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PubMed1985

Filiform polyposis: an unusual complication of inflammatory bowel disease.

Filiform polyposis is an unusual form of inflammatory polyposis which complicates inflammatory bowel disease. Recognition of this variant is important in that its radiographic and endoscopic picture may mimic villous adenoma or adenocarcinoma. Filiform polyposis may precipitate obstruction by stricture formation or give rise to major hemorrhage. We report five patients with inflammatory bowel disease complicated by asymptomatic filiform polyposis to emphasize the pathology of this lesion. We also review the literature regarding this topic.

Adult↗
PubMed1997

Management of varicella infection during the course of inflammatory bowel disease.

OBJECTIVE: To study the natural history and outcome of varicella infection developing in steroid treated inflammatory bowel disease. BACKGROUND: Varicella infection occurring in immunosuppressed or immunocompromised patients is a common problem with a significant mortality. Varicella infection during the course of inflammatory bowel disease has been reported in a small number of patients with at least one fatality. METHODS: Four young patients with inflammatory bowel disease who developed varicella infection while on immunosuppressive therapy, steroids, or azathioprine were studied. In each patient the infection was severe, and the three most recently treated patients received acyclovir. RESULTS: All four patients developed severe varicella infection while receiving immunosuppressive therapy for their disease. Three patients were treated with intravenous acyclovir with concomitant reduction of steroid dosage and recovered completely. One patient, treated in 1980 with antibiotics and reduction in steroids, did not receive acyclovir and also survived. CONCLUSIONS: Varicella infection is a relatively uncommon occurrence in inflammatory bowel disease. If varicella infection occurs, prompt diagnosis and treatment with acyclovir and concomitant reduction in immunosuppressive therapy (reduction in steroid dosage and discontinuation of azathioprine) should be initiated immediately to limit viremia and avoid fatal complications.

Acyclovir↗
PubMed1999

Chronic recurrent multifocal osteomyelitis associated with chronic inflammatory bowel disease in children.

Chronic recurrent multifocal osteomyelitis (CRMO) is a rare disease of children characterized by aseptic inflammation of the long bones and clavicles. No infectious etiology has been identified, and CRMO has been associated with a number of autoimmune diseases (including Wegener's granulomatosis and psoriasis). The relationship between CRMO and inflammatory bowel disease is poorly described. Through an internet bulletin board subscribed to by 500 pediatric gastroenterologists, we identified six inflammatory bowel disease patients (two with ulcerative colitis, four with Crohn's colitis) with confirmed CRMO. In all cases, onset of the bony lesions preceded the onset of bowel symptoms by as much as five years. Immunosuppressive therapy for the bowel disease generally resulted in improvement of the bone inflammation. Chronic recurrent multifocal osteomyelitis should be considered in any inflammatory bowel disease patient with unexplained bone pain or areas of uptake on bone scan. CRMO may be a rare extraintestinal manifestation of inflammatory bowel disease; alternatively, certain individuals may be genetically predisposed to the development of both diseases.

Adolescent↗
PubMed2006

Nutrition in inflammatory bowel disease.

Nutrition has an important role in the management of inflammatory bowel disease. This role includes the prevention and correction of malnutrition, the prevention of osteoporosis and in children the promotion of optimal growth and development. In active Crohn's disease nutritional therapy (in the form of enteral feeding) is an effective primary therapy for many patients. Corticosteroids, however, are more effective than enteral diet therapy in adults. Enteral diets should be considered as primary therapy in pediatric Crohn's disease, especially in children with poor nutritional status or growth impairment. Enteral nutrition does not have a proven primary therapeutic role in ulcerative colitis. There are many theories that suggest that diet may be implicated in the aetiology of inflammatory bowel disease, however, there are, as yet, no dietary approaches proven to reduce the risk of developing IBD.

Adult↗
PubMed1986

Zinc absorption in inflammatory bowel disease.

Zinc absorption was measured in 29 patients with inflammatory bowel disease and a wide spectrum of disease activity to determine its relationship to disease activity, general nutritional state, and zinc status. Patients with severe disease requiring either supplementary oral or parenteral nutrition were excluded. The mean 65ZnCl2 absorption, in the patients, determined using a 65Zn and 51Cr stool-counting test, 45 +/- 17% (SD), was significantly lower than the values, 54 +/- 16%, in 30 healthy controls, P less than 0.05. Low 65ZnCl2 absorption was related to undernutrition, but not to disease activity in the absence of undernutrition or to zinc status estimated by leukocyte zinc measurements. Mean plasma zinc or leukocyte zinc concentrations in patients did not differ significantly from controls, and only two patients with moderate disease had leukocyte zinc values below the 5th percentile of normal. In another group of nine patients with inflammatory bowel disease of mild-to-moderate severity and minimal nutritional impairment, 65Zn absorption from an extrinsically labeled turkey test meal was 31 +/- 10% compared to 33 +/- 7% in 17 healthy controls, P greater than 0.1. Thus, impairment in 65ZnCl2 absorption in the patients selected for this study was only evident in undernourished persons with moderate or severe disease activity, but biochemical evidence of zinc deficiency was uncommon, and clinical features of zinc depletion were not encountered.

Adult↗
PubMedDate not supplied

Differential behavior of coagulation factor XIII in patients with inflammatory bowel disease and in patients with giant cell arteritis.

The aim of this prospective study was to examine the role of coagulation factor XIII (FXIII) in relation to disease activity in inflammatory bowel disease (IBD) and in giant cell arteritis. Plasma FXIII activity was studied during active and inactive disease in newly diagnosed patients with Crohn's disease (CD; n = 20), ulcerative colitis (UC; n = 18) and giant cell arteritis (GCA; n = 19), in 3-month intervals (median follow-up 12 months). FXIII was also measured in two noninflammatory control groups, age and sex matched for IBD (n = 25) and GCA (n = 26). FXIII activity was significantly lower in active CD or UC than in active GCA or the noninflammatory controls. Both in CD and UC, FXIII activity correlated inversely with indices of clinical disease activity, the erythrocyte sedimentation rate, fibrinogen and C-reactive protein levels. Low FXIII activity is a characteristic feature of active IBD, and serial measurements may be useful to assess IBD activity.

Adult↗
PubMed2006

Complications of biological therapy for inflammatory bowel diseases.

PURPOSE OF REVIEW: The purpose of this review is to analyze the complications associated with treatment of inflammatory bowel disease with biologic agents. RECENT FINDINGS: There have been various biologic agents evaluated in patients with inflammatory bowel disease; that is, Crohn's disease and ulcerative colitis. Thus far only infliximab has been approved by the US Food and Drug Administration as induction and maintenance treatment in patients with active Crohn's disease (moderate-to-severe and/or fistulizing) who are refractory to conventional therapy. Recent data from two large multicenter, multicountry, randomized controlled clinical trials have demonstrated that infliximab is efficacious also for the treatment of ulcerative colitis. Other biologics considered potentially efficacious are still undergoing evaluation in various clinical trials. SUMMARY: The data concerning biologics' associated toxicity in patients with inflammatory bowel disease are the most robust in the case of infliximab. These data are derived from both prospective, randomized clinical trials and from post-marketing experience. In the case of the remaining agents the data concerning safety in inflammatory bowel disease are limited, as these agents were not evaluated in as many trials as infliximab; indeed, some of them included only several patients.

Biological Therapy↗
PubMed2002

A review of leukofiltration therapy for decreasing the morbidity associated with cardiopulmonary bypass and acute inflammatory bowel disease.

Complications of cardiopulmonary bypass (CPB) and acute inflammatory bowel disease (IBD) are associated with increased morbidity and cost. During reperfusion post-CPB, activated neutrophils adhere to microvascular endothelial cells mediated by cell adhesion molecules (CAMs) and cytokines/chemokines with subsequent myocardial damage caused by activated neutrophil-derived oxidants and enzymes. Leukofiltration was shown to reduce myocardial reperfusion injury and improve gas exchange as suggested by improvements in surrogate markers of inflammation and clinical end points. In acute IBD, characterized by rectal bleeding and protracted hospital stays, circulating neutrophils emigrate to the inflamed colon and adhere to microvascular endothelial cells by CAMs. Multiple treatments with leukofiltration in IBD were shown to induce long-term remission of acute IBD. Hence, leukofiltration may reduce reperfusion injury and rectal bleeding in CPB and IBD, respectively, and therefore decrease the morbidity and cost associated with these diseases.

Acute Disease↗
PubMed2001

Renal tubular injury is present in acute inflammatory bowel disease prior to the introduction of drug therapy.

BACKGROUND: 5-aminosalicylic acid (5-ASA) has been associated with renal complications in inflammatory bowel disease. Renal function is typically monitored using serum creatinine; however, significant disease may predate increases in creatinine. AIMS: To identify whether markers of early renal disease (urinary albumin, alpha-1-microglobulin [alpha-1-M] and N-acetyl-beta-D-glucosaminidase [NAG], and serum cystatin C) are useful in the assessment of renal function in inflammatory bowel disease patients receiving 5-ASA. METHODS: Twenty-one patients with a new diagnosis of inflammatory bowel disease were investigated. Samples were taken at diagnosis, and at 3-monthly intervals after the commencement of 5-ASA, for 1 year. RESULTS: Mean creatinine clearance was 100 mL/min and did not change following treatment. Inflammatory bowel disease was not associated with albuminuria. Urinary N-acetyl-beta-D-glucosaminidase and alpha-1-microglobulin at diagnosis were increased in 10 (48%) and 11 (52%) patients, respectively: treatment was not associated with consistent changes in urinary protein excretion. There was a significant correlation between cystatin C and creatinine clearance both at diagnosis (r=-0.533, P=0.0275) and combining the initial and follow-up data (r=-0.601, P < 0.01), but not between creatinine and creatinine clearance (P > 0.05). CONCLUSIONS: Tubular proteinuria is an extra-intestinal manifestation of inflammatory bowel disease irrespective of 5-ASA treatment. Tubular proteins are not useful predictors of an adverse renal response to 5-ASA. Serum cystatin C may be an improved marker of glomerular filtration rate in this setting.

Acetylglucosaminidase↗
PubMed1991

Colonic glycoproteins in monozygotic twins with inflammatory bowel disease.

Colonic glycoprotein composition was evaluated in monozygotic twins with inflammatory bowel disease using ion-exchange chromatography. Fifty-three individuals, 12 pairs and 1 single twin with ulcerative colitis and 14 pairs with Crohn's disease, were evaluated. Seven twin pairs were concordant for the presence of ulcerative colitis or Crohn's disease, whereas twin siblings of 10 ulcerative colitis probands and 9 Crohn's disease probands were not known to have inflammatory bowel disease. Content of one chromatographically defined component of colonic mucin, designated HCM species IV, was reduced in both patients with ulcerative colitis (1040 +/- 300 cpm/10,000 cpm total HCM) and their apparently healthy twins (1340 +/- 540 cpm/10,000 cpm total HCM) compared with control subjects (4030 +/- 1,000 cpm/10,000 cpm total HCM). Composition of mucin in Crohn's disease patients and their nonaffected twins was not significantly different than in controls. These observations suggest that altered profiles of mucin glycoprotein may be present before the onset of ulcerative colitis and may be genetically defined. Conversely, it appears that alterations in glycoproteins only are not sufficient to initiate mucosal inflammation.

Adolescent↗
PubMed2007

Colonic expression of leukotriene-pathway enzymes in inflammatory bowel diseases.

BACKGROUND: Leukotrienes derived from the 5-lipoxygenase pathway are proinflammatory lipid mediators that possibly play a role in inflammatory bowel diseases. The expression of 5-lipoxygenase pathway proteins has not previously been examined in colonic mucosa in inflammatory bowel disease. RESULTS: Quantitative immunohistochemical analyses showed that, compared to those of the control subjects (n = 9), colonic biopsies from patients with active inflammatory bowel disease (n = 17) had 3- to 7-fold higher mean counts of cells expressing 5-lipoxygenase (P = 0.03), 5-lipoxygenase-activating protein (P = 0.005), and the leukotriene A(4) hydrolase (P = 0.004), which make up the biosynthetic pathway of the potent neutrophil chemotaxin leukotriene B(4). Immunoexpression of the leukotriene C(4) synthase was unaltered (P > 0.2). The increased representation of leukotriene B(4)-pathway enzymes was associated with higher counts of neutrophils (P = 0.0001), macrophages (P = 0.03), eosinophils (P = 0.0004), CD8(+) T cells (P < 0.001), activated T cells (P < 0.05), and B cells (P < 0.05) but not of mast cells (P > 0.9). These eicosanoid and cellular changes were most marked in the subgroup of patients with ulcerative colitis (n = 9), and were absent in patients with quiescent disease (n = 6). The anomalies in the 5-lipoxygenase pathway were accompanied as expected by more cells immunostaining for cytokine-inducible COX-2 (P = 0.004, n = 17), but this study also revealed a greater number of cells expressing COX-1 in the samples from the patients in the ulcerative colitis subgroup (P = 0.03, n = 9). CONCLUSIONS: The 5-lipoxygenase data provide a cellular basis for increased tissue synthesis of the leukotriene B(4), as reflected in the colonic mucosa and rectal dialysates of patients with active inflammatory bowel disease, which contributes to neutrophil influx and colonic injury. The COX-1/COX-2 data highlight the ambiguous functional role of prostanoid pathways in inflammatory bowel diseases.

Adult↗
PubMedDate not supplied

Non-calculus suppurative cholangitis in Danish patients with inflammatory bowel disease.

BACKGROUND/AIMS: We examined the risk of non-calculus suppurative cholangitis in patients with inflammatory bowel disease in the entire Danish population. METHODOLOGY: The study included all patients discharged from Danish hospitals with a diagnosis of Crohn's disease or ulcerative colitis as registered in the Danish National Registry of Patients from January 1, 1977 to December 31, 1992. We compared the observed number of patients hospitalized with suppurative cholangitis with expected numbers on the basis of age, gender, and calendar-specific incidence rates in the general population. RESULTS: Overall, 15,317 eligible patients with inflammatory bowel disease were discharged during the study period. Among these were 52 cases of non-calculus suppurative cholangitis. The incidence rate of non-calculus suppurative cholangitis in the cohort with inflammatory bowel disease was 46.1 per 100,000 person-years. The standardized incidence ratio (SIR) for suppurative cholangitis was increased similarly for patients with Crohn's disease [SIR=6.7, 95% confidence interval (CI): 3.1-12.7] and for patients with ulcerative colitis (SIR=6.6, 95% CI: 4.7-9.1). The highest relative risk was found in male patients younger than 40 years of age, for both Crohn's disease and ulcerative colitis (SIR=70.5 and 78.7, respectively). CONCLUSIONS: Patients with inflammatory bowel disease have an increased risk of non-calculus suppurative cholangitis.

Adult↗
PubMed2005

Activation of A2A adenosine receptor attenuates intestinal inflammation in animal models of inflammatory bowel disease.

BACKGROUND & AIMS: Adenosine has been implicated as an important regulator of the inflammatory response. Four subtypes of adenosine receptors (A 1 , A 2A , A 2B , and A 3 ) have been described, of which A 2A potentially inhibits inflammation. The aim of this study was to investigate the role of A 2A in mucosal inflammation by administering a selective A 2A agonist (ATL-146e) to experimental models of inflammatory bowel disease. METHODS: The anti-inflammatory effects of ATL-146e were studied in the acute and chronic rabbit formalin-immune complex models of colitis and the SAMP1/YitFc mouse model of spontaneous ileitis. RESULTS: ATL-146e significantly reduced the acute inflammatory index and tissue necrosis compared with vehicle ( P < .01) in the acute model of rabbit immune colitis. In the chronic rabbit immune colitis model, ATL-146e significantly suppressed inflammatory cell infiltration into the colonic mucosa ( P < .05) and prevented mortality. The administration of ATL-146e significantly decreased the chronic inflammatory index ( P < .01) and villus distortion index ( P < .01) in the ileum of SAMP1/YitFc mice, and ameliorated adoptively transferred ileitis in severe combined immunodeficient mice injected with CD4 + T cells from SAMP1/Yit mice ( P < .05). Tumor necrosis factor, interferon gamma, and interleukin 4 concentrations were significantly suppressed by ATL-146e treatment in supernatants from cultures of mesenteric lymph node cells of SAMP1/YitFc mice ( P < .05 vs vehicle-treated mice). CONCLUSIONS: A 2A adenosine receptor activation by ATL-146e significantly reduced inflammation in the intestinal mucosa. This effect was associated with decreased leukocyte infiltration and inhibition of proinflammatory cytokines. Activation of A 2A by selective agonism may therefore serve as a novel therapy for the treatment of inflammatory bowel disease.

Acute Disease↗
PubMed1988

Leukergy in inflammatory bowel disease.

In the phenomenon of leukergy, white blood cells agglomerate in peripheral blood slides. This agglomeration has been described in inflammatory infections of various causes. This study assesses this phenomenon in inflammatory bowel disease. A correlation was found between the severity of inflammatory bowel disease activity and the percentage of leukergy. Leukergy was found to parallel the clinical and endoscopic findings of inflammatory bowel disease. Furthermore, leukergy was found to be more accurate than white blood count and erythrocyte sedimentation rate. It is also found to accurately assess the course of the disease when clinical and other laboratory tests were masked by steroid and antibiotic administrations. Leukergy is a quick, inexpensive test that can easily be performed at the patient's bedside.

Adolescent↗
PubMed2002

Validation of the EuroQol questionnaire in patients with inflammatory bowel disease.

OBJECTIVE: The EuroQol EQ-5D is a generic questionnaire for describing and valuing patients' health-related quality of life. The purpose of the study was to analyse the construct validity, criterion validity, test-retest reliability and responsiveness of the EQ-5D in patients with inflammatory bowel disease. METHODS: 152 consecutive patients with inflammatory bowel disease (123 with Crohn's disease and 29 with ulcerative colitis) completed the EQ-5D, the SF-36 and the Inflammatory Bowel Disease Questionnaire (IBDQ). Of the study group, 66 patients filled in the EQ-5D a second time after a 2-week gap, including a transition question. Disease activity was measured by the Crohn's Disease Activity Index (CDAI) and by Rachmilewitz's Clinical Activity Index (CAI). RESULTS: The EQ-5D showed a moderate ceiling effect. Correlation between the EQ-5D visual analogue scale (EQ VAS) score and CDAI/CAI was r = -0.65/r = -0.71 (both P < 0.001). Levels of responses to EQ-5D items and the EQ VAS score were significantly better for patients in remission than for patients with active disease (all P < 0.01). For the total sample, coefficients of correlation between the EQ VAS score and SF-36 and IBDQ scores ranged between 0.37 and 0.73 (all P < 0.0001). When repeated, the EQ-5D was reliable in stable patients (intraclass correlation coefficient for EQ VAS = 0.77, kappa statistic for items 0.39 to 1.00); the EQ VAS was responsive in patients who, in the transition question, indicated an improvement in health state (effect size 0.79). CONCLUSIONS: The EQ-5D is reasonably valid, reliable and responsive in patients with inflammatory bowel disease. It can be used to generate preference-based valuations of health-related quality of life in inflammatory bowel disease.

Adolescent↗
PubMed1974

A study of peripheral leucocyte migration in agarose medium in inflammatory bowel disease.

THE MIGRATION OF PERIPHERAL LEUCOCYTES FROM PATIENTS WITH INFLAMMATORY BOWEL DISEASE WAS INVESTIGATED USING AN AGAROSE PLATE TECHNIQUE AND THREE ANTIGENIC MATERIALS: (1) the enterobacterial common antigen of Kunin; (2) extract from germ-free rat faeces; and (3) Kveim suspension from a sarcoid spleen K19. Inhibition of migration was obtained only with Kunin antigen. It was present in 11 out of 20 patients with ulcerative colitis and in four out of 20 patients with Crohn's disease but in only one out of 33 control subjects. These findings suggest the possibility that a state of cellular immunity to enterobacterial common antigen may exist in inflammatory bowel disease. Lack of cellular reactivity to extract from germ-free faeces and Kveim suspension is in contrast with the results obtained by others by means of the capillary tube method and requires further investigation.

Adolescent↗
PubMed1997

Reduced bone density in patients with inflammatory bowel disease.

BACKGROUND: Reduced bone mineral density in patients with inflammatory bowel disease is thought to be due to disturbances in calcium homeostasis or the effects of corticosteroid treatment. AIMS: To assess the prevalence and mechanism of reduced bone mineral density in 79 patients with inflammatory bowel disease (44 with Crohn's disease, 35 with ulcerative colitis) who did not have significant risk factors for low bone densities. METHODS: Dual x ray absorptiometry was used to measure bone mineral density and serum and urinary markers of osteoblast (alkaline phosphatase, procollagen 1 carboxy terminal peptide and osteocalcin) and osteoclast (pyridinoline, deoxypyridinoline, and type 1 collagen carboxy terminal peptide) activities to assess bone turnover. RESULTS: There was a high prevalence of low bone mineral density (prevalence of T scores < -1.0 from 51%-77%; T scores < -2.5 (osteoporosis) from 17%-28%) with hips being more often affected than vertebrae (p < 0.001). Reduced bone mineral density did not relate to concurrent or past corticosteroid intake, or type, site, or severity of disease. Whereas calcium homeostasis was normal, bone markers showed increased bone resorption without a compensatory increase in bone formation. CONCLUSIONS: The greater prevalence of reduced hip bone mineral density, as opposed to vertebral, mineral density and the pattern of a selective increase in bone resorption contrasts with that found in other known causes of metabolic bone disease.

Absorptiometry, Photon↗
PubMed1999

Fibromyalgia in inflammatory bowel disease.

OBJECTIVE: Studies of the rheumatological complications of inflammatory bowel disease (IBD; Crohn's disease and ulcerative colitis) have focused on peripheral arthritis and spondylitis, and less is known about soft tissue rheumatism, specifically the fibromyalgia syndrome (FM). Our aim was to estimate the prevalence of FM and assess pain thresholds in patients with Crohn's disease (CD) and ulcerative colitis (UC). METHODS: Seventy-two patients with UC and 41 with CD attending consecutively at the Gastroenterology Outpatient Clinic were assessed for the presence of FM and tenderness thresholds. FM was diagnosed according to the American College of Rheumatology 1990 criteria. Tenderness was measured by manual palpation and with a dolorimeter. One hundred twenty healthy subjects served as controls. RESULTS: FM was documented in 30 of 113 patients with IBD (30%), specifically in 49% of patients with CD and 19% with UC (p = 0.001); in controls the rate was 0%. Subjects with CD exhibited more tenderness and reported more frequent and more severe FM associated symptoms than subjects with UC. Patients with CD had a higher tender point count, 11.3 (+/- 6.5), than those with UC, 6.4 (+/- 5.7) (p = 0.001); in healthy controls, the count was 0.1 (+/- 0.5). Tenderness thresholds (kg) were lower in CD 2.9 (+/- 1.7) than UC 3.9 (+/- 2.0) (p = 0.005) and controls 5.8 (+/- 0.9). CONCLUSION: FM is common in IBD, particularly Crohn's disease. The lower pain threshold in Crohn's disease may suggest a disease-specific effect. Recognizing FM in patients with IBD will prevent misdiagnosis and ensure correct treatment.

Adult↗