Administration, Oral↗
PubMed1995

Neurologic aspects of inflammatory bowel disease.

UNLABELLED: To determine the frequency, spectrum, and clinical features of neurologic disorders associated with ulcerative colitis (UC) and Crohn's disease (CD). BACKGROUND: Extraintestinal manifestations of inflammatory bowel disease (IBD) are well documented, but the association of IBD with neurologic involvement is rare and often controversial. METHODS: Tertiary care center ambulatory and hospital services data bank retrospective computerized search with subsequent file review. PATIENTS: From among 638 IBD patients diagnosed from 1981 to 1991, we identified 10 CD patients and nine UC patients with neurologic involvement unrelated to a defined systemic or iatrogenic cause. Neurologic disorders diagnosed 15 or more years before the intestinal symptomatology were excluded. RESULTS: Three percent of IBD patients had neurologic involvement. In 14 of 19 (74%), it started within a mean of 5.7 years (range, 0.7 to 12 years) after the diagnosis of bowel disease, and in two of 19 (10%) it occurred at the time of IBD exacerbation. During the course of IBD, 10 of 19 patients (53%) exhibited other extraintestinal manifestations. Peripheral nerve disorders were observed in six UC patients. Myelopathy (5 patients), myopathy (3), and myasthenia gravis (1) were diagnosed in eight CD patients and one UC patient. Cerebrovascular disorders occurred in two UC and two CD patients. CONCLUSIONS: Neurologic disorders associated with IBD are more common than appreciated and follow a different pattern of involvement in UC and CD. A prospective study is required to define the nature of this association.

Adult↗
PubMed2002

The effect of nonmalignant systemic disease on tolerance to radiation therapy.

PURPOSE: Some patients with nonmalignant systemic diseases, like collagen vascular disease (CVD), hypertension, diabetes mellitus, and inflammatory bowel disease (IBD), tolerate radiation therapy poorly. Although the mechanisms of each of these disease processes are different, they share a common microvessel pathology that is potentially exacerbated by radiotherapy. This article reviews and evaluates available data examining the effects of these benign disease processes on radiation tolerance. METHODS: We conducted a thorough review of the Anglo-American medical literature from 1960 to 2001 on the effects of radiotherapy on CVD, hypertension, diabetes mellitus, and IBD. RESULTS: Fifteen studies were identified that examined the effects of radiation therapy for cancer in patients with CVDs. Thirteen of 15 studies documented greater occurrences of acute and late toxicities (range 7%-100%). Higher rates of complications were noted especially for nonrheumatoid arthritis CVDs. Nine studies evaluated the effects of hypertension and diabetes on radiation tolerance. All nine studies documented higher rates of late toxicities than in a "control" group (range 34%-100%). When patients had both diabetes and hypertension, the risk of late toxicities was even higher. Six studies examined radiation tolerance of patients with IBD irradiated to the abdomen and pelvis. Five of these six studies showed greater occurrences of acute and late toxicities for patients with IBD, even with precautionary measures like reduced fraction size and volume and patient immobilization (13%-29%). CONCLUSION: The majority of published studies documented lower radiation tolerance for patients who have CVD, diabetes mellitus, hypertension, and IBD. This may reflect a publication bias, as the majority of these studies are retrospective with small numbers of patients and use different scoring scales for complications. These factors may contribute to an overestimation of true radiation-induced morbidity. Although the paucity of data makes precise estimates difficult, a subset of patients, in particular, those with active CVD, IBD, or a combination of uncontrolled hypertension with type I diabetes, is likely to be at higher risk. Future prospective trials need to document these disease entities when reporting treatment-related complications and also must monitor toxicities associated with quiescent versus active IBD and CVD, type I versus type II diabetes, and levels of hypertension (controlled versus uncontrolled) matched for radiation-specific treatment sites, field size, fractionation, and total dose.

Collagen Diseases↗
PubMedDate not supplied

Chronic idiopathic inflammatory bowel diseases of the horse.

A review of reported cases of inflammatory bowel diseases (IBDs) of horses for which no etiology was identified included cases of granulomatous enteritis (GE), multisystemic eosinophilic epitheliotropic disease (MEED), lymphocytic-plasmacytic enterocolitis (LPE), and idiopathic eosinophilic enterocolitis (EC). The terms EC and MEED were both used to describe a disease in horses characterized by infiltration of intestine and extraintestinal tissues with eosinophils. We use EC to describe IBD characterized by only intestinal infiltration by eosinophils. Horses with GE, MEED, or LPE are usually examined because of weight loss and depression, but horses with EC are usually examined because of signs of abdominal pain. Typically, horses with IBD have low concentrations of serumal proteins, especially albumin, and fail to adequately absorb glucose or xylose. Antemortem diagnosis of IBD can only be made by histologic examination of affected intestine. In some cases, antemortem diagnosis is made from histologic examination of rectal mucosa obtained by biopsy. Suspected causes of IBD in the horse include abnormal immune response to bacterial, viral, parasitic, or dietary antigens. Most horses with IBD do not survive, but horses with EC are more likely than those with LPE, MEED, or GE to respond to treatment. Successful treatments of horses with IBD include resection of grossly affected intestine and administration of corticosteroids.

Animals↗
PubMedDate not supplied

Cerebrospinal fluid and plasma concentration of soluble intercellular adhesion molecule 1, vascular cell adhesion molecule 1 and endothelial leukocyte adhesion molecule in patients with acute ischemic brain disease.

BACKGROUND: Leukocyte migration into the ischemic area is a complex process, controlled by adhesion molecules (AM) in leukocytes and endothelium, by migratory capacity of leukocytes and the presence of hemotaxic agents in the tissue. In this research it was supposed that in the blood and cerebrospinal fluid (CSF) of patients in the acute phase of ischemic brain disease (IBD) there were relevant changes in the concentration of soluble AM (sICAM-1, sVCAM-1 and sE-selectin), that could have been the indicators of the intensity of damaging processes in central nervous system (CNS). METHODS: The study included 45 IBD patients, 15 with transient ischemic attack (TIA), 15 with reversible ischemic attack (RIA), and 15 with brain infarction (BI), of both sexes, mean age 66 +/- 7. Control group consisted of 15 patients with radicular lesions of discal origin, subjected to diagnostic radiculography, without the signs of interruption in the passage of CSF. Changes of selected biochemical parameters were determined in all patients in frame 72 hours since the occurrence of an ischemic episode. Concentrations of soluble AM were determined in plasma and CSF by ELISA. Total number of leukocytes (TNL) in peripheral blood was determined by hematological analyzer. RESULTS: The results showed that during the first 72 hrs of IBD significant increases occurred in TNL and that the increase was progressive compared to the severeness of the disease. Significant increase of soluble AM concentration was shown in plasma of IBD patients. The increase was highest in BI, somewhat lower in RIA and the lowest in TIA patients compared to the control. In CSF concentrations of sICAM-1, sVCAM-1 and sE-selectin demonstrated similar increasing trend as in plasma. CONCLUSION: TNL, as well as the soluble AM concentrations in plasma and CSF, were increased during the acute IBD phase and progressive in relation to the severeness of the disease, so that they might have been the indicators of CNS inflammatory reaction intensity. Furthermore, the results indicated their role in IBD pathogenesis and offered the possibility of researching the application of antagonists and/or activity modulators of some of them in IBD therapy.

Acute Disease↗