Inflammatory changes of the gastric mucosa and serum concentration of chosen growth factors in children

Maciorkowska, Elżbieta; Marcinkiewicz, S; Kaczmarski, Maciej; Kemonä, A

doi:10.2478/v10039-010-0007-6

Cited by 5 publications

(5 citation statements)

References 16 publications

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“…( 13,20,21 ) The VEGF may have originated from gastric cancer cells ( 8 ) and the production and secretion may be increased with the progression of the cancer, but whether the cancer is intestinal or diffuse may have little influence on the VEGF level. It has been reported that H. pylori infection elevates serum VEGF level, ( 22,23 ) which can be a reason for the elevated VEGF level in gastric cancer patients. However, no association was observed between H. pylori serology and VEGF, sVEGFR‐1 or sVEGFR‐2 level in controls of this study.…”

Section: Discussionmentioning

confidence: 99%

Reduced serum vascular endothelial growth factor receptor‐2 (sVEGFR‐2) and sVEGFR‐1 levels in gastric cancer patients

et al. 2011

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The relationship between gastric cancer and serum vascular endothelial growth factor receptor‐1 (sVEGFR‐1) and sVEGFR‐2, which are soluble form receptor proteins of vascular endothelial growth factor (VEGF), has not been extensively studied. VEGF, sVEGFR‐1 and sVEGFR‐2 were measured in the sera obtained before surgical operation from 164 gastric cancer patients and from 164 healthy controls matched for age and gender. Compared with controls, the cases showed elevated VEGF (P < 0.01) and reduced sVEGFR‐1 (P = 0.07) and sVEGFR‐2 (P = 0.02). The difference in VEGF levels was small among men and when the outcome was early cancer. The difference in sVEGFR‐1 levels was significant or borderline significant only in men and when the outcome was diffuse type cancer. The difference in sVEGFR‐2 levels was significant only in men and when the outcome was advanced or diffuse type cancer. The sensitivities and specificities of VEGF, sVEGFR‐1 and sVEGFR‐2 were all approximately 60%. For diffuse type cancer, sVEGFR‐2 showed a sensitivity of 62.4% and a specificity of 63.4%, which was similar to serum pepsinogen. In conclusion, elevated VEGF and reduced sVEGFR‐1 and sVEGFR‐2 in serum are characteristic of gastric cancer patients, and the value of serum sVEGFR‐2 in the diagnosis of diffuse type gastric cancer should be further evaluated. (Cancer Sci 2011; 102: 866–869)

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Section: Discussionmentioning

confidence: 99%

Reduced serum vascular endothelial growth factor receptor‐2 (sVEGFR‐2) and sVEGFR‐1 levels in gastric cancer patients

et al. 2011

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“…About 11% of the US population are experiencing this problem. [1][2][3][4][5] Associated with virulence, this bacteria is able to produce a kind of protein that has long been regarded as a marker. This protein known as CagA which is also associated with increased inflammation, cell proliferation, and gastric mucosal metaplasia.…”

Section: Introductionmentioning

confidence: 99%

“…This protein known as CagA which is also associated with increased inflammation, cell proliferation, and gastric mucosal metaplasia. 5 Vascular endothelial growth factor (VEGF), a well-known angiogenic factor, plays a role in many processes in the formation of new mucosal tissue after H. pylori inflammation by stimulated the formation of angiogenesis, which are aimed to supply the nutrients and oxygen to newly formed tissues. Many studies have shown that levels of VEGF increased in cases of malignancy, including gastric tumors.…”

Section: Introductionmentioning

confidence: 99%

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Vascular endothelial growth factor (VEGF) serum levelsof patients with Helicobacter pylori gastritis with cytotoxin-associated gene A positive (CagA + )status

Siregar

Sungkar

2019

JMedScie

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Helicobacter pylori (H.pylori) is an agent that causes gastritis and the ulcer of gaster, which are ultimately caused gastric tumors. The prevalence is about 80% average in developing country and 20-50 % in developed countries. One of the virulence factor is cytotoxin-associated gene A (CagA) that plays a role in the inflammation process, cell proliferation and metaplasia in gastric mucosa. Vascular endothelial growth factor (VEGF) is one of angiogenic factors that plays a role in the process of making new mucosal tissue after the inflammation by H.pylori. The escalation of VEGF expression levels contribute to the beginning of gastric carcinogenesis. The study was aimed to analyze of VEGF serum levels between CagA(+) and CagA(-) in patients with H.pylori gastritis. Cross sectional study was conducted on 30 patients with H.pylori gastritis after conducted gastroscopy, biopsy and CLO test, which were continued with VEGF serum examination using ELISA test and perfomed PCR test to determine the CagA status. The data was analyzed with SPSS 22 version and p value <0.05 was considered significant. The results of this study were18 men (60 %) and 12 women (46%) from 30 total subjects, with a median age average was 53.5 years old. Majority ethnic was Batak with 16 subjects (53.3%). Helicobacterpylori gastritis with CagA(+) was about 21 subjects (70%) and H.pylori gastritis with CagA(-) was about 9 subjects (30%). We found that median VEGF serum levels of patients with H.pylori gastritis with CagA(+)[480.3 pg/dL (115.5-2185.2)] significantly higher compared to that with CagA(-) [291.1 pg/dL (158.4-556.7)] (p<0.05). In conclusion, the VEGF serum levels of patients with H.pylori gastritis with CagA(+) is higher compared to that with CagA(-).

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“…Επιπρόσθετα, οι αυξημένες συγκεντρώσεις τόσο του TGF-α όσο και του TGF-β1 έχουν παρατηρηθεί σε διάφορες φλεγμονώδεις καταστάσεις, αντανακλώντας πιθανώς έναν μηχανισμό αντιρρόπησης στην εξέλιξη της φλεγμονής (421)(422)(423)(424). Σύμφωνα με τα παραπάνω, ο TGF-α και ο TGF-β1, δρώντας ως σημαντικές αντιφλεγμονώδεις κυτταροκίνες, παρουσιάζουν εκεσεσημασμένη έκκριση ώστε να αντισταθμίσουν την φλεγμονή που χαρακτηρίζει την ΕΥΑ.…”

Section: μετατρεπτικοί αυξητικοί παράγοντες Tgf-α και Tgf-β1 και ευαunclassified

Ενδομήτρια Υπολειπόμενη Αύξηση Και Ανοσολογικοί Παράγοντες Του Γαστρεντερικού

Λιόση¹

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Objective: To determine cord blood levels of calprotectin, a protein that is increased in inflammatory states and released by activated neutrophils has apoptosis-inducing activity. Materials and methods: Cord-blood calprotectin concentrations were determined in intrauterine-growth-restricted (IUGR, usually associated with increased neutrophil activation and apoptosis, ns50) and appropriate-for-gestationalage (AGA, ns110) single full-term pregnancies, and were correlated with perinatal demographic parameters. Results: No significant differences exists between the IUGR and AGA groups, implying that calprotectin at birth does not reflect increased neutrophil activation and apoptosis expected in IUGR. However, in IUGRs, calprotectin concentrations increased with every gestational week wbs45.3, 95% confidence interval (CI): 13.5-77.1, Ps0.006x, suggesting concomitant up-regulation of neutrophil activation and apoptosis. A combined group showed significantly decreased calprotectin concentrations in cesarean sections wbs-74.5, 95% CI: -115.2-(-33.9), P-0.001x, pointing to excessive inflammatory response in vaginal deliveries. Finally, birth weight, customized centile, gender, maternal age and parity do not impact on cord blood calprotectin concentrations. Conclusions: Cord blood calprotectin concentrations at term are independent of intrauterine growth, gender, parity and maternal age and probably do not reflect the increased neutrophil activation and excessive apoptosis expected in IUGR.

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Inflammatory changes of the gastric mucosa and serum concentration of chosen growth factors in children

Cited by 5 publications

References 16 publications

Reduced serum vascular endothelial growth factor receptor‐2 (sVEGFR‐2) and sVEGFR‐1 levels in gastric cancer patients

Reduced serum vascular endothelial growth factor receptor‐2 (sVEGFR‐2) and sVEGFR‐1 levels in gastric cancer patients

Vascular endothelial growth factor (VEGF) serum levelsof patients with Helicobacter pylori gastritis with cytotoxin-associated gene A positive (CagA + )status

Ενδομήτρια Υπολειπόμενη Αύξηση Και Ανοσολογικοί Παράγοντες Του Γαστρεντερικού

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