The +1059G/C polymorphism in the C‐reactive protein (CRP) gene is associated with involvement of the terminal ileum and decreased serum CRP levels in patients with Crohn's disease

Thalmaier, D.; Dambacher, Julia; Seiderer, Julia; Konrad, Astrid; Schachinger, Veronika; Pfennig, Simone; Otte, Jan-Michel; Crispin, Alexander; Göke, Burkhard; Ochsenkühn, Thomas; Lohse, Peter; Brand, Stephan

doi:10.1111/j.1365-2036.2006.03093.x

Cited by 30 publications

(15 citation statements)

References 56 publications

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“…CRP, as a biomarker in this study for the evaluation of inflammatory status in ESRD patients, should be understood objectively. Although it has been widely accepted as a valuable and well recognized index of inflammation, some studies recently have reported that CRP partly depends upon commonly unmeasured factors (e. g. genetic traits) [18], [19]. In addition, as each patient had different conditions, such as age, complications, treatments, serum levels of phosphate, calcium, and intact parathyroid hormone, the data could be not well-controlled.…”

Section: Discussionmentioning

confidence: 99%

Inflammation Disrupts the LDL Receptor Pathway and Accelerates the Progression of Vascular Calcification in ESRD Patients

et al. 2012

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BackgroundChronic inflammation plays a crucial role in the progression of vascular calcification (VC). This study was designed to investigate whether the low-density lipoprotein receptor (LDLr) pathway is involved in the progression of VC in patients with end-stage renal disease (ESRD) during inflammation.Methods and ResultsTwenty-eight ESRD patients were divided into control and inflamed groups according to plasma C-reactive protein (CRP) level. Surgically removed tissues from the radial arteries of patients receiving arteriovenostomy were used in the experiments. The expression of tumour necrosis factor-α (TNF-α) and monocyte chemotactic protein-1 (MCP-1) of the radial artery were increased in the inflamed group. Hematoxylin-eosin and alizarin red S staining revealed parallel increases in foam cell formation and calcium deposit formation in continuous cross-sections of radial arteries in the inflamed group compared to the control, which were closely correlated with increased LDLr, sterol regulatory element binding protein-2 (SREBP-2), bone morphogenetic proteins-2 (BMP-2), and collagen I protein expression, as shown by immunohistochemical and immunofluorescent staining. Confocal microscopy confirmed that inflammation enhanced the translocation of the SREBP cleavage-activating protein (SCAP)/SREBP-2 complex from the endoplasmic reticulum to the Golgi, thereby activating LDLr gene transcription. Inflammation increased alkaline phosphatase protein expression and reduced α-smooth muscle actin protein expression, contributing to the conversion of the vascular smooth muscle cells in calcified vessels from the fibroblastic to the osteogenic phenotype; osteogenic cells are the main cellular components involved in VC. Further analysis showed that the inflammation-induced disruption of the LDLr pathway was significantly associated with enhanced BMP-2 and collagen I expression.ConclusionsInflammation accelerated the progression of VC in ESRD patients by disrupting the LDLr pathway, which may represent a novel mechanism involved in the progression of both VC and atherosclerosis.

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Section: Discussionmentioning

confidence: 99%

Inflammation Disrupts the LDL Receptor Pathway and Accelerates the Progression of Vascular Calcification in ESRD Patients

et al. 2012

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“…This may have been due to the fact that the C-reactive protein levels peak at the beginning of the disease process and then decrease rapidly. Alternatively, this may have been due to genetic polymorphism, which has been repeatedly described in humans [33,34] the microscopic and macroscopic disease scores were very closely related to the serum calprotectin levels, which suggest that this protein reflects the state of the bowel mucosa. In medical practice, a real-time assessment of disease activity during a clinical visit has paramount importance for deciding which therapeutic strategy or diagnostic imaging technique to employ (e.g., colonoscopy).…”

Section: Discussionmentioning

confidence: 92%

Serum calprotectin levels correlate with biochemical and histological markers of disease activity in TNBS colitis

Cury

Mizsputen

Versolato

et al. 2013

Cellular Immunology

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Background and aim Serum calprotectin is elevated in patients with inflammatory bowel disease (IBD). Whether it correlates other markers of disease activity is unknown. The aim of this study was to correlate serum calprotectin with biochemical and histological measures of intestinal inflammation. Materials and methods TNBS colitis was induced in wistar rats, and serial blood samples were collected at 0, 3, and 12 days. Animals were subsequently sacrificed for pathological evaluation at day 12. Serum calprotectin and cytokines were measured by ELISA. Pathologic changes were classified at the macroscopic and microscopic levels. Results TNBS colitis induced elevated serum calprotectin, TNF and IL-6 within 24 h. Levels of serum calprotectin remained elevated in parallel to persistence of loose stool and weight loss to day 12. Serum calprotectin levels correlated with serum levels of TNF-α and IL6 (p < 0.001), but not CRP. Animals with liquid stool had significantly higher levels of serum calprotectin than control animals. There was a correlation between macroscopic colitis scores, and levels of serum calprotectin. Conclusion Serum calprotectin levels correlate with biochemical and histological markers of inflammation in TNBS colitis. This biomarker may have potential for diagnostic use in patients with IBD.

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“…The overlapping function may be inferred from synergistic effects on disease risk and behavior. Variants in the Wnt pathway transcription factor ( TCF-4 ) 17 and hetero- or homozygosity for the + 1059G/C polymorphism in the C-reactive protein gene 18 have also been associated with terminal ileal involvement in CD.…”

Section: Genotype-phenotype Correlations In Ibdmentioning

confidence: 99%

How Does Genotype Influence Disease Phenotype in Inflammatory Bowel Disease?

Ananthakrishnan

Xavier

2013

Inflammatory Bowel Diseases

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Inflammatory bowel diseases (Crohn’s disease (CD); ulcerative colitis (UC)) are chronic immunologically mediated diseases of the gut. Advances in genetics have revolutionized our understanding of the pathogenesis of these conditions with 163 risk loci identified, encompassing a variety of immunologic functions. There is substantial heterogeneity in the natural history of these diseases with respect to disease onset, course, and progression to complications. There are also significant variations in response to therapies, and susceptibility to therapy-related and disease-related complications. An important need in the field is to identify predictors of disease course, complications, and likelihood of response and adverse events to allow for targeted therapeutic decision making. The genotype of an individual in constant and non-modifiable, and thus could potentially fulfill the role of important predictors of these outcomes. In this review, we discuss the existing literature on the prediction of various disease phenotypes in CD and UC utilizing underlying genotype. We also identify gaps in the literature and suggest future directions for research. There is need for large, multi-institution, and international collaborative consortia with efficient and detailed cohort accrual, phenotypic definition, genotyping, and dynamic assessments of external (for example, diet) and internal (microbiome) environment to allow us to progress towards personalized and precision medicine in the management of these complex diseases.

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The +1059G/C polymorphism in the C‐reactive protein (CRP) gene is associated with involvement of the terminal ileum and decreased serum CRP levels in patients with Crohn's disease

Abstract: SUMMARYBackground Serum C-reactive protein (CRP) levels influence the response to antitumour necrosis factor (TNF) therapies.

Cited by 30 publications

References 56 publications

Inflammation Disrupts the LDL Receptor Pathway and Accelerates the Progression of Vascular Calcification in ESRD Patients

Inflammation Disrupts the LDL Receptor Pathway and Accelerates the Progression of Vascular Calcification in ESRD Patients

Serum calprotectin levels correlate with biochemical and histological markers of disease activity in TNBS colitis

How Does Genotype Influence Disease Phenotype in Inflammatory Bowel Disease?

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