Background: Autoimmune gastritis (AIG) and Helicobacter pylori gastritis are distinct etiologies of chronic gastritis, yet comparative data on their long-term progression remain limited. Objectives: We compared the evolution of precancerous gastric lesions in patients with AIG and H. pylori-associated gastritis. Methods: This retrospective single-center cohort included 116 patients (52 histologically defined AIG, 64 H. pylori-associated gastritis) who underwent two upper endoscopies with Sydney-protocol biopsies at least 12 months apart between 2013 and 2024 (median follow-up 60 and 49 months). The primary outcome was the development of glandular atrophy or intestinal metaplasia (IM) not present at baseline. Results: New atrophy or IM developed in 61.5% (32/52) of AIG and 34.4% (22/64) of H. pylori patients (adjusted odds ratio [OR] 3.81, 95% confidence interval [CI] 1.53–9.49). Incident atrophy was more frequent in AIG (65.1% vs. 31.5%), including in comparison with baseline H. pylori-positive patients only (adjusted OR 3.02, 95% CI 1.08–8.46), whereas differences in IM were less consistent. Progression occurred in 42.9% of patients who were H. pylori-negative after treatment and 55.6% of persistently infected patients (p = 0.70). Proton pump inhibitor (PPI) use, an exploratory clinical risk score, and symptom changes were not associated with progression. Conclusions: In this selected cohort with repeat endoscopy, histologically defined AIG was associated with more frequent histological progression, particularly glandular atrophy, than H. pylori-associated gastritis. Prospective studies with serologically confirmed AIG and neoplastic endpoints are needed to inform risk stratification.

Background: Liver cirrhosis is associated with portal hypertension and its gastrointestinal complications, but non-variceal gastroduodenal mucosal injury and its relationship to Helicobacter pylori (H. pylori) infection and hepatic disease severity remain incompletely characterized. Methods: This retrospective, cross-sectional study included 162 patients undergoing first upper gastrointestinal endoscopy (61 with cirrhosis, 101 controls), assessed using a composite gastroduodenal mucosal injury score (range 0–16) across the antrum, gastric corpus, duodenal bulb, and second duodenal portion. Results: Cirrhosis was independently associated with a higher injury burden after adjusting for H. pylori status, nonsteroidal anti-inflammatory drug (NSAID), antiplatelet, anticoagulant, and proton pump inhibitor (PPI) use (adjusted count ratio [aCR] = 1.33, 95% CI: 1.09–1.63, p = 0.006); and H. pylori infection was independently and separately associated with higher injury burden (aCR = 1.25, 95% CI: 1.01–1.54, p = 0.037), while none of the four medication classes showed an independent association. This excess injury was concentrated almost exclusively in the gastric corpus (adjusted aCR = 3.04, p < 0.0001), with no significant differences at other sites. Injury severity did not correlate with Child–Pugh class or tests of the liver’s biosynthetic capacity (all p > 0.05). Only patients with concurrent cirrhosis and H. pylori infection showed significantly elevated injury relative to unexposed controls (adjusted aCR = 1.87, 95% CI: 1.38–2.53, p < 0.0001), with a significant, exploratory cirrhosis × H. pylori interaction (aCR = 1.56, p = 0.037). Conclusions: Cirrhosis is therefore associated with a corpus-predominant pattern of gastroduodenal injury, compatible with, though not proof of, a portal hypertension-related mechanism, and shows a significant positive multiplicative interaction with concurrent H. pylori infection; given the exploratory nature of this analysis, these findings are hypothesis-generating and warrant prospective confirmation before informing endoscopic screening or infection-screening practice.

Background/Objectives: Vascular patches used in cardiovascular reconstruction remain limited by thrombosis, calcification, restricted remodeling, and inability to accommodate somatic growth. This proof-of-concept study aimed to fabricate and characterize porous vascular patches by fused deposition modeling (FDM) using polylactic acid (PLA) and thermoplastic polyurethane (TPU) in single-material and multilayer configurations. Methods: PLA/TPU patches with different polymer compositions, layer sequences, interfilament spacing, and staggered layer arrangements were fabricated by FDM. Mass and dimensional changes during in vitro immersion were assessed for the constituent polymers (n = 3 per polymer) and selected patch configurations (n = 1 per configuration). Patch microstructure and the in-plane dimensions of surface-visible pore openings were evaluated by top-view optical microscopy and ImageJ analysis, while time to first visually detectable fluid passage was assessed using a 22% (w/w) aqueous glycerol test solution under low hydrostatic pressure. Results: PLA and TPU exhibited distinct mass and dimensional profiles during 140 days of immersion, with mean mass increases of 1.37% and 3.68%, respectively. Selected patch specimens showed different temporal mass-change profiles during 42 days of immersion in phosphate-buffered saline (PBS). Descriptive pore measurements varied among the investigated configurations; V7b showed mean dimensions of 96.5 × 93.2 µm. In the exploratory test, fluid passage was first visually detected at 18 min (V5-TPU), 59 min (V6b) and 135 min (V7b). Conclusions: FDM enabled the fabrication of porous PLA/TPU vascular patch prototypes with different material composition and multilayer architectures. These findings establish a preliminary basis for further physicochemical, mechanical, biological, and hemodynamic evaluations of FDM-fabricated PLA/TPU vascular patches.