Kronik aktif gastritli olan çocuklarda çölyak arter kan akımının değerlendirilmesi

Year 2021, Volume: 14 Issue: 1, 21 - 29, 04.01.2021

Ulaş Emre Akbulut , Mehmet Burak Özkan İshak Işık , Atike Atalay

https://doi.org/10.31362/patd.724121

Abstract

Purpose: There is no information about gastric blood flow in children with chronic gastritis. In this study, we aimed to evaluate hemodynamic changes of the celiac artery by trans-abdominal duplex Doppler ultrasonography, in children with chronic gastritis.
Materials and Methods: We examined 64 children with duplex Doppler ultrasonography. 36 children (group 1) with chronic active gastritis (diagnosed by endoscopy and histology) and 28 healthy children (group 2) were included the study. Children with chronic gastritis were classified again according to the presence of Helicobacter pylori infection and the severity of inflammation. End diastolic velocity, mean peak systolic velocity, pulsatility index and resistive index of the celiac artery were compared.
Results: While the mean pulsatility index and the mean resistive index were significantly higher in the group 1 (p < 0.001) the mean peak systolic velocity and the mean end diastolic velocity were significantly lower in group 1 than in controls (p < 0.001). In addition, mean peak systolic velocity was significantly higher in patients without Helicobacter pylori than in patients with Helicobacter pylori than (p < 0.05).
Conclusions: In this study, children with chronic active gastritis was shown that the decreased blood flow in celiac artery. Doppler ultrasonography can be used in first step diagnostic investigation before further invasive tests in children with suspicion of gastritis.

Amaç: Kronik gastritli çocuklarda mide kan akımı hakkında bilgi bulunmamaktadır. Bu çalışmada kronik gastritli çocuklarda transabdominal dupleks Doppler ultrasonografi ile çölyak arterin hemodinamik değişikliklerini değerlendirmeyi amaçladık.
Gereç ve Yöntem: Dupleks Doppler ultrasonografi ile 64 çocuğu inceledik. Kronik aktif gastritli (endoskopi ve histoloji tanısı alan) 36 çocuk (grup 1) ve 28 sağlıklı çocuk (grup 2) çalışmaya dahil edildi. Kronik gastritli çocuklar Helicobacter pylori enfeksiyonunun varlığına ve inflamasyonun şiddetine göre tekrar sınıflandırıldı. Çölyak arterin uç diyastolik hızı, ortalama pik sistolik hızı, pulsatilite indeksi ve rezistif indeksi karşılaştırıldı.
Bulgular: Grup 1'de ortalama pulsatilite indeksi ve ortalama rezistif indeksi anlamlı olarak daha yüksekken (p <0.001), grup 1'de ortalama pik sistolik hızı ve ortalama uç diyastolik hızı kontrollerden (p <0.001) anlamlı olarak daha düşüktü. Ayrıca, ortalama pik sistolik hızı Helicobacter pylori olmayan hastalarda Helicobacter pylori hastalarına göre anlamlı olarak daha yüksekti (p <0.05).
Çıkarımlar: Bu çalışmada, kronik aktif gastritli çocukların çölyak arter kan akımında azalma olduğu gösterilmiştir. Doppler ultrasonografi gastrit şüphesi olan çocuklarda daha ileri invaziv testlerden önce ilk basamak tanı incelemesinde kullanılabilir.

Keywords

Doppler ultrasonography, Celiac artery, Chronic gastritis, Children, Helicobacter pylori

Evaluation of celiac artery blood flow in children with chronic active gastritis

Abstract

Purpose: Knowledge on gastric blood flow in children with chronic gastritis is scarce. In this study, we aimed to evaluate hemodynamic changes of the celiac artery (CA), in children with chronic gastritis assessed using trans-abdominal duplex Doppler ultrasonography.
Methods: We examined 36 children (group 1) with chronic active gastritis (diagnosed by endoscopy and histology) and 28 asymptomatic control children (group 2) with duplex Doppler ultrasonography. Children with chronic gastritis were classified again according to the severity of inflammation and the presence of Helicobacter pylori infection. Mean peak systolic velocity (PSV), enddiastolic velocity (EDV), resistive index (RI), and pulsatility index (PI) of the CA were compared.
Results: The mean PSV and the mean EDV were significantly lower in patients than in controls (p<0.001). The mean PI and the mean RI were significantly higher in the patient group than in the controls (p<0.001). In addition, mean PSV was significantly lower in patients with H. pylori than in patients without H. pylori (p<0.05).
Conclusions: In this first study, children with chronic active gastritis were associated with a decrease in CA flow velocities that could be seen on Doppler ultrasonography. Doppler ultrasonography can be used in preliminary diagnostic work-up before further invasive tests.

Keywords

Doppler ultrasonography, celiac artery, gastritis, children, helicobacter pylori

References

• Sierra D, Wood M, Kolli S, Felipez LM. Pediatric Gastritis, Gastropathy, and Peptic Ulcer Disease. Pediatr Rev 2018; 39: 542-9
• Lee EJ, Lee YJ, Park JH. Usefulness of Ultrasonography in the Diagnosis of Peptic Ulcer Disease in Children. Pediatr Gastroenterol Hepatol Nutr 2019; 22: 57-62.
• Akbulut UE, Emeksiz HC, Kocak FG, Livaoglu A. Diagnostic yield of esophagogastroduodenoscopy in children with chronic abdominal pain. Arch Med Sci 2018; 14: 74-80.
• Thomson M, Tringali A, Dumonceau JM, et al. Paediatric Gastrointestinal Endoscopy: European Society for Paediatric Gastroenterology Hepatology and Nutrition and European Society of Gastrointestinal Endoscopy Guidelines. J Pediatr Gastroenterol Nutr 2017; 64: 133-53
• Whittle BJR. The defensive role played by gastric microcirculation. Meth Find Exp Clin Pharmacol 1989; 11 (Suppl 1): 35–43.
• Guslandi M. Mucosal blood flow and gastric protection – effect of neurohormonal and pharmacological agents. Int J Clin Pharmacol Ther Toxicol 1986; 24: 143–7
• Guslandi M, Sorghi M, Tittobello A. Does Helicobacter pylori affect gastric microcirculation? Ital J Gastroenterol 1994; 26: 383-4
• Koktener A, Turkay FGG, Erarslan E, et al. Doppler sonography of hemodynamic changes of the celiac artery in chronic active gastritis. Turk J Med Sci 2012; 42: 1273-7
• Dixon MF, Genta RM, Yardley JH, Correa P. Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994. Am J Surg Pathol 1996; 20: 1161-81.
• Tytgat GNJ. The Sydney System: Endoscopic Division. Endoscopic appearances in gastritis/duodenitis. J Gastroenterol Hepatol 1991; 6: 223-34
• Wang Y, Yuan SY, Zhang ZY. A study of gastric mucosal blood flow of peptic ulcer, chronic gastritis and gastric carcinoma. Zhonhua Nei Ke Za Zhi 1993; 32: 239–42.
• Henriksnas J, Atuma C, Phillipson M, Sandler S, Engstrand L, Holm L. Acute effects of Helicobacter pylori extracts on gastric mucosal blood flow in the mouse. World J Gastroenterol 2009; 15: 219-25
• Moorchung N, Srivastava AN, Gupta NK, Malaviya AK, Achyut BR, Mittal B. The role of mast cells and eosinophils in chronic gastritis. Clin Exp Med 2006; 6: 107-14
• Carusu RA, Parisi A, Crisafulli C, et al. Intraepithelial infiltration by mast cells in human Helicobacter pylori active gastritis. Ultrastruct Pathol 2011; 35: 251-5
• Hu Y, Liu JP, Zhu Y, Lu NH. The Importance of Toll-like Receptors in NF-κB Signaling Pathway Activation by Helicobacter pylori Infection and the Regulators of this Response. Helicobacter. 2016; 21: 428-40.
• Rahmani A, Moradkhani A, Hafezi Ahmadi MR, et al. Association between serum levels of high sensitive C-reactive protein and inflammation activity in chronic gastritis patients. Scand J Gastroenterol. 2016; 51: 531-7
• Gimbrone MA Jr, García-Cardeña G. Endothelial Cell Dysfunction and the Pathobiology of Atherosclerosis. Circ Res. 2016; 118: 620-36
• Judaki A, Norozi S, Ahmadi MRH, Ghavam SM, Asadollahi K, Rahmani A. Flow mediated dilation and carotid intima media thickness in patients with chronic gastritis associated with Helicobacter pylori infection. Arq Gastroenterol 2017; 54: 300-4.
• Lee M, Baek H, Park JS, et al. Current Helicobacter pylori infection is significantly associated with subclinical coronary atherosclerosis in healthy subjects: A cross-sectional study. PLoS One 2018; 13: e0193646.
• Atuma C, Engstrand L, Holm L. Helicobacter pylori extracts reduce gastric mucosal blood flow by a nitric oxideindependent but mast cell- and platelet-activating factor receptor-dependent pathway in rats. Scand J Gastroenterol 1999; 34: 1183-9