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At least 1,135 records · Page 63Linked to original sources
PubMed1996

Enhanced expression and production of monocyte chemoattractant protein-1 in inflammatory bowel disease mucosa.

Peripheral blood monocytes are recruited to the inflamed mucosa of inflammatory bowel disease but the specific chemotactic signals responsible for their attraction are not known. Monocyte chemoattractant protein-1 (MCP-1) is a chemokine with potent monocyte attracting and activating properties and the aim of this study was to examine its expression and production in inflammatory bowel disease. In situ hybridization demonstrated mRNA for MCP-1 in macrophages, some of which had been recently recruited from the circulation as demonstrated by their co-expression of the monocyte marker CD 14, as well as in smooth muscle and endothelial cells in inflamed mucosa. Immunohistochemical studies showed a corresponding distribution of MCP-1 protein production by macrophages, smooth muscle, and endothelial cells. By contrast minimal MCP-1 mRNA expression and protein were found in histologically normal mucosa. Macrophages isolated from surgically resected inflammatory bowel disease colons and examined by Northern analysis expressed MCP-1 mRNA significantly more frequently (15/24 vs. 0/19, P< 0.0001) than macrophages from histologically normal mucosa from colon cancer resections. Blood monocytes stimulated by lipopolysaccharide and treated with hydrocortisone, 5-aminosalicylic acid, or cyclosporin A showed reduced MCP-1 expression and production in the presence of these agents. This study demonstrates increased expression of MCP-1 mRNA and protein and cells of origin of MCP-1 in inflamed intestinal mucosa. Together with the demonstrated influence of therapeutic agents on monocyte MCP-1 production the findings suggest a role for MCP-1 in monocyte attraction to the mucosal lesion of inflammatory bowel disease.

Adolescent↗
PubMed1996

A longitudinal study of alexithymia and psychological distress in inflammatory bowel disease.

A group of 104 patients with inflammatory bowel disease (IBD) was followed longitudinally for 6 months. While anxiety and depression scores were influenced over time by changes in the level of disease activity, there was no significant change in alexithymia scores. The findings support the contention that alexithymia is a stable personality characteristic in some IBD patients, in contrast to anxiety and depression which are state phenomena influenced by the level of disease activity.

Adult↗
PubMed2003

Extraintestinal complications of inflammatory bowel disease.

Recent studies of extraintestinal manifestations (EIMs) of inflammatory bowel disease (IBD) have demonstrated the importance of genetic predisposition in the etiology of musculoskeletal and cutaneous manifestations. In addition, small studies have shown infliximab to be effective in treating troublesome EIMs, particularly in pyoderma gangrenosum. Other trials have examined the safety of cyclooxygenase-2-specific nonsteroidal inflammatory drugs in IBD. Further work has been done on osteoporosis in IBD, and the American Gastroenterological Association has published a technical review and management guidelines for osteoporosis in a range of gastrointestinal disorders. However, despite further publications, debate remains concerning whether IBD patients with osteoporosis have a significant increase in fracture risk, and whether the bone loss is related to the disease or to its treatment.

Bone Diseases, Metabolic↗
PubMed2006

[Inflammatory bowel disease and lung].

Ulcerative colitis and Crohn's disease are associated with a variety of systemic manifestations. Pulmonary disease has been described much less frequently than other organ systems, yet more than 400 cases have been reported. Lung and gastrointestinal system are originated from primitive gut and they have same pathogenetic changes in these patients. Major patterns of pulmonary disease associated with inflammatory bowel disease (IBD) are pleuritis, airway disease, interstitial lung disease, necrobiotic nodules, pulmonary eosinophilia, thromboembolic disease, vasculitis, granulomatous lung disease, etc. Colectomy may aggravate respiratory symptoms. Drug induced disease must be kept in mind in patients taking sulfasalazine, mesalamine, methotrexate, and anti-TNF-alpha. Latent pulmonary abnormalities are evident either at pulmonary function tests or induced sputum or bronchoalveolar lavage, have been also reported in patients with inflammatory bowel disease in the absence of clinical evidence of airway disease. The treatment of IBD related respiratory involvement depends on the specific pattern of involvement, if left untreated, especially in airway disease, puts the patient at risk of developing irreversible destruction of the air passage. A high degree of suspicion is necessary to detect early the respiratory disease in association with any form of bowel disease.

Colitis, Ulcerative↗
PubMed1996

Renal tubular damage: an extraintestinal manifestation of chronic inflammatory bowel disease.

OBJECTIVE: To investigate whether treatment of inflammatory bowel disease (IBD) with 5-aminosalicylate or sulphasalazine in IBD may induce renal tubular damage. DESIGN AND METHODS: The urinary enzymes beta-N-acetyl-D-glucosaminidase ( beta-NAG), dipeptidylpeptidase 4 (DPP4) and alanine aminopeptidase (AAP) were measured as markers of renal tubular damage in 104 consecutive patients with Crohn's disease and in 43 consecutive patients with ulcerative colitis (all with normal serum creatinine values). Control values were gained from 65 healthy persons. RESULTS: The normal values (mean +/- SD) for the urinary enzymes investigated (U/g creatinine in the urine) were: DPP4 4.5 +/- 2.2, beta-NAG 1.6 +/- 1.4, AAP 11.4 +/- 6.5. In 28% of the patients with ulcerative colitis elevated beta-NAG levels of more than the mean + 2 x SD were measured. This pathological enzymuria was nearly exclusively found in patients with active disease (CAI > 6): DPP4 15.6 +/- 25.3, beta-NAG 8.3 +/- 10.1, AAP 24.7 +/- 50.1 (all three enzymes were significantly elevated). The highest values were measured in patients with active ulcerative colitis before start of therapy. Nineteen per cent of the patients with Crohn's disease had elevated beta-NAG levels of more than the mean + 2 x SD. There was no significant difference in enzymuria between patients with active (CDAI > 150) and patients with inactive Crohn's disease (CDAI < or = 150). DPP4 and AAP were normal in both groups. A correlation between the enzymuria and the cumulative doses of 5-aminosalicylic acid, sulphasalazine or prednisolone could not be found. The courses of enzymuria in three patients who presented with the first severe manifestation of IBD are described. They were treated with either corticosteroids and 5-aminosalicylic acid or corticosteroids and sulphasalazine. Before onset of therapy, very high urine enzyme values were measured. They almost normalized in the course of successful medical therapy despite increasing cumulative doses of 5-aminosalicylic acid or sulphasalazine. CONCLUSIONS: Renal tubular damage can frequently be observed in IBD. Our results suggest that this is an extraintestinal manifestation of the disease and not a toxic side-effect of anti-inflammatory therapy using 5-aminosalicylic acid or sulphasalazine.

Adolescent↗
PubMed1976

Association of inflammatory bowel disease and large vascular lesions.

A case of inflammatory bowel disease with associated multiple large vessel vascular lesions similar to that seen in Takayasu's arteritis is described in a 15-year-old female. It is suggested that this type of vascular lesion may represent another rare systemic manifestation of inflammatory bowel disease.

Adolescent↗
PubMed2004

Azathioprine dose escalation in inflammatory bowel disease.

BACKGROUND: Forty per cent of patients with inflammatory bowel disease fail to respond to standard dose azathioprine (2 mg/kg/day). AIMS: To evaluate the efficacy and safety of increasing the azathioprine dose according to a fixed schedule and guided by clinical response and adverse effects. METHODS: We reviewed the records of all patients with inflammatory bowel disease treated by a single clinician over 6 years, unresponsive to at least 3 months treatment with standard dose azathioprine, and whose dose was subsequently increased. RESULTS: Forty patients (27 male; 24 Crohn's, 16 ulcerative colitis) with chronic active disease or recurrent flares despite standard dose azathioprine for a median 8 months (range 3-114) increased their dose from a median 2.02 (1.61-3.19) mg/kg/day to 2.72 (2.37-3.99) mg/kg/day in one to four increments of 0.5 mg/kg/day, and were followed over a median 6 (0.5-54) months. Eleven of the 40 patients (seven Crohn's, four ulcerative colitis) responded or had reduced frequency of flare-ups at the end of follow-up, while 17 of the 40 patients had no benefit. Response was more likely for maximum doses < or =2.5 mg/kg/day (six of 11 patients) than for doses >2.5 mg/kg/day (five of 29 patients) (P = 0.042). Twelve patients (11 of whom received maximum doses >2.5 mg/kg/day) were unable to maintain an increased azathioprine dose because of leukopenia in eight, nausea in three, and raised liver enzymes in one (all transient and reversible). CONCLUSIONS: Increasing the azathioprine dose up to 2.5 mg/kg/day appears beneficial in patients who have not responded to 2 mg/kg/day. Further increase above 2.5 mg/kg/day is less likely to be efficacious, and is associated with a substantial risk of adverse reactions.

Adult↗
PubMed1986

Assessing nutritional state in inflammatory bowel disease.

Nutrient depletion is a common complication of inflammatory bowel disease, and some of the consequences can be severe. Although it is often easy to recognise the most severely undernourished subjects, those with lesser degrees of malnutrition may prove more difficult to detect. Measurements of many nutritional variables will be abnormal in patients with inflammatory bowel disease, especially in those with Crohn's disease, but are not always relevant to the clinical management of patients. Anthropometric means of assessment, in particular, measurement of mid arm circumference, can act as a simple, reproducible method of detecting those most at risk of appreciable undernutrition.

Anthropometry↗
PubMed2006

Anemia in inflammatory bowel disease.

Anemia is a frequent extraenteric complication of inflammatory bowel disease (IBD, Crohn's disease and ulcerative colitis). A systematic review of the literature shows that the overall prevalence of anemia ranges from 8.8% to 73.7% but differs whether in a setting of Crohn's disease or ulcerative colitis. A disabling complication of IBD, anemia worsens the patient's general condition and quality of life, and increases hospitalization rates. Different factors, including vitamin B12 and folic acid deficiency, bone marrow suppression secondary to drug therapy, autoimmune hemolytic anemia and the coexistence of myelodysplastic syndromes are involved in the pathogenesis of anemia in IBD. The main types of anemia in IBD are iron deficiency anemia and anemia accompanying chronic diseases. Correct diagnostic definition of anemia is a fundamental step in guiding the choice of therapeutic options, since the co-presence of different pathogenetic factors may sometimes require a more complex treatment plan. A review of anemia in IBD, its pathogenetic features, epidemiology, diagnosis and therapy based on evidence from recent studies is the focus of this article.

Anemia↗
PubMed1992

New therapeutic agents in the treatment of inflammatory bowel disease.

Despite intense investigation, the etiology of inflammatory bowel disease (IBD) remains unknown. Recent studies with new therapeutic agents provide insight into the pathogenesis of IBD through analysis of the clinical response to pharmacologic agents whose mechanism of action is understood. Until new agents are established, IBD will be treated with conventional drugs directed toward modifying the inflammatory responses responsible for gastrointestinal mucosal damage. Sulfasalazine, mesalamine (5-aminosalicylic acid), and corticosteroids will continue to be the mainstay of therapy for the foreseeable future. Antibiotics such as metronidazole and immunosuppressants such as 6-mercaptopurine and methotrexate are useful in Crohn's disease and ulcerative colitis in selected cases. Many new exciting agents are being investigated and show encouraging results in the treatment of IBD. This article reviews the agents used in IBD with an emphasis on new therapeutic agents.

Adjuvants, Immunologic↗
PubMed2005

Inflammatory bowel diseases: clinical update of practical guidelines.

Idiopathic inflammatory bowel disease (IBD) includes a collection of disorders of the gastrointestinal tract of unknown aetiology, characterized by intestinal inflammation and a chronic relapsing course associated with local and systemic complications. Traditionally, IBD comprises two prototype entities, ulcerative colitis (UC) and Crohn's disease (CD) and an intermediate variant of these diseases, indeterminate colitis which shows overlapping features of the two major forms. Over the last few years, considerable progress has been made in our knowledge of the pathogenesis of IBD, which is complex and derives from genetic, environmental and immunological interactions. The aetiology remains unclear, but it is well established that the lesions and symptoms are associated with over-production of pro-inflammatory cytokines. In this paper we briefly review the pathophysiology and the new therapeutic approaches to IBD, since from these, new achievement depends the appropriate diagnostic exams to be performed and diagnostic flow charts.

Anti-Inflammatory Agents↗
PubMed2002

Etiopathogenesis of inflammatory bowel disease: the importance of the pediatric perspective.

Inflammatory bowel disease (IBD) is now recognized as a common chronic disease affecting children and adolescents. This article will review recent advances made in the fields of genetics, epidemiology, gut ecology, and immunology regarding the etiopathogenesis of IBD, with particular emphasis on the contributions made by pediatric studies. Areas where further study of the pediatric age group would be beneficial will be highlighted.

Child↗
PubMed2002

Increased serum levels of YKL-40 in patients with inflammatory bowel disease.

BACKGROUND AND AIMS: Initiation of a fibrotic process has been suggested as part of the intestinal response to chronic inflammation in inflammatory bowel disease. YKL-40 has been proposed as a new serum marker of fibrosis. We studied compared the serum levels of YKL-40 in patients with ulcerative colitis or Crohn's disease with inflammatory and healthy controls. PATIENTS AND METHODS: YKL-40 serum levels were measured in 179 patients with inflammatory bowel disease (94 ulcerative colitis, 85 Crohn's disease), in 23 with intestinal inflammation of other causes, and 70 matched healthy controls using a commercially available enzyme-linked immunosorbent assay. YKL-40 levels were assessed in terms of disease activity, type and localization. RESULTS: Mean serum YKL-40 levels were 102.6+/-82.7 ng/ml in ulcerative colitis patients and 112.2+/-83.7 ng/ml in Crohn's disease patients, significantly higher than in healthy controls (64.1+/-21.4 ng/ml) but not significantly different from inflammatory controls (77.8+/-23.1 ng/ml). Disease activity and C-reactive protein levels were significantly correlated with YKL-40 levels in both ulcerative colitis and Crohn's disease. Crohn's disease patients with ileum localization had significantly higher YKL-40 levels than those with ileocolonic or colonic disease. Patients with stenotic disease had mean YKL-40 levels not significantly different than those with nonstenotic disease. CONCLUSION: Serum levels of YKL-40 are increased in patients with inflammatory bowel disease, and this is associated with the inflammatory process rather than with the degree of fibrosis.

Adipokines↗
PubMed2006

Vitamin D status in children and young adults with inflammatory bowel disease.

OBJECTIVES: Previous studies of vitamin D status in pediatric patients with inflammatory bowel disease have revealed conflicting results. We sought to report (1) the prevalence of vitamin D deficiency (serum 25-hydroxy-vitamin D concentration < or = 15 ng/mL) in a large population with inflammatory bowel disease, (2) factors predisposing to this problem, and (3) its relationship to bone health and serum parathyroid hormone concentration. PATIENTS AND METHODS: A total of 130 patients (8-22 years of age) with inflammatory bowel disease, 94 with Crohn disease and 36 with ulcerative colitis, had serum 25-hydroxy-vitamin D, intact parathyroid hormone, and lumbar spine bone mineral density (using dual-energy x-ray absorptiometry) measured at Children's Hospital Boston. RESULTS: The prevalence of vitamin D deficiency was 34.6%. Mean serum 25-hydroxy-vitamin D concentration was similar in patients with Crohn disease and ulcerative colitis, 52.6% lower among patients with dark skin complexion, 33.4% lower during the winter months (December 22 to March 21), and 31.5% higher among patients who were taking vitamin D supplements. Serum 25-hydroxy-vitamin D concentration was positively correlated with weight and BMI z score, disease duration, and serum albumin concentration and negatively correlated with erythrocyte sedimentation rate. Patients with Crohn disease and upper gastrointestinal tract involvement were more likely to be vitamin D deficient than those without it. Serum 25-hydroxy-vitamin concentration was not associated with lumbar spine bone mineral density z score or serum parathyroid hormone concentration. CONCLUSIONS: Vitamin D deficiency is highly prevalent among pediatric patients with inflammatory bowel disease. Factors predisposing to the problem include having a dark-skin complexion, winter season, lack of vitamin D supplementation, early stage of disease, more severe disease, and upper gastrointestinal tract involvement in patients with Crohn disease. The long-term significance of hypovitaminosis D for this population is unknown at present and merits additional study.

Adolescent↗
PubMed1999

Colorectal cancer in inflammatory bowel disease: a continuing problem.

PURPOSE: Because of the increased risk of colorectal cancer in patients with inflammatory bowel disease, surveillance colonoscopy with mucosal biopsies for dysplasia has been advocated to prevent malignancy or permit its early diagnosis. However, despite adoption of colonoscopic surveillance programs by many clinicians, we have noted a pattern of continued referrals for inflammatory bowel disease-associated malignancy. This study was undertaken in an effort to characterize this cohort of patients. METHODS: We reviewed the operative records of a large metropolitan colorectal practice from 1983 to 1995. During this period 40 large-bowel resections were performed for patients with documented inflammatory bowel disease and concomitant carcinoma. A retrospective analysis was conducted with emphasis on clinical presentation, pathologic description, and most recent follow-up. RESULTS: Mean age at the time of diagnosis of cancer was 48 years with an average inflammatory bowel disease duration of 19 years. Seven patients had documented inflammatory bowel disease for less than eight years before their cancer diagnosis. Carcinomas were identified preoperatively by colonoscopy in 92 percent of patients. One-half of these patients had the colonoscopy to investigate a recent change in inflammatory bowel disease symptoms or signs, whereas the other half underwent endoscopy as routine surveillance. For the remaining 8 percent of patients, operated on for worsening symptoms, the carcinoma was detected in the pathological specimen only. The majority of patients (68 percent) did not have a preoperative diagnosis of dysplasia. Twenty-five percent of tumors were mucinous, 20 percent were multicentric, and 70 percent were located distal to the splenic flexure. Among the seven patients who died, four had pancolitis, six had a recent worsening of symptoms, and all had cancer involving the rectum. CONCLUSION: Cancer occurs at a younger age in patients with long-standing inflammatory bowel disease. The tumors are often mucinous, multiple, and located in the left colon. Despite increasing acceptance of surveillance colonoscopy as a recommended strategy in cancer prevention, almost one-half of the patients in this study had their cancer diagnosed because increased colitis symptoms led to colonoscopic examination. Eighteen percent of patients developed cancer with less than an eight-year history of inflammatory bowel disease. These data call into question the effectiveness of dysplasia surveillance as a population-based strategy to decrease the colorectal cancer mortality in inflammatory bowel disease patients.

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↗
PubMed1985

CT of complicated inflammatory bowel disease in children.

Most children with inflammatory bowel disease do not need a CT scan. However, when the course becomes complicated it often is necessary to evaluate what is happening outside the bowel lumen. CT is the examination of choice for that evaluation. With CT, the presence and extent of an abscess can be diagnosed and followed; fistulae can be detected; bowel wall and mesenteric thickening can generally be differentiated from an abscess.

Abdominal Muscles↗
PubMed1984

T-cell abnormalities in inflammatory bowel disease are mediated by interleukin 2.

Inflammatory bowel disease (IBD) may be an immunologically mediated disorder in which T cells are unable to respond appropriately to cell surface-associated antigens. To test this possibility, 37 patients with IBD, 24 with Crohn's disease and 13 with ulcerative colitis who were not being treated with immunosuppressive therapy were studied. The ability of T cells to proliferate in response to autologous or allogeneic cells, i.e., the autologous or allogeneic mixed-lymphocyte reaction (MLR) was tested. The autologous MLR was depressed using patient cells compared to control cells, regardless of disease type or activity (1564 +/- 223 cpm versus 3300 +/- 381 cpm, P less than 0.05) while the allogeneic MLR was depressed in patients with active disease only (29,833 +/- 2871 cpm versus 46,799 +/- 3340 cpm, P less than 0.01). The ability of T cells to recognize and lyse allogeneic cells, allogeneic cell-mediated lympholysis (CML), was also low in patients with active disease (24 +/- 4% versus 37 +/- 3%, P less than 0.05). Since T-cell proliferation and cytotoxicity depend upon adequate production of and response to a T-cell growth factor, interleukin 2 (IL-2), IL-2 production and responsiveness in IBD were studied. IL-2 production by patient T cells in response to phytohemagglutinin was only 39% of control values, P less than 0.05. The response to IL-2 was measured by the increase in T-cell proliferation in the autologous MLR in medium alone or medium supplemented with IL-2. Control T-cell proliferation rose from 3300 +/- 381 cpm to 10,761 +/- 428 cpm with exogenous IL-2 (P less than 0.001). Patient T-cell proliferation rose from 1564 +/- 223 cpm to 6817 +/- 771 cpm with IL-2 (P less than 0.001) but did not reach the level of the IL-2-supplemented control autologous MLR (P less than 0.05). In addition, the percentage of activated patient T cells having Tac antigen (IL-2 receptor) was depressed (P less than 0.05). These findings did not vary with disease type or activity. It is concluded from these data that peripheral blood T lymphocytes from patients with IBD have a diminished response to cell surface antigens which is associated with a decrease in IL-2 production and receptor generation. These defects may be responsible for the depressed T-cell proliferation and cytotoxicity that accompany IBD.

Adolescent↗