Vmist prostahlandynu E2 v syrovattsi krovy patsiientiv iz erozyvno-vyrazkovymy urazhenniamy hastroduodenalnoi zony bez i z komorbidnoiu hipertonichnoiu khvoroboiu

Abstract

Introduction. The combination of erosive-ulcerative lesions (EUI) of the gastroduodenal zone with hypertension (HT) is a common phenomenon and is a modern medicine’s pressing issue. Taking nonsteroidal anti-inflammatory drugs (NSAIDs), including by patients with HT, is accompanied by prostaglandin synthesis suppression due to cyclooxygenase inhibition and results in an arterial pressure increase. Moreover, it should be mentioned that patients with HT have a higher risk of gastroduodenal lesions. The aim of the study. To explore the prostaglandin E2 content in the blood serum of patients with gastroduodenal erosive-ulcerative lesions without and with comorbid hypertension. Materials and methods. The research involved 20 patients with gastroduodenal EUI without comorbid HT and 30 patients with gastroduodenal EUI suffering comorbid HT. All patients went through general clinical examinations, esophagogastroduodenofibroscopy (EGDFS), and stool tests to verify H.pylori infection, with prostaglandin E2 (PGE2) content in blood serum being determined. Results. EGDFS showed that among patients with gastroduodenal EUI without comorbid HT, 25.00 % were diagnosed with gastric EUI; half of the cases (50.00 %) revealed duodenum lesions, and another 25.00 % – combined stomach and duodenum lesions. At the same time, patients with EUI combined with comorbid HT manifested more frequent (p-value less than 0.05) gastric localization of mucosal EUI (50.00 %); 16.67 % of patients had the duodenum lesions, while combined stomach and duodenum defects were observed in 33.33 %. H. pylori infection was confirmed in 13 patients (65.00 %) with EUI without comorbid HT and in 22 examined individuals (73.33 %) with the gastroduodenal zone EUI and comorbid HT. The endogenous PGE2 was significantly higher in patients who had only gastric mucosa and duodenum EUI without comorbid HT and amounted to 2135.79 ± 80.94 pg/ml (p-value less than 0.05), while patients with EUI and comorbid HT were tested a significantly lower PGE2 level in blood serum – 1513.55 ± 92.48 pg/ml. At the same time, the significantly lower PGE2 level in patients with EUI and comorbid HT compared to the similar indicator in patients without it explains the differences in the EUI distribution in both groups of patients revealed during endoscopic examination. Since a significantly weakened PGE2 synthesis leads to lower bicarbonate and mucus secretion and more intensive acid production, the balance between the aggression and protection factors is upset, which contributes to the EUI emergence mainly in the stomach’s antral part. The research has exposed no significant difference in PGE2 content in patients with duodenum mucosa EUI and those with a combination of gastric and duodenum mucosa lesions (p-value more than 0.05). Besides, the PGE2 content was tested significantly lower in patients with EUI gastric localization, than in those with combined ulcers (p-value less than 0.05). The presence or absence of H. pylori infection also did not affect the endogenous PGE2 level (p-value more than 0.05). Conclusions. The prostaglandin E2 content in the blood serum of patients with gastroduodenal erosive-ulcerative lesions with comorbid hypertension was notably lower than in patients with erosive-ulcerative lesions of the gastroduodenal zone without comorbid hypertension. Moreover, a significant prostaglandin E2 decrease in the blood serum of patients with gastroduodenal erosive-ulcerative lesions with comorbid hypertension upsets the balance between aggression and protection factors, which contributes to the emergence of erosive-ulcerative defects, mostly in the stomach.