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PubMed2001

Inflammatory cytokines and mucosal injury.

The cause of mucosal injury in inflammatory bowel disease (IBD) is not clear but likely involves infectious agents or other toxins followed by an abnormal immune response in genetically susceptible individuals. The inflammatory cytokines appear to play a key role in both the susceptibility of some individuals and the tissue damage that accompanies IBD. The generation of transgenic and gene-targeted (knockout) animals has provided invaluable information regarding the cytokines and cellular immune effectors that are important in IBD. Information from these and other preclinical animal models, such as those involving interleukin 11, has led to human trials testing novel therapies for IBD and other diseases in which inflammation of the gut mucosa is an important component. Thus, expression of inflammatory cytokines appears to be an important target for the development of novel therapies for IBD and other diseases in which intestinal mucosal damage occurs, such as mucositis and graft-versus-host disease.

Animals↗
PubMed1995

Different abdominal scintigraphy pattern in patients with ulcerative colitis, Crohn's disease and seronegative spondylarthropathies.

The aim was to analyse the abdominal scintigraphy pattern in patients with seronegative spondylarthropathy (SSp), ulcerative colitis (UC) and Crohn's disease (CD). A total of 117 patients with defined histological lesions of inflammatory bowel disease (IBD) (68 UC and 49 CD), 32 patients with active SSp [European Spondylarthropathy Study Group (ESSG) 1991 criteria] without clinical evidence of IBD and 21 controls without IBD or SSp were studied. All patients with SSp and controls received similar doses of non-steroidal anti-inflammatory drugs. Abdominal scintigraphy images were obtained at 30 and 120 min after injection of 99m-technetium hexamethyl propylene amine oxime (99mTc-HMPAO)-labelled leucocytes. The 99mTc-HMPAO-labelled leucocyte scan was positive in 17 patients with SSp (53.1%), 45 patients with UC (66.1%) and 33 patients with CD (67.3%). Rectum and sigma involvement was more frequent in patients with UC (68.8%) than in patients with SSp (23.5%) or CD (33.3%) (P < 0.05) [odds ratios (OR): 7.1 and 4.4, respectively]. Terminal ileum involvement was more frequent in patients with CD (63.6%) than in patients with SSp (23.5%) or UC (8.8%) (P < 0.05) (OR: 5.6 and 17.9, respectively). The 99mTc-HMPAO-labelled leucocyte scan shows an increased uptake in patients with SSp without evidence of IBD. Perhaps these patients represent one end of the spectrum of IBD, but rectal and terminal ileum involvement were less frequent in patients with SSp than in patients with UC or CD.

Abdomen↗
PubMed2001

The prevalence and incidence of peripheral arthritis in patients with inflammatory bowel disease, a prospective population-based study (the IBSEN study).

OBJECTIVES: To estimate the occurrence of peripheral arthritis (PA) 6 yr after diagnosis of inflammatory bowel disease (IBD). METHODS: In a population-based cohort of 654 patients with a definite diagnosis of IBD, 521 patients (80%) were clinically examined by a rheumatologist 6 yr after IBD diagnosis. RESULTS: PA related to IBD (PAIBD) was detected at examination in four patients (point prevalence 0.8%). If the patients' own reports of PA were accepted, 12% of the cases had developed such manifestations. The striking difference may be explained by the nature of PAIBD exhibiting a short-lasting, self-limiting, non-destructive course and by possible differences in the validity of both methods of ascertainment. CONCLUSION: Our results indicate that PAIBD occurs in a considerable number of IBD patients during the first years after diagnosis, but the point prevalence of PAIBD is low.

Adolescent↗
PubMed1999

Pathogenesis of inflammatory bowel disease.

In spite of expanding knowledge of cellular and molecular mechanisms of intestinal inflammation, the etiology and pathogenesis of inflammatory bowel disease (IBD) remain obscure. The link between the environment and IBD is still circumstantial, but definite progress is occurring in defining genetic susceptibility loci for Crohn's disease (CD) and ulcerative colitis (UC). The notion that normal enteric flora play a role in initiating or maintaining IBD is gaining momentum. Some components of the flora may act as noxious agents, whereas others (probiotics) seem to have a protective effect. The importance of the mucosal immune system to IBD is established, and evidence is accumulating that nonimmune components, such as epithelial, mesenchymal, and endothelial cells, also contribute to gut inflammation. The effect of cytokines in intestinal immunity is being elucidated by studies on their molecular mechanism, particularly the activation of nuclear factor (NF)-kappaB. Finally, the beneficial effects of cytoprotective prostaglandins and cell adhesion molecule (CAM) blockade promise novel therapeutic opportunities derived from an improved understanding of IBD pathogenesis.

Journal Article↗
PubMed2003

Genotype-based phenotyping heralds a new taxonomy for inflammatory bowel disease.

Inflammatory bowel disease (IBD) has traditionally been categorized as either ulcerative colitis or Crohn disease on the basis of clinical, radiologic, and histologic criteria. Within these diseases, however, significant heterogeneity is observed, suggesting the existence of phenotypic subtypes, based on features such as location and behavior of disease. Evidence for a possible genetic basis of these subgroups first emerged in the 1990s from epidemiologic studies in multiply affected families. Recent advances in our understanding of the genetics of IBD, in particular the identification of NOD2/CARD15, have provided the opportunity to explore the genetic basis for this heterogeneity. This article reviews recent studies investigating the contribution of genetics to IBD phenotype. Although many of the genes remain unidentified, the emerging data suggests that IBD comprises a heterogeneous family of oligogenic inflammatory disorders in which the specific clinical manifestations of disease in any individual are determined by the interaction of genetic and environmental factors. These data have validated the approach of classifying patients into accurately defined clinical subgroups, and they raise the possibility that a genetic basis for the observed disease heterogeneity may account for the discrepant findings from earlier genetic studies. A future molecular classification will provide the framework to understanding the different biologic mechanisms that underlie the clinical subgroups of IBD and, by patient stratification, permit the unraveling of the complex interaction between the genetic and environmental causes of disease.

Journal Article↗
PubMed2000

Pediatric inflammatory bowel disease imaged with Tc-99m white blood cells.

Studies have suggested that Tc-99m white blood cell (WBC) imaging is superior to contrast radiology for assessing the extent and activity of inflammatory bowel disease (IBD). The Tc-99m WBC scan seems ideally suited to obtain, in only one examination, a precise temporal snapshot of the distribution and intensity of inflammation, whereas radiographic methods of investigation tend to represent changes that are more chronic. The test is useful in children with inconspicuous signs suggesting IBD in whom laboratory test results are either normal or slightly abnormal. In those cases, a negative Tc-99m WBC study will obviate endoscopic investigations. The author's current experience, in more than 500 patients, indicates that the Tc-99m WBC scan is a virtual gold standard to establish, or exclude, the diagnosis of IBD. The minimal invasiveness of the Tc-99m WBC scan makes it an especially attractive method for evaluating children with IBD. It is economical compared with endoscopy, and its diagnostic sensitivity is excellent. The ability to evaluate the small and large bowel simultaneously is an important advantage for the patient. In conclusion, the Tc-99m WBC scan is a useful tool to evaluate IBD and should be added to the clinician's investigative armamentarium.

Child↗
PubMed1991

Parental distress and social interaction in families with children with inflammatory bowel disease.

Twenty families who had children with inflammatory bowel disease (IBD) and 20 comparison families with healthy children were studied concerning parental distress and social interaction. The mothers in the IBD group scored very high on parental distress, whereas the fathers did not differ from the comparison group. Both parents in the IBD group reported significantly lower scores on a social support scale. The dimension of social integration was normal, but deeper relations and attachment were negatively affected among parents in the IBD group. The mental health of the children with IBD correlated with the social support, especially the qualitative aspects.

Adaptation, Psychological↗
PubMed1990

Limitations in the evaluation of therapy in inflammatory bowel disease: suggestions for future research.

The current treatment of inflammatory bowel disease (IBD), though improved over earlier therapies, remains variable rather than consistent and supportive rather than curative. The similar management of ulcerative colitis (UC) and Crohn's disease (CD), which are thought to be differing though related disorders, suggests that therapy is nonspecific. The variation in therapeutic practices results from the fact that the etiologies of the diseases are obscure, from limited knowledge of the biological and pharmacological actions of drugs commonly prescribed (sulfasalazine, 5-ASA compounds, steroids, 6-MP and azathioprine), from an inadequate understanding of genetic differences influencing drug metabolism, from insufficient awareness of the factors influencing drug efficiency (concurrent use of antimotility drugs, cigarette smoking, food combinations), from the variability of the patient groups studied (extent and severity of disease), and from incomplete documentation of the clinical status of patients at the time of therapeutic trial. Future advances in treatment will depend on gaining new information about the nature of IBD and of drug pharmacology and bioavailability, derived from collaborative studies by clinicians, clinical investigators, and basic scientists. Important areas for IBD research include the biology of intestinal epithelium, the nature of the IBD inflammatory reaction and of gut mucosal immune regulation (via the application of new biotechnologies) and more representative experimental animal models. Decisive multicenter therapeutic studies require agreement on definitions of ulcerative colitis and Crohn's disease, accurate characterization of patient groups, acceptable objective criteria of IBD severity and activity, and reliable indicators of therapeutic response.(ABSTRACT TRUNCATED AT 250 WORDS)

Forecasting↗
PubMed1990

Refractory parastomal ulcers: a multidisciplinary approach.

Chronic parastomal ulcers in patients with ileostomy or colostomy stomas are unusual. Previous reports have implicated infections, fistulas, recurrent inflammatory bowel disease (IBD), pyoderma gangrenosum, and trauma. Over the past 8 years we have evaluated 10 cases of such refractory parastomal ulcers that occurred at a mean of 11 years after stomal surgery. Eight patients had had an ileostomy for IBD while two had undergone colostomy for colon cancer. Five patients with IBD were diagnosed as having pyoderma gangrenosum ulcerations. They required systemic treatment for a mean of 25 weeks to effect ulcer healing. The other five patients had either parastomal ulcers on the basis of dermatoses (contact dermatitis, eczema, or bullous pemphigoid) or contact ulcers due to face-plate pressure and parastomal dermatitis. These patients received topical treatment with healing of ulcers in a mean of 4 weeks. We conclude that parastomal ulcers occurring in patients without IBD or IBD patients without classic pyoderma gangrenosum require early dermatologic evaluation as they respond relatively quickly to appropriate local therapy.

Chronic Disease↗
PubMed1992

Microbic superinfection in relapse of inflammatory bowel disease.

To assess the association between symptomatic relapse of inflammatory bowel disease (IBD) and superinfection with enteropathogenic microorganisms, we determined prospectively the incidence of infections with enteropathogenic bacteria, protozoa, and helminths in patients with confirmed longstanding IBD. Sixty-four patients with IBD (49 with Crohn's disease [CD] and 15 with ulcerative colitis [UC]) were consecutively enrolled in the study when relapse occurred. Multiple biopsies for histological and microbiological investigations were taken from all patients who were evaluated by colonoscopy. Parallel stool specimens were investigated for the presence of enteropathogenic bacteria, protozoa, and helminths. In six patients, we detected Clostridium difficile or toxin B (five CD, one UC), in one patient Campylobacter jejuni (CD), and in another patient Salmonella typhimurium (UC). Enteropathogenic Escherichia coli were isolated from three patients. Investigation of biopsies for Mycobacteria, microscopic examination of stool samples for helminths, and immunofluorescence for chlamydia were negative in all patients. In summary, as we found enteropathogenic microorganisms so infrequently in patients with relapse of IBD, despite intensive microbiological screening by tissue sampling for detection of gut adherent bacteria, we believe that microorganisms play only a minor role in the exacerbation of IBD.

Adult↗
PubMed1998

Factor V Leiden mutation is not increased in patients with inflammatory bowel disease.

Individuals with inflammatory bowel disease (IBD) are known to have an increased incidence of thromboembolic disease. Activated protein C resistance (APCR) has been identified as one of several inherited disorders of coagulation that predispose individuals to thromboembolic problems. This resistance results from a single point mutation in the factor V gene, called factor V Leiden. It has been suggested that many patients with IBD have APCR, as tested by a clotting assay. We have evaluated a series of 49 patients with IBD, none of whom had a history of thromboembolic disease. We assayed for the factor V Leiden mutation by polymerase chain reaction and found only one heterozygote. Seventeen of the 49 patients were negative for APCR by the clotting assay. Factor V Leiden mutation is not more common in patients with IBD than in the general population. We were unable to confirm a prior report indicating that patients with IBD have a higher prevalence of resistance to activated protein C.

Activated Protein C Resistance↗
PubMed2001

Primary sclerosing cholangitis in patients with inflammatory bowel disease in Turkey.

BACKGROUND: Primary sclerosing cholangitis (PSC), which is a progressive cholestatic liver disease of unknown etiology, is strongly correlated with inflammatory bowel disease (IBD). GOALS: To determine the prevalence and describe the characteristics of PSC in patients with IBD in Turkey. STUDY: We determined the prevalence of PSC in patients with IBD admitted to our department during a 6-year period. Also, patients with PSC were investigated from an IBD aspect. Regardless of whether the patient had symptoms such as itching, jaundice, and abdominal pain, endoscopic retrograde cholangiopancreatography was performed on those with elevated alkaline phosphatase, and liver biopsy was done if endoscopic retrograde cholangiopancreatography failed to bring about the diagnosis. RESULTS: Overall prevalence of PSC was 9 of 386 (2.3%) patients with ulcerative colitis (UC) and 4 of 110 (3.6%) patients with Crohn's disease (CD). Inflammatory bowel disease was established in 13 of 18 (72.2%; UC, 50.0%; CD, 22.2%) patients who were being observed for PSC. The male-to-female ratio was 5:4 in UC and 3:1 in CD patients with PSC. The mean age at diagnosis of PSC was 43.6 years (range, 30-54 years) in patients with UC and 30.5 years (range, 26-41 years) in patients with CD. In patients with UC, the extension of colitis was total in seven patients (7/110, 6.3%) and left-sided in two patients (2/142, 1.4%). In patients with CD, the disease was located in the ileum and colon in one patient (1/47, 2.1%) and in colon alone in three patients (3/21, 14.2%). CONCLUSIONS: Prevalence of PSC-associated IBD in the Turkish community appear to be similar to the results of western origin studies.

Adult↗
PubMed1997

Antineutrophil cytoplasmic antibodies in children with inflammatory bowel disease: prevalence and diagnostic value.

BACKGROUND: Antineutrophil cytoplasmic antibodies (ANCA), particularly perinuclear ANCA (p-ANCA), have been found more frequently in sera from patients with ulcerative colitis (UC) than in sera from Crohn's disease (CD) or unclassified enterocolitis (UE) patients. This 2-center study examined sera from 102 pediatric patients with inflammatory bowel disease (IBD) to evaluate their diagnostic value and assess their relationship with disease features, distribution, activity and treatment. METHODS: The serum ANCA of 102 children with IBD were measured: 33 UC, 64 CD and 5 UE with various disease locations and degrees of activity. The mean age at the onset of symptoms was 10.7 years (1 to 16.3 years). Sera from 26 unaffected first degree relatives and 20 children without IBD were also investigated. ANCA were detected using indirect immunofluorescence of ethanol-fixed granulocytes. RESULTS: There were ANCA in the sera of 24/33 children with UC (73%), 9/64 with CD (14%) and 4/5 with UE (80%). p-ANCA were more frequent than cytoplasmic-ANCA in positive sera: UC = 67%, CD = 57% and UE = 75%. The presence of ANCA was 73% sensitive and 81% specific for a diagnosis of UC, compared to other IBD (p < 0.001). Three children with proved sclerosing cholangitis associated with UC were all positive. There was no link between ANCA-positive sera and disease activity, or other endoscopic or clinical criteria. ANCA were detected in 4/26 first degree relatives (15%) and in 1/20 control subjects (5%). CONCLUSIONS: Because of their sensitivity and specificity, ANCA may be helpful in the clinical assessment of patients with IBD, and especially those with UC. However, there is no link between the pressure of p-ANCA and the site of UC or its activity, so that it cannot be used to monitor medical treatment or surgical indications.

Adolescent↗
PubMed2001

Fecal calprotectin as a measure of disease activity in childhood inflammatory bowel disease.

BACKGROUND: Calprotectin is an abundant neutrophil protein that is extremely stable in feces. The aim of this study was to assess the effectiveness of fecal calprotectin as a noninvasive measure of disease activity in childhood inflammatory bowel disease (IBD) by comparison to a modified Lloyd-Still and Green score and laboratory inflammatory indices. METHODS: Spot fecal samples from 37 children with IBD and 31 control children were sent by ordinary mail to the laboratory. Fecal calprotectin concentration was measured by an in-house enzyme linked immunosorbent assay (ELISA). A modified Lloyd-Still & Green score (mLSS) was calculated for each child with IBD within 10 days of obtaining the fecal sample. RESULTS: Compared with control values (median, range) (2.1, 0.5-6.3 mg/L), fecal calprotectin was increased in 16 children with ulcerative colitis, (11.5, 0.6-272.5 mg/L, P < 0.001) and in 21 children with Crohn disease, (14.0, 0.7-59.7 mg/L, P < 0.001). Twelve "moderately affected" children (mLSS of 35-65) had higher fecal calprotectin concentrations (22.2, 2.7-141.7 mg/L) than 25 "mildly affected" children (mLSS > 65), (10.3, 0.6-272.5 mg/L, P = 0.002). For the total IBD group, fecal calprotectin concentration correlated negatively with the mLSS (r = -0.61, P < 0.001). It also correlated negatively with serum albumin concentration (r = -0.49, P = 0.002) and positively with erythrocyte sedimentation rate (r = 0.40, P = 0.01). CONCLUSIONS: Fecal calprotectin seems to reflect bowel inflammation in children with IBD. As a simple, safe, noninvasive test, it has the potential to reduce the number of invasive investigations performed in these children.

Adolescent↗
PubMed2002

Prevalence of factor V G1691A (Leiden), prothrombin G20210A, and methylene tetrahydrofolate reductase C677T thrombophilic mutations in children with inflammatory bowel disease.

BACKGROUND: Patients with inflammatory bowel disease (IBD) have an increased incidence of thromboembolic events. This risk may be caused by an increased frequency of thrombophilic mutations such as factor V Leiden G1691A (FVL), prothrombin G20210A (PT), or methylene tetrahydrofolate reductase C667T (MTHFR). Prevalence rates of heterozygous mutations in FVL, PT, and MTHFR are reported for whites (1.8%, 1.3%, 26.6%, respectively), blacks (0.8%, 0.3%, and 12.4%, respectively), and Hispanics (1.2%, 2.4%, and 41.5%, respectively). We sought to determine the prevalence of these thrombophilic mutations in a large cohort of children with IBD. METHODS: Children aged 21 years or younger with IBD were genotyped for FVL, PT, and MTHFR mutations by polymerase chain reaction amplification and restriction enzyme digestion. Prevalence rates were compared with established rates in the respective populations. RESULTS: Of 92 patients enrolled, 89 (62 with Crohn disease, 24 with ulcerative colitis, and 3 with indeterminate colitis) had genotype results available. The mean age was 13.3 +/- 4.2 years (range, 2-21 years). Statistical analysis was performed on 89 FVL, PT, and MTHFR allele pairs. Polymerase chain reaction genotyping identified 5 patients with heterozygous FVL mutations, 3 patients heterozygous for the PT mutation, and 36 patients heterozygous and 4 patients homozygous for the MTHFR mutation. The thrombophilic allele mutation frequencies in our sample were not significantly different from predicted weighted average values: FVL, 2.8% versus 1.5%; PT, 1.7% versus 1.1%; and MTHFR, 24.7% versus 24.4%. In 24 patients with a family history of thrombosis, 1 was heterozygous for FVL and for MTHFR, 1 was heterozygous for FVL and homozygous for MTHFR, 2 were heterozygous for PT, and 9 were heterozygous MTHFR. There was no significant correlation between family history of thrombosis and presence of a thrombophilic mutation. The four patients with homozygous mutations for MTHFR, two of whom also were heterozygous for FVL, did not have either a personal history of thrombosis or a family history of thrombotic events. Two patients had thrombotic events without mutations in these genotypes: one had protein S deficiency and the other had no identifiable cause. CONCLUSIONS: The presence of genetic mutations that predispose to hypercoagulable states does not appear to correlate with the prevalence of IBD or to thromboembolic events in patients with IBD. There was no statistical difference between the proportions of the mutated allele frequency in our study patients and the general population.

Adolescent↗
PubMed2003

The insulin-like growth factor axis in children with inflammatory bowel disease.

BACKGROUND: The insulin-like growth factor (IGF) axis consists of two IGFs and six IGF-binding proteins (IGFBPs) that regulate proliferation and differentiation of many cell types. Malnutrition and inflammation alter the IGF axis. The authors evaluated circulating IGFs and IGFBPs in patients with inflammatory bowel disease (IBD) at the time of presentation and compared them with values obtained during remission. METHODS: Seventeen newly diagnosed pediatric IBD patients were studied on presentation and during remission. Nutritional status was assessed by body mass index (BMI) and serum protein assay. The Lloyd-Still and Green IBD clinical scoring system was used. IGF-I and IGF-II levels were measured by radioimmunoassay, and IGFBP-3 levels were measured by immunoradiometric assay. IGFBPs were quantified on ligand blots with a PhosphorImager. RESULTS: Body mass index and IBD clinical scores improved after treatment: 18.7 +/- 3.0 versus 21.3 +/- 3.0 kg/m (P = 0.023) and 74.6 +/- 16.7 versus 93.1 +/- 7.4 (P< 0.001), respectively. Protein changes were insignificant. IGFBP-3 levels increased from time of first evaluation to remission: 3,470 +/- 850 versus 4,700 +/- 473 ng/mL (P< 0.001). The ratio of IGFBP-3 to IGFBP-2 increased from first evaluation to remission: 1.7 +/- 1.9 versus 3.9 +/- 1.9 (P= 0.003). IGF-I and IGF-II levels also increased: 139 +/- 167 versus 223 +/- 118 ng/mL (P= 0.011) and 307 +/- 111 versus 386 +/- 73 ng/mL (P= 0.007), respectively. CONCLUSIONS: Circulating IGFBP-3 levels were low during active IBD and increased at remission in parallel with the IGF-I levels. The IGFBP-3 to IGFBP-2 ratio was altered in the presence of active disease in a manner that would reduce IGF-I action. This abnormality improved after treatment.

Acute Disease↗
PubMed2004

Colonic expression of MUC2, MUC5AC, and TFF1 in inflammatory bowel disease in children.

BACKGROUND: The quantity and quality of mucins are affected in inflammatory bowel disease (IBD) both because of a reduction in the number of goblet cells and a decrease in the number of sugar residues per oligosaccharide side chain. Alteration in the types of mucins and aberrant location may contribute to the underlying pathology by affecting the mucus barrier function or may instead be a response to inflammation. The authors used the periodic acid-Schiff/Alcian blue stain to distinguish neutral and acidic mucins, and used specific antibodies to the mature goblet cell mucin MUC2, MUC2 core antigen, foveolar cell mucin MUC5AC, and gastric trefoil factor (TFF1), to characterize their presence and distribution in colonic tissue sections from patients with IBD. RESULTS: Both core and mature MUC2 were expressed in all colonic goblet cells from patients with ulcerative colitis (UC) and Crohn disease and from healthy controls. MUC5AC and TFF1, which are not normally expressed by colonic tissue, also were expressed in scattered goblet cells, coexpressing with MUC2. In areas of goblet cell depletion, MUC2 was present in cytoplasmic granules of flattened, cuboidal, nongoblet-cell-like surface cells. The staining was more intense and homogenous with the MUC2 core antibody, suggesting expression of relatively immature mucin. Some of these cells also coexpressed MUC5AC but to a lesser extent. These findings are not unique to IBD but were also found in other types of intestinal inflammation. CONCLUSION: The study confirms earlier observations that MUC2 is the major colonic mucin in IBD. It appears in two forms: mature MUC2 in goblet cells and immature MUC2 especially in secretory granules of cells that are not phenotypically goblet cells. MUC5AC and TFF1 expression in goblet cells is common in IBD and other inflammatory conditions of the colon. These changes may represent a nonspecific repair function of the colon cells to compensate for damage to barrier function.

Adolescent↗
PubMed1992

Pulmonary granulocyte margination is increased in patients with inflammatory bowel disease.

The pulmonary granulocyte content of the lung was quantified in patients with inflammatory bowel disease (IBD) after injection of 111In-labelled granulocytes and compared with patient controls, who, on the basis of their negative white cell scans, were not considered to have active inflammation. The mean ratios of lung:liver count rates per pixel on the posterior gamma camera image in patient controls was 0.34 (S.D. 0.16, n = 8) at 1-1.5 h after injection of the cells, and 0.29 (S.D. 0.14, n = 18) at 2-4 h. This ratio was higher in patients with active IBD at both imaging times: 0.45 (0.13, n = 13, P > 0.05) and 0.44 (0.1, n = 19, P < 0.001). Patients with inactive IBD also had increased ratios at both imaging times: 0.6 (0.14, n = 7, P < 0.01) and 0.54 (0.15, n = 12, P < 0.001), respectively. In a further group of 12 patients with active IBD, there was no correlation between the lung:liver ratio and the severity of the IBD as assessed by whole-body 111In retention at 4-6 days after labelled cell injection. These patients were treated for 3 weeks with an oral, non-absorbable corticosteroid, after which there was a significant decrease in disease activity but no significant change in the lung:liver ratio. Inflammatory bowel disease appears to be associated with abnormal pulmonary granulocyte accumulation. It is not apparently related to disease activity but may be the result of an associated pulmonary abnormality.

Adhesiveness↗