Non-invasive investigation of inflammatory bowel disease

Tibble, J; Bjarnason, Ingvar

doi:10.3748/wjg.v7.i4.460

Cited by 139 publications

(98 citation statements)

References 65 publications

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“…Genetic and environmental factors were assumed to play a significant role in the etiology of the disease [1,2] . The role of genetic factors was supported by ethnical and familial differences and also by twin studies [19][20][21][22] , while the differences in incidence rates among various geographical areas suggest a role for certain environmental factors.…”

Section: Discussionmentioning

confidence: 99%

“…Inflammatory bowel disease (IBD) is a multifactorial polygenic disease with probable genetic heterogeneity. Based on this hypothesis, the disease may develop in a genetically predisposed host as a consequence of disregulated immune response to environmental factors, in particular enteric antigens, resulting in continuous immune-mediated inflammation [1,2] . However, the disease phenotype may be affected by various other factors.…”

Section: Introductionmentioning

confidence: 99%

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Striking elevation in incidence and prevalence of inflammatory bowel disease in a province of western Hungary between 1977-2001

Lakatos¹,

Mester

Erdélyi

et al. 2004

WJG

121

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Striking elevation in incidence and prevalence of inflammatory bowel disease in a province of western Hungary between 1977-2001

Lakatos¹,

Mester

Erdélyi

et al. 2004

WJG

121

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“…Increased calprotectin levels have been detected in intestinal diseases associated with inflammation such as necrotizing enterocolitis, and its quantitation provides a measure of the degree of tissue inflammation in adults with irritable bowel disease (31,32). Neopterin and calprotectin appears to play a regulatory role in the inflammatory process as well as calprotectin (33,34).…”

Section: Bowel Inflammation In Gastroschisismentioning

confidence: 99%

Biochemical Investigations of Bowel Inflammation in Gastroschisis

et al. 2006

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ABSTRACT:Neonates with gastroschisis have perivisceritis resulting from contact between the bowel and amniotic fluid. Here, we characterized the mediators involved in this inflammatory process in humans and ewes, to find a reliable marker of this process. We have diagnosed 41 cases of gastroschisis since 1995. Amniotic fluid sampled for karyotyping between 15 and 32 wk of gestation was also used to assay cytokines and inflammatory proteins. The findings were compared with those in 93 age-matched controls. Amniotic fluid cells were analyzed by means of cytology. Histologic examination of the bowel was performed when neonatal appendectomy was performed. The findings were compared with those obtained in a ewe model of gastroschisis. In gastroschisis, amniotic total protein, IL-6, IL-8, and ferritin levels were significantly higher than in controls. Gastroschisis was associated with significantly higher cell counts (mainly mononuclear cells) in amniotic fluid. At birth, macrophages were abundant in the fibrous peel covering the bowel. Similar results were obtained in the ewe model. Gastroschisis may be associated with a subchronic inflammatory process of variable intensity. This inflammation is restricted to the bowel wall and involves inflammatory cells such as macrophages, which may secrete ferritin, neopterin, and calprotectin. G astroschisis is an abdominal wall defect in which various segments of the bowel extrude through a small paraumbilical defect, usually situated on the right side. Prenatal diagnosis is usually made in the second trimester, when sonography shows bowel loops floating freely in amniotic fluid (1). Gastroschisis is rare (1/6000 to 1/10,000 pregnancies) and generally isolated. Its cause is unknown, but probably involves premature regression of the omphalomesenteric artery, leading to failure of the mesodermal components of the abdominal wall (2). The survival rate exceeds 90%. Factors of poor prognosis include intrauterine growth retardation, oligohydramnios, and the degree of perivisceritis at birth (3).Perivisceritis in this setting is due to aseptic peritonitis, probably secondary to prolonged exposure of the bowel to amniotic fluid (4). The components of amniotic fluid involved in this reaction are controversial, but we have previously obtained evidence incriminating high levels of digestive enzymes, which may aggress the gut; this is also supported by experimental findings (5,6). The inflammatory process includes edema, fibrin deposition, and cell infiltration of the bowel wall (7,8). We and Morrison et al. (9,10) have shown on restricted studies that the degree of inflammation should be used to evaluate gut damage. Here we studied a series of human cases of gastroschisis and used a ewe experimental model to examine the involvement of inflammatory cells and soluble mediators. MATERIALS AND METHODSPatients and samples. Forty-one human pregnancies complicated by fetal gastroschisis have been managed at Robert Debré Hospital since 1995. Gastroschisis was diagnosed between 15 and 32 wk of pre...

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“…The diagnosis of IBD presents some difficulties in clinical practice due to overlapping of symptoms with non-inflammatory functional bowel disorders (3). Since recognition of IBD requires extensive, invasive and expensive investigation, low-cost and noninvasive biochemical markers facilitating differential diagnosis are needed (4).…”

Section: Introductionmentioning

confidence: 99%

Clinical relevance of circulating midkine in ulcerative colitis

Krzystek−Korpacka

Neubauer

Matusiewicz

2009

Clinical Chemistry and Laboratory Medicine

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Background: Non-invasive biochemical markers are needed to support the diagnosis of ulcerative colitis (UC), an incurable disease of unknown pathology. Midkine is an angiogenic cytokine, chemotactic towards neutrophils and macrophages, and a T-regulatory cell suppressor. Methods: Serum midkine was measured immunoenzymatically in 93 UC patients and 108 healthy subjects, and evaluated with respect to disease status, endoscopic, inflammatory and angiogenic activity. The diagnostic value of midkine was compared to Creactive protein (CRP) using receiver operating characteristics (ROC) analysis. Results: Midkine was higher (p-0.0001) in inactive (199 ng/L) and active UC (351 ng/L) compared with controls (93 ng/L), and reflected disease activity (rs0.427, p-0.001). Midkine was correlated with CRP, erythrocyte sedimentation rate (ESR), leukocytes, platelets, interleukin-6, paraoxonase-1, albumin, transferrin, iron, hemoglobin, and hematocrit. Midkine correlated with angiogenic factors: vascular endothelial growth factor-A and platelet-derived growth factor-BB. As a marker of UC, midkine showed a diagnostic accuracy of 85%, sensitivity of 72%, specificity of 82%, whereas CRP showed 83%, 65% and 91%, respectively. As a marker of active UC, midkine showed a diagnostic accuracy of 87%, sensitivity of 84%, specificity of 75%, whereas CRP showed 75%, 63% and 83%, respectively. Combined assessment of midkine and CRP improved sensitivity but substantially decreased specificity. Conclusions: UC is associated with increased circulating midkine, which corresponds with clinical, endoscopic, inflammatory and angiogenic activity, and anemia. Performance of midkine as a marker of UC or active UC was comparable to that of CRP. Clin Chem Lab Med 2009;47:1085-90.

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Non-invasive investigation of inflammatory bowel disease

Cited by 139 publications

References 65 publications

Striking elevation in incidence and prevalence of inflammatory bowel disease in a province of western Hungary between 1977-2001

Striking elevation in incidence and prevalence of inflammatory bowel disease in a province of western Hungary between 1977-2001

Biochemical Investigations of Bowel Inflammation in Gastroschisis

Clinical relevance of circulating midkine in ulcerative colitis

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