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S Vermeire

Publications and source records attributed to S Vermeire.

48 records · Page 3Linked to original sources
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↗
PubMed2000

Exclusion of linkage of Crohn's disease to previously reported regions on chromosomes 12, 7, and 3 in the Belgian population indicates genetic heterogeneity.

Susceptibility to inflammatory bowel disease (IBD) is significantly determined by genetic factors. Linkage data from genome-wide searches have identified regions on chromosomes 16, 12, 7, and 3. Our goal was to replicate these four regions in a Belgian population of IBD families. Fifty-four IBD families were studied (47 with Crohn's disease [CD] and 7 with mixed CD and ulcerative colitis, containing 79 affected sibpairs (68 CD only, 11 mixed) for the regions previously implicated to chromosomes 16, 12, 7, and 3. In this study, no evidence for linkage was found on any of the four chromosomal regions studied for either the whole IBD dataset or the CD subgroup. The multipoint maximum logarithm of odds scores were less than 0.7 for all four regions. Exclusion mapping could significantly exclude chromosomes 3, 7, and 12. Despite earlier findings, we could significantly exclude linkage of CD with previously reported regions on chromosomes 12, 7, and 3, and could not find evidence for linkage to chromosome 16. It is important to report these findings in light of the genetic heterogeneity of IBD. A genome-wide search on a larger group of affected siblings is being analyzed to detect other possible susceptibility loci in the Belgian population.

Belgium↗
PubMed1998

Structural, functional, and genetic characterization of Gastrophilus hemoglobin.

Hemoglobin of Gastrophilus intestinalis (Insecta, Diptera), was purified and characterized. At least two isoforms have been identified by isoelectrofocusing, mass spectrometry, and genomic Southern blotting. Functional studies show a high oxygen affinity due to a low ligand dissociation rate (koff = 2.4 s-1) and a relatively high autoxidation rate (t1/2 = 1.6/h). The globins were separated under denaturing conditions, and the sequence of Hb1 (Mr = 17,965 +/- 2) was determined at the protein and DNA level. The open reading frame codes for a polypeptide of 150 amino acids. Although the globin is distantly related to globins from other species, it has a low penalty score against globin templates. Freshly isolated hemoglobin was crystallized from polyethylene glycol. Crystals contain two hemoglobin molecules per asymmetric unit. Solution of the three-dimensional structure by molecular replacement could not be achieved, possibly due to the presence of three protein isoforms in the crystals. In order to determine its three-dimensional structure, G. intestinalis Hb1 was overexpressed in Escherichia coli, resulting in a fully functional molecule as confirmed by ligand binding affinity. The globin gene contains two introns at positions D7.0 and G7.0. The D7.0 intron is unprecedented, suggesting that globin gene evolution is much more complex than originally thought.

Amino Acid Sequence↗
PubMed1998

[Drug prevention of Crohn disease recurrence in the neo-terminal ileum after ileocolic resection].

Crohn's recurrence is the appearance of objective signs defined radiologically, endoscopically or pathologically of Crohn's disease in the bowel of a patient who has previously had a resection of all macroscopically diseased tissue. New lesions can be visualized endoscopically within weeks to months after ileal resection and ileocolonic anastomosis in the neoterminal ileum. The evolution of these lesions mimics the natural history of ileal Crohn's disease at the onset. If we are able to prevent recurrence of early lesions we would probably interrupt the natural course of the disease. The drugs tested until today include different 5-ASA formulations, metronidazole and budesonide. 5-ASA seems to have a limited protective effect. High dose metronidazole started immediately after surgery decreases endoscopic and symptomatic recurrence rates but is associated with a lot of side effects. Budesonide 6 mg/day o.m. reduces endoscopic recurrence after one year only in patients operated upon for inflammatory activity. Studies with immunosuppression for recurrence prevention are currently underway. Thus, today 5-ASA-formulations are recommended as general pharmaco-prophylaxis.

Anti-Inflammatory Agents↗
PubMed1997

Clustering of increased small intestinal permeability in families with Crohn's disease.

BACKGROUND & AIMS: Small intestinal permeability is increased in a proportion of patients with Crohn's disease (CD) and a subset of their healthy relatives. A primary permeability defect was postulated in the pathogenesis of the disease. The aim of this study was to identify a possible genetic pattern in the distribution of CD and/or abnormal permeability. METHODS: Differential urinary excretion of lactulose and mannitol (L/ M) in complete CD families was determined. Controls included healthy families and families with ulcerative colitis. Pedigrees were used to compare the distribution of CD and/or increased permeability. RESULTS: The L/M was significantly increased in patients with CD. Seventeen of 67 first-degree relatives (25%) had a ratio greater than the upper limit (P95 = 0.0170). Permeability results of CD families showed a highly significant familial aggregation. The lack of a genetic pattern in relation with CD and occurrence of disturbed permeability especially within generation, points toward a shared environmental factor. Five of 14 healthy spouses (36%) of patients with CD had also an increased permeability, and prevalence of increased permeability was not higher in families with known familial occurrence (P = 0.85). CONCLUSIONS: This large family study confirms an increased permeability in a subset of healthy relatives of patients with CD. However, the absence of a typical family pattern and the high prevalence in spouses is in favor of a common nongenetic factor or a subclinical disease manifestation.

Adolescent↗
PubMed1990

Independent control of the production of insulin-like growth factor I and its binding protein by cultured testicular cells.

The production of insulin-like growth factor I (IGF-I) and IGF-I binding protein (BP) was investigated in Sertoli, Leydig and peritubular cells derived from the immature rat testis and cultured in vitro. It is demonstrated that all these cells secrete not only IGF-I but also IGF-I BP. In Sertoli cells follitropin (FSH) and other agonists which increase intracellular cAMP stimulate IGF-I secretion but inhibit IGF-I BP release. The response of the BP is pronounced and very sensitive which makes it a new and useful parameter of FSH action. The calcium ionophore A23187 markedly decreases IGF-I BP production in Sertoli cells without noticeable effect on IGF-I itself. This effect can only partially be mimicked by a phorbol ester suggesting that intracellular calcium itself may play a major role in the control of IGF-I BP secretion. Peritubular cells produce high amounts of IGF-I and low amounts of IGF-I BP. Androgens do not affect the production of IGF-I or its BP neither by monocultures nor by cocultures of peritubular and Sertoli cells. In Leydig cells, lutropin (LH) and cAMP stimulate both IGF-I and IGF-I BP secretion. The production of IGF-I by Leydig-Sertoli cocultures clearly exceeds that expected from the monocultures suggesting that cell-cell interactions may also play a role in the control of testicular IGF-I production. The observation that the production of IGF-I and its activity are tightly and independently controlled supports the contention that this growth factor plays an important role in the paracrine and autocrine control of testicular function. Whether IGF-I BP increases or decreases the effects of IGF-I in the testis remains to be investigated.

Animals↗
PubMedDate not supplied

Management of ulcerative colitis and Crohn's disease.

The conventional medical treatment of IBD consists of aminosalicylates, corticosteroids, immunosuppressive drugs (azathioprine, 6-mercaptopurin, methotrexate, cyclosporin) and antibiotics. The only drugs able to modify the disease course are azathioprine, its metabolite 6-mercaptopurin and methotrexate. However, these drugs have a slow onset of action and are associated with important side-effects in some patients, necessitating the discontinuation of the drug. Moreover, up to 60% of patients do not respond to these drugs long-term. Fortunately, the management of IBD has entered a new era in the beginning of the 1990s with the development of new biological therapies, selectively blocking the inflammatory cascade. The novel molecules have arisen from the increasing knowledge about the disease pathogenesis and their production has been precipitated by the techniques of molecular biology. Infliximab, the first available biological for Crohn's disease has certainly revolutionised standard treatment. Because of its profound clinical, endoscopic and histological effects, the standard step up approach in the treatment of IBD has been challenged. A large array of new rationally designed biologicals, with a better safety profile and equally selectively acting is underway, and is likely to change our current practise even more dramatically in the next decade.

Aminosalicylic Acids↗
PubMedDate not supplied

Diagnostic approach to IBD.

Inflammatory bowel disease, with Crohn's disease and ulcerative colitis as the two main disorders, is a heterogeneous group of disorders of unknown etiology. Clinical initial presentation is sometimes misleading and causing diagnostic delay which may be important. Identification of subgroups of patients on the basis of genetic, immunologic and clinical markers will be important for exact diagnosis, but also for new drug trials. The current diagnosis depends on clinical, radiographic, endoscopic and laboratory data. The introduction of serological markers such as pANCA and ASCA will allow an increase in the diagnostic accuracy at initial diagnosis of inflammatory bowel disease and may play a role in defining subgroups of the disease.

Barium Sulfate↗
PubMedDate not supplied

Miliary tuberculosis following infliximab therapy for Crohn disease: A case report and review of the literature.

We present a case of miliary tuberculosis diagnosed 15 months after infliximab treatment despite negative screening for previous exposure to Mycobacteria on skin PPD and chest X-ray. This case shows that--although screening for TB with a skin PPD and a chest X-ray should be performed in all patients--this is not 100% effective and may be a problem in patients on concomitant immunosuppression. The clinical course of this patient further shows that in a patient treated with anti-TNF antibodies who's condition does not improve one should always be aware of the possibility of a tuberculosis infection. Even though tuberculosis is usually not rapidly fatal, the disease may show a fulminant course in immunocompromised patients.

Aged↗