High Serum Pepsinogen I and beta Helicobacter pylori Infection Are Risk Factors for Aspirin-Induced Gastroduodenal Injury

Abstract

Background: Whether gastric hyperchlorhydria and Helicobacter pylori infection contribute to aspirin-induced gastroduodenal injury still lacks evidence. Because serum pepsinogens (PGs) and gastrin-17 (G17) can reflect gastric acid secretion, this study intended to elucidate whether serum PGs, serum G17, and H. pylori infection are associated with aspirin-induced gastrointestinal injury. Summary: A total of 60 patients taking low-dose aspirin for more than 1 month were enrolled in this study. Serum PG I, PG II, and G17 were determined using ELISA. A 14C-urea breath test was used for the detection of an H. pylori infection. The modified Lanza score was used to evaluate the degree of gastroduodenal injury under endoscopy. The median serum PG I level was significantly higher in the intensive gastroduodenal injury (IGI) group compared to that in the mild gastroduodenal injury group (155.0 vs. 116.6 ng/mL, p = 0.006). The H. pylori infection rate was significantly higher in the IGI group (73 vs. 40%, p = 0.037). Receiver operator characteristic curves analysis revealed that the cutoff value of PG I was 123 ng/mL, with 80% sensitivity and 61.4% specificity. H. pylori infection combined with PG I at >123 ng/mL had an OR (95% CI) of 15.8 (2.4 ± 104.5) for the prediction of aspirin-induced gastroduodenal injury. Key Messages: Serum PG I and H. pylori infection could be used to identify potential high-risk aspirin-induced gastroduodenal injury patients.

Association between serum pepsinogen and atherosclerotic cardiovascular disease

“…In fact, many studies have defined the thresholds of serum PGs based on the characteristics of the data [24,33,34]. It has been reported that the cutoff value of PGI was 123 ng/mL in the aspirin-induced gastroduodenal injury [24]. This threshold was similar to the one acquired in our experimental results (PGI Z 131 ng/mL).…”

“…Further, demographic, lifestyle, lipids, renal function and inflammatory indicators were adjusted in the Model 2, and Model 3 (Table 2), the correlation between PGI/PGR has been slightly weakened. The concentrations of serum PGs can also be affected by the usage of nonsteroidal anti-inflammatory drugs (NSAIDs) through inducing GMI [24,25]. Aspirin, one of the most commonlyused NSAIDs, can cause digestive bleeding, perforation, and ulceration, by disrupting the gastric epithelial cell barrier and systematically inhibiting gastric mucosal protection [25e30].…”

“…In the screening of gastrointestinal diseases, PGI 70 ng/mL and PGR 3 was a commonly accepted cutoff [10]. In fact, many studies have defined the thresholds of serum PGs based on the characteristics of the data [24,33,34]. It has been reported that the cutoff value of PGI was 123 ng/mL in the aspirin-induced gastroduodenal injury [24].…”

What Is New in Helicobacter pylori Diagnosis. An Overview

“…A similar association between a decreased PG I/II ratio and precancerous gastric conditions was also confirmed in several European countries, although the authors criticized the PG low specificity and its testing limitation for assessing gastric cancer risks [ 114 ]. Moreover, the measurement of PG I levels in the serum and the assessment of H. pylori infection may also be used to identify patients at high-risk for gastroduodenal injury induced by aspirin [ 115 ]. Interestingly, a cutoff value of PG I ≤ 31.2 ng/mL and PG I/II ratio ≤ 4.6 was able to discriminate for a past H. pylori infection in patients with Group A blood in a multicenter study [ 116 ].…”

Diagnosis of Helicobacter pylori infection

“…vs 61.7% and 39.2% for CRP. Among these biomarkers, Shan et al demonstrated that combination of increased serum PG 1 level and presence of H. pylori infection, in the group of patients taking aspirin, can indicate aspirininduced gastrointestinal damages 34. …”