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PubMed1996

Relationship between inflammatory hepatic disease and inflammatory bowel disease, pancreatitis, and nephritis in cats.

OBJECTIVE: To determine whether cats with inflammatory hepatic disease had concurrent inflammatory bowel disease (IBD), pancreatitis, or chronic interstitial nephritis. DESIGN: Prospective case series. SAMPLE POPULATION: 78 tissue sections of liver, intestine, pancreas, and kidney from cats that had previous necropsy examinations at the teaching hospital. PROCEDURE: We reviewed histologic sections of liver, intestine, pancreas, and kidney from cats that had previous necropsy examinations and determined the prevalence of lymphocytic portal hepatitis, cholangiohepatitis, IBD, pancreatitis, and chronic interstitial nephritis, and the relationship among them. RESULTS: 36 cats had lymphocytic portal hepatitis, 18 had cholangiohepatitis, and 24 did not have inflammatory hepatic disease. The prevalence of IBD (10/36; 28%) and pancreatitis (5/36; 14%) in cats with lymphocytic portal hepatitis was not significantly different from cats without inflammatory hepatic disease. The prevalence of IBD (15/18; 83%) and pancreatitis (9/18; 50%) was greater (P < 0.05) for cats with cholangiohepatitis, compared with cats without inflammatory hepatic disease. Thirty-nine percent of cats (7/18) with cholangiohepatitis had IBD and pancreatitis. Evidence of IBD in association with cholangiohepatitis was characterized by infiltration of lymphocytes and plasma cells into the lamina propria; however, neutrophilic infiltrates also were found in 6 of 15 (40%) cats with cholangiohepatitis. Pancreatitis was mild in all cats. CLINICAL IMPLICATIONS: Cats with a diagnosis of cholangiohepatitis should be evaluated for IBD and pancreatitis.

Age Distribution↗
PubMedDate not supplied

History of infectious bursal disease in the U.S.A.--the first two decades.

Infectious bursal disease (IBD) emerged in 1957 as a clinical entity responsible for acute morbidity and mortality in broilers on the Delmarva peninsula. The condition spread rapidly and was recognized throughout the U.S. broiler and commercial egg production areas by 1965. Early attempts to isolate the etiologic agent were impeded by a lack of specific-pathogen-free (SPF) eggs and by deficiencies in viral and serologic techniques. By 1967, the highly infectious nature of the agent was recognized. Reliable methods were developed to isolate the virus in embryonated eggs and to adapt it to tissue culture. The agent was characterized as a virus belonging to a new taxonomic group in 1976. The immunosuppressive property of IBD virus was first recognized in 1970 and was confirmed in structured trials in 1976. An early method of control involved planned infection of chickens. This technique lowered IBD mortality but often resulted in immunosuppression and further dissemination of field virus. A live attenuated vaccine was then developed, based on mild field isolates passaged in SPF eggs. This vaccine was federally licensed as the first of its kind for interstate use in 1968. It remains widely used today in breeders as a primer and in the control of very virulent IBD in many countries. The first two decades following emergence of IBD were characterized by close cooperation among scientists in academia, the biologics industry, and the USDA. By 1976, mortality caused by IBD was effectively controlled by vaccination. However, the more subtle effects of immunosuppression and the tremendous economic impact of the disease were just starting to be appreciated. Recognition of Delaware variants in the mid-1980s and emergence of very virulent forms of the condition in Europe and Asia beginning in 1989 attest to the continuing importance of IBD.

Animals↗
PubMed1997

Optimizing therapy for inflammatory bowel disease.

This review focuses on current developments in the major categories of therapy used in the management of inflammatory bowel disease (IBD). Conventional corticosteroids, although a mainstay of the acute treatment of IBD for many years, have many drawbacks, including a variety of side effects--particularly with chronic use. Budesonide appears to be relatively safe and at least moderately effective in inducing remission in active distal ulcerative colitis (UC) and Crohn's disease. Aminosalicylates, both oral and topical, have proven useful in managing mild-to-moderate active UC and mild active Crohn's disease, as well as in maintaining remission. Data from recent trials suggest that higher doses of mesalamine are generally more efficacious than lower doses. In addition, a combination of oral and rectal formulations may succeed when one route, alone, is not successful. The immunomodulatory agents azathioprine, 6-mercaptopurine, and methotrexate have been shown to be effective in the treatment of IBD and are now widely accepted as valuable parts of the therapeutic armamentarium. Cyclosporine, although effective, is associated with many toxicities, and patients must be monitored closely in centers experienced with this agent. Clinical trials of IL-10, IL-11, and anti-TNFalpha have also shown promise. Antibiotics have been used empirically for many years in the treatment of IBD. Larger clinical trials are warranted to explore the potential efficacy of antibiotic therapy. This has been accomplished with metronidazole in Crohn's disease, and other antibiotic trials are underway at this time. The investigational agents acemannan, heparin, and transdermal nicotine have also shown variable degrees of promise as possible therapies for IBD. Despite the variety of agents available for the treatment of IBD, none is ideal or universally accepted. Ongoing research into the well-established therapeutic agents, as well as novel drugs with more precise targets, may contribute to the design of a more nearly optimal regimen for IBD in the not-too-distant future.

Adrenal Cortex Hormones↗
PubMed1998

[Comparison of endoscopy, radiology and scintigraphy with Tc-99m-exametazine labeled leukocytes and In-111 labeled human polyclonal immunoglobulin G in the diagnosis of inflammatory bowel disease].

BACKGROUND: The 99mTc-exametazine labelled leukocytes (99mTc-WBC) scintigraphy is an established method for the inflammatory bowel disease (IBD) diagnosis, but the labelled procedure is a large and laborious process. The 111In-labelled human polyclonal immunoglobulin G (111In-IgG) can be an alternative in the non invasive IBD diagnosis. PATIENTS AND METHODS: Thirty-four patients routinely referred for investigation of IBD were studied. The 99mTc-WBC and 111In-IgG were simultaneously injected and images were obtained at 30 min, 3 and 24 h post-injection. The diagnostic was established by histology of endoscopy and/or surgery samples. Images were blindly evaluated by two experienced observers who only knew of the clinical suspicion of IBD. IBD was confirmed in 27 patients (17 with Crohn's disease [CD] and 10 with ulcerative colitis [UC]). RESULTS: Sensitivity, specificity and accuracy were 88.5, 100 and 90.3% respectively for endoscopy, 73.7, 75 and 73.9% for radiology, 59.3, 85.7 and 64.7% for 111In-IgG scan and 96.3, 85.7 and 94.1% for 99mTc-WBC scan. In the diagnosis of CD involvement of small bowel, the 99mTc-WBC scan identified 9/11 patients with confirmed disease, whereas the 111In-IgG scan diagnosed only four of them. In the evaluation of colonic disease, the 99mTc-WBC scan correctly diagnosed 21/22 confirmed patients, being the 111In-IgG scan positive in 13 of them. As far as disease extension concerned, the 99mTc-WBC demonstrated a statistically significance rather number of disease segments than endoscopy, radiology and 111In-IgG scan. CONCLUSIONS: The 99mTc-WBC was an effective method in the diagnosis of suspected IBD patients, both in the evaluation of small bowel disease and colonic disease, with slightly best results for colonic disease, whereas the 111In-IgG scan seems to have no utility neither in diagnosis nor in extension evaluation of IBD.

Adolescent↗
PubMed2004

"Best practice" in inflammatory bowel disease: an international survey and audit.

Background: An observational study was conducted at eight university and four district hospitals in eight countries collaborating in clinical and epidemiological research in inflammatory bowel disease (IBD) to compare European health care facilities and to define current "best practice" with regard to IBD. Methods: The approach used in this multi-national survey was unique. Existing quality norms, developed for total hospital care by a specialized organization, were restricted to IBD-specific care and adapted to the frame of reference of the study group. In each center, these norms were surveyed by means of questionnaires and professional audits in all participating centers. The collected data were reported to the center, compared to data from other hospitals, and used to benchmark. Group consensus was reached with regard to defining current "best practice". Results: The observations in each center involved patient-oriented processes, technical and patient safety, and quality of the medical standard. Several findings could be directly implemented to improve IBD care in another hospital (benchmarks). These included a confidential relationship between health care worker(s) and patients, and availability of patient data. Conclusions: The observed benchmarks, in combination with other subjectively chosen "positive" procedures, have been defined as current "best practice in IBD", representing practical guidelines towards better quality of care in IBD.

Journal Article↗
PubMed2001

Cancer risk in patients with inflammatory bowel disease: a population-based study.

BACKGROUND: The objective of the current study was to determine the incidence of cancer among persons with inflammatory bowel disease (IBD) and to compare these incidence rates with those of the non-IBD population using population-based data from the administrative claims data of Manitoba's universal provincial insurance plan (Manitoba Health). METHODS: IBD patients were matched 1:10 to randomly selected members of the population without IBD based on year, age, gender, and postal area of residence. The incidence of cancer was determined by linking records from the IBD and non-IBD cohorts with the comprehensive Cancer Care Manitoba registry. Incidence rates and rate ratios (IRR) were calculated based on person-years of follow-up (Crohn's disease = 21,340 person-years and ulcerative colitis [UC] = 19,665 person-years) for 1984-1997. RESULTS: There was an increased IRR of colon carcinoma for both Crohn disease patients (2.64; 95% confidence interval [95% CI], 1.69-4.12) and UC patients (2.75; 95% CI, 1.91-3.97). There was an increased IRR of rectal carcinoma only among patients with UC (1.90; 95% CI, 1.05-3.43) and an increased IRR of carcinoma of the small intestine only in Crohn disease patients (17.4; 95% CI, 4.16-72.9). An increased IRR of extraintestinal tumors was observed only for the liver and biliary tract in both Crohn disease patients (5.22; 95% CI, 0.96-28.5) and UC patients (3.96; 95% CI, 1.05-14.9). There was an increased IRR of lymphoma for males with Crohn disease only (3.63; 95% CI, 1.53-8.62), and this finding did not appear to be related to use of immunomodulatory therapy. Compared with controls, Crohn's disease was associated with an increased risk of cancer overall, but UC was not. CONCLUSIONS: There appear to be similar increased risks for developing colon carcinoma and hepatobiliary carcinoma among patients with Crohn disease and UC. There is an increased risk of developing rectal carcinoma in UC patients, an increased risk of developing carcinoma of the small bowel in Crohn disease patients, and an increased risk of developing lymphoma among males with Crohn disease.

Adult↗
PubMed2004

Inflammatory bowel diseases as an intermediate stage between normal and cancer: a FTIR-microspectroscopy approach.

Elucidation of the evolution of inflammatory bowel disease (IBD) to cancer by clinical symptoms and histopathology of biopsies is important. Fourier transform infrared microspectroscopy (FTIR-MSP) has shown promise as a diagnostic tool for distinction of normal and cancer cells and tissues. In the present work, FTIR-MSP is used to evaluate IBD cases and to study the IR spectral characteristic with respect to cancer and normal tissues from formalin-fixed colonic biopsies from patients. Specific regions of the spectra were analyzed by statistical tools to study variations in metabolites that signified changes between the two pathological conditions: IBD and cancer. IBD tissues can be grouped with cancer or normal tissue using certain parameters such as phosphate content and RNA/DNA ratio as calculated from the spectra and show intermediate levels with regard to these metabolites. Further classification of the spectra by cluster analysis indicated which cases of Crohn's disease (3 of 10 cases) or ulcerative colitis (7 of 10 cases) were more likely to progress to cancer. The study exhibits that FTIR-MSP can detect gross biochemical changes in morphologically identical IBD and cancer tissues and suggest which cases of IBD may require further evaluation for carcinogenesis.

Cell Transformation, Neoplastic↗
PubMed2004

Commentary: the role of the IL-18 system and other members of the IL-1R/TLR superfamily in innate mucosal immunity and the pathogenesis of inflammatory bowel disease: friend or foe?

Crohn's disease and ulcerative colitis are examples of inflammatory bowel disease (IBD), and are multifaceted chronic autoimmune disorders with unknown etiology; to date, there is no known cure. IBD is thought to occur as a result of an inappropriate immune response to environmental factors in a genetically predisposed host, and it has become increasingly clear that cytokines play an important role in this process. In recent years, several groups have provided evidence that IL-18 is significantly up-regulated during the course of chronic intestinal inflammation and appears to play a pivotal role in the pathogenesis of human IBD, particularly in Crohn's disease. IL-18 is a pleiotropic cytokine with several biological functions, but is most commonly associated with its ability to synergistically induce the expression of IFN-gamma. However, although IL-18 has been extensively studied in both human IBD as well as in murine models of colitis, no definitive function of IL-18 during the initiation and perpetuation of chronic gut inflammation has been firmly established, and its precise role in the pathogenesis of IBD has yet to be determined. In light of the recent observation that the transcription factor interferon regulatory factor-1 has the ability to regulate the functional activity of IL-18, and concomitantly disease severity, in a murine model of colitis through altered expression of its endogenous inhibitor, IL-18-binding protein, this commentary will review what is currently known regarding the role of IL-18 in normal mucosal immunity and during the pathogenesis of IBD.

Animals↗
PubMed2005

Characterization of genotype-phenotype relationships and stratification by the CARD15 variant genotype for inflammatory bowel disease susceptibility loci using multiple short tandem repeat genetic markers.

The classification of ulcerative colitis (UC), Crohn disease (CD), and indeterminate colitis (IC) as forms of inflammatory bowel disease (IBD) is based on clinical, radiological, and histological criteria. The genetic basis of IBD is well founded, and susceptibility loci have been identified on several different chromosomes. We aimed to define genotype-phenotype relationships and interactions with the IBD susceptibility gene CARD15for various IBD susceptibility loci (IBD1, IBD2, IBD5, IBD6, IBD7, and chromosome 4) by characterizing previously described peak LOD score short tandem repeat (STR) markers. The study population consisted of 484 severely affected Caucasian patients with IBD, 144 healthy controls, and 348 nonaffected first-degree relatives of IBD patients. Associations were defined with the use of population- and family-based methodology. Correction for multiple testing was performed with a method based on an experimental false discovery rate. We provide novel evidence to show that IBD2 is involved in susceptibility to IC and terminal ileal CD in this population, with overrepresentation of IBD2 STR D12S83 (GenBank Z16592.1) allele 7 (g.49_60del[CA](6)) in IC (q = 0.038, P = 0.014) and underrepresentation of allele 8 (g.51_60del[CA](5)) in terminal ileal CD (q = 0.038, P = 0.016). The association of IBD2 with IC was confirmed by family-based testing. We also provide novel evidence to show that IBD5 is involved in susceptibility to IC and colonic/ileocolonic CD in this population, with overrepresentation of IBD5 STR D5S1984 (GenBank Z52623.1) allele 5 (g.183_186del[CA](2)) in both IC (q = 0.040, P = 0.005) and colonic/ileocolonic CD (q = 0.040, P = 0.004). Evidence is also given for potential interactions between CARD15and IBD2/IBD5. Other findings include an association of IBD2 with UC, and an association of IBD1 with terminal ileal and colonic/ileocolonic CD.

Adult↗
PubMed2007

Estimation of the period prevalence of inflammatory bowel disease among nine health plans using computerized diagnoses and outpatient pharmacy dispensings.

BACKGROUND: There are few contemporary estimates of prevalence rates for inflammatory bowel disease (IBD) in diverse North American communities. METHODS: We estimated the period prevalence of IBD for January 1, 1999, through June 30, 2001, among 1.8 million randomly sampled members of nine integrated healthcare organizations in the US using computerized diagnoses and outpatient pharmaceutical dispensing. We also assessed the positive predictive value (PPV) and sensitivities of 1) the case-finding algorithm, and 2) the 30-month sampling period using medical chart review and linkage to a 78-month dataset, respectively. RESULTS: The PPV of the case-finding algorithm was 81% (95% confidence interval [CI], 78-87) and 84% (95% CI, 79-89) in two different organizations. In both, the sensitivity of the optimal algorithm, compared with the most inclusive, exceeded 90%. The sensitivity of the 30-month sampling period compared with 78 months was 61% (95% CI, 57-64) in one organization. Applying a slightly more sensitive case-finding algorithm, the average period prevalence of IBD across the nine organizations, standardized to the age- and gender-distribution of the US population, 2000 census, was 388 cases (95% CI, 378-397) per 100,000 persons (range 209-784 per 100,000; average follow-up 26 months). The prevalence of Crohn's disease, ulcerative colitis, and unspecified IBD was 129, 191, and 69 per 100,000, respectively. CONCLUSIONS: The observed average prevalence was similar to prevalence proportions reported for other North American populations (369-408 per 100,000). Additional research is needed to understand differences in the occurrence of IBD among diverse populations as well as practice variation in diagnosis and treatment of IBD.

Adolescent↗
PubMed2007

Changes in clinical characteristics, course, and prognosis of inflammatory bowel disease during the last 5 decades: a population-based study from Copenhagen, Denmark.

BACKGROUND: It remains uncertain whether the increasing incidence of inflammatory bowel disease (IBD) during the last decades has been accompanied by an alteration in the presentation, course, and prognosis of the disease. To answer this question, 3 consecutive population-based IBD cohorts from Copenhagen, Denmark (1962-2005), were assessed and evaluated. METHODS: Phenotype, initial disease course, use of medications, cumulative surgery rate, standardized incidence ratio of colorectal cancer (CRC), and standardized mortality ratio (SMR) were compared in the 3 cohorts, which had a total of 641 patients with Crohn's disease (CD) and 1575 patients with ulcerative colitis (UC). RESULTS: From 1962 to 2005, the proportion of IBD patients suffering from CD increased (P < 0.001), time from onset of symptoms to diagnosis of CD decreased (P = 0.001), and median age at diagnosis of UC increased (P < 0.01). The prevalence of upper gastrointestinal involvement and pure colonic CD varied significantly between cohorts. UC patients diagnosed in the 1990s had a higher prevalence of proctitis, received more medications, and had a milder initial disease course than did previous patients. The surgery rate decreased significantly in CD but not in UC. The risk of CRC in IBD was close to expected over the entire period, whereas the mortality of patients with CD increased (overall SMR, 1.31; 95% CI, 1.07-1.60). CONCLUSIONS: Despite variations in the presentation and initial course of IBD during the last 5 decades, its long-term prognosis remained fairly stable. Treatment of IBD changed recently, and future studies should address the effect of these changes on long-term prognosis.

Adolescent↗
PubMed2007

Effect of the anti-tumor necrosis factor-alpha antibody infliximab on the ex vivo mucosal matrix metalloproteinase-proteolytic phenotype in inflammatory bowel disease.

BACKGROUND: Previous studies have shown an upregulation of matrix metalloproteinases (MMPs) in intestinal tissue of patients with inflammatory bowel disease (IBD) and significant clinical improvement after administration of the anti-TNF-a antibody infliximab. The aims of our study were to determine expression and secretion of MMP-1, -2, -3, -9, and their inhibitors TIMP-1, -2 by IBD versus control intestinal mucosa ex vivo and to assess the regulatory capacity by infliximab of the proteolytic phenotype. METHODS: Intestinal mucosal explants from 20 IBD and 15 control patients were cultured with or without infliximab and/or the T-cell activator pokeweed mitogen (PWM). Explants and culture supernatants were analyzed for MMPs, TIMPs, and TNF-alpha protein, activity and/or mRNA levels. All patients were genotyped for functional TNF-alpha, MMP, and TIMP single nucleotide polymorphism (SNP) loci. RESULTS: Expression of MMP and TIMP protein/activity in basal medium was higher in IBD versus control explants. Dependent on genotype at SNP loci, infliximab downregulated MMP-1, -3, and -9 relative to TIMP-1 and -2 and also decreased MMP-1 and -3 activities, while PWM enhanced these levels, partly counteracted again by infliximab. The expression of MMP-2 relative to TIMP did not change by treatment with infliximab and/or PWM. CONCLUSIONS: The high expression of MMPs in patients with IBD suggests a role for these proteinases in the pathogenesis of this disease. Infliximab seems to induce a genotype-associated matrix protective phenotype, which may contribute to the observed therapeutic efficacy of this drug in IBD, particularly at the mucosal surface.

Adolescent↗
PubMed2007

Long-standing colonic inflammation is associated with a low prevalence of diverticuli in inflammatory bowel disease patients.

BACKGROUND: Diverticulosis is associated with high intracolonic pressure and a weakened bowel wall. Chronic colitis is characterized by liquid stools suggestive of low intracolonic pressure and a thickened bowel wall. Therefore, the aim of this study was to assess the prevalence of diverticulosis in colitis patients. METHODS: Colonoscopy results of patients with inflammatory bowel disease (IBD)-associated colitis older than 50 years were retrospectively evaluated and compared with those of patients who underwent screening colonoscopy. Only patients with biopsy-proven disease, disease duration of more than 5 years, and disease beyond the distal 20 cm were included. RESULTS: In all, 1037 patients were diagnosed by colonoscopy as suffering from IBD-associated colitis between 1987-2005. After exclusion of patients who did not meet the inclusion criteria the study population consisted of 314 IBD patients and 1023 age-matched control patients. A significantly higher percent of diverticuli was detected in the control group compared with the IBD group (15% versus 3.5%, P < 0.001). No significant difference in the prevalence of diverticuli was detected between the three subtypes of IBD patients (2% in ulcerative colitis versus 4.7% in Crohn's colitis versus 7.6% in indeterminant colitis). Neither disease duration nor the specific colonic segment involved had a significant influence on the prevalence of diverticulosis. CONCLUSIONS: Long-standing colonic inflammation in IBD patients is associated with a lower prevalence of diverticuli.

Colitis↗
PubMed2007

5-Aminosalicylic acid therapy and the risk of colorectal cancer among patients with inflammatory bowel disease.

BACKGROUND: Patients with inflammatory bowel disease (IBD) affecting the colon are at increased risk of developing colorectal cancer (CRC). Published data are conflicting about whether 5-aminosalicylic acid (5-ASA) has chemopreventive properties against IBD-related carcinogenesis. The objective of this observational study was to determine if an association between 5-ASA therapy and CRC risk exists in IBD patients. METHODS: Adult patients with a new CRC diagnosis (n = 18,440) were identified from 2 large administrative claims databases. For each case, 20 control patients with no record of CRC diagnosis or bowel surgery (n = 368,800) were identified. RESULTS: An IBD diagnosis was associated with a 6- to 7-fold increased risk of CRC (ulcerative colitis, crude odds ratio [OR] = 6.72, 95% CI, 5.79-7.81; Crohn's disease, crude OR = 6.60, 95% CI, 5.56-7.82). Among patients with IBD (364 CRC cases, 1172 controls), exposure to 5-ASA therapy of any dose or duration during the 12 months before CRC diagnosis was not associated with a reduced risk of CRC (OR = 0.97; 95% CI, 0.77-1.23). However, there was a trend toward a decreased risk of CRC with increasing number of mesalamine prescriptions in the previous year, though statistical significance was not achieved (trend P = 0.08). CONCLUSIONS: Treating IBD patients with 5-ASA medications was not found to have a protective effect against colitis-related CRC when assessed over a short period of exposure.

Aged↗
PubMed2000

Familial and sporadic inflammatory bowel disease: different entities?

The strongest risk factor for developing inflammatory bowel disease (IBD) is having a relative with the disease. Familial IBD may be one homogeneous subgroup, phenotypically different from sporadic IBD. Several observations support a role for familiarity in disease site and behavior, particularly in Crohn's disease (CD), but published findings do not all concur. Early disease onset is often found in children with IBD who have a parent with the disease. Genetic anticipation may explain this finding but other explanations and/or observational biasis are more likely. Location and type may differ between familial and sporadic CD cases: family studies report many cases involving both small bowel and colon, and few cases of colonic disease alone, although such features may be secondary to early age at onset. Most studies found no effect of positive family history on severity and course of CD. In ulcerative colitis (UC), phenotypic differences between familial and sporadic cases appear to be limited, but little data are available for analysis. No difference has been found between familial and sporadic IBD as far as disease markers such as pANCA, ASCA, or intestinal permeability are concerned. In conclusion, the only message available for clinical practice is that the relative risk of IBD in first-degree relatives is increased by a factor of 10-15 compared with the general population. Families should not receive genetic counseling/information about age at onset and disease severity.

Genetic Predisposition to Disease↗
PubMed2001

Decreased CD44v6 expression in lamina propria lymphocytes of patients with inflammatory bowel disease.

Splice variants of the glycoprotein CD44 are transiently expressed on lymphocytes during T cell activation. Increased expression of CD44v6 on peripheral blood lymphocytes (PBL) of patients with inflammatory bowel disease (IBD) was described recently. The aim of this study was therefore to characterize CD44v6 expression on CD4(+) lamina propria lymphocytes (LPL) of patients with active IBD in comparison to controls. CD44v6 expression on CD4(+) LPL (n = 19) of controls and patients with active IBD (Crohn's disease n = 14, ulcerative colitis n = 15) was analyzed by flow cytometry and compared to that on autologous PBL. Thereby, in vitro regulation of CD44v6 on LPL and PBL via CD3 and CD2 and the costimulatory signal B7-1 was examined. In addition, the role of protein kinase C (PKC) in CD44v6 expression was tested. CD44v6 expression was increased in CD4(+) LPL (median, 45%) compared to PBL (median, 38%). Surprisingly, in IBD CD44v6 was downregulated on CD4(+) lamina propria T cells, irrespective of their state of inflammation (median, 28%). CD44v6 expression on LPL was not upregulated upon CD3 activation alone but following costimulation with B7-1. However, CD2-mediated T cell activation sufficiently induced upregulation of CD44v6 on LPL and PBL. In our study, downregulation of CD44v6 on LPL of patients with IBD was not due to defective PKC activation. Taken together, these data indicate that decreased CD44v6 expression on LPL in IBD might be a feature of an inappropriate costimulatory signal in T cell activation.

Adult↗
PubMed1996

Familial aggregation of inflammatory bowel disease in a Mediterranean area.

To evaluate familial aggregation of inflammatory bowel disease (IBD) in the Mediterranean area and to estimate the disease risk in first degree relatives. 427 patients with IBD were consecutively interviewed in order to obtain a complete pedigree of first degree relatives. Sufficient information was obtained in 98% of 2,685 family members. The prevalence ratio of IBD in family members was estimated and compared to the prevalence ratio of IBD in general population; the ratio was then standardized by age since the prevalence of the disease is age-dependent. The lifetime risk was assessed by the Kaplan Meier method. Thirty index cases (7%) had at least one affected first degree relative. As compared with the general population, first degree relatives of the 427 patients with IBD had a 4.38-fold increase in the age corrected risk of having the same disease. The kaplan-Meier curve showed a higher risk at 25 years of age for offsprings (3%) than for parents (1%) and siblings (1%) whereas the crude ratio showed a higher risk for siblings (1.9%) compared to parents (0.8%) and offsprings (1%). In the Mediterranean area, the familial prevalence of IBD is higher than in the general population and comparable to North European rates.

Adolescent↗
PubMed1995

Simultaneous administration of 111In-human immunoglobulin and 99mTc-HMPAO labelled leucocytes in inflammatory bowel disease.

Technetium-99m hexamethylpropylene amine oxime (HMPAO) labelled leucocytes and indium-111 polyclonal immunoglobulin (IgG) were simultaneously injected into a group of 27 patients routinely referred for the investigation of inflammatory bowel disease (IBD). Ten-minute anterior abdomen and tail on detector views were obtained at 30 min, 4 h and 24 h p.i. of both tracers. The diagnosis of IBD was obtained in all cases by endoscopy with biopsy and/or surgery. Images were blindly evaluated by two experienced observers who only knew of the clinical suspicion of IBD. IBD was confirmed in 20 patients (12 with Crohn's disease and eight with ulcerative colitis). Sensitivity, specificity and accuracy were 100%, 85% and 96% respectively for labelled leucocytes and 70%, 85% and 74% for IgG. Both IgG and leucocyte scans were normal in six out of seven patients in whom a diagnosis of IBD was excluded; the remaining patient, with ischaemic colitis, was falsely positive with both agents. As far as disease extension is concerned, the IgG study localized 27 diseased segments, whereas 49 were seen with the leucocyte study. Eighty-four segments were normal and 25 showed tracer uptake with both agents. Twenty-four were positive only with the leucocyte study and two were positive only with the IgG study. Agreement between the agents was 80.7%. These results confirm that 111In-human polyclonal scintigraphy is less sensitive than 99mTc-HMPAO scintigraphy both for the diagnosis of IBD and in the evaluation of disease extension. Nevertheless, if leucocyte labelling is not available, labelled IgG can be used only for diagnostic purposes.

Adolescent↗