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Mucosal immunity plays an important role in the pathogenesis of IgA nephropathy (IgAN). This study aimed to investigate if infection of Helicobacter pylori (H. pylori), a common bacteria in the gastrointestinal tract, associated with IgAN. This study included 261 patients with IgAN and 46 healthy controls. Clinical information and plasma samples were collected from patients and healthy controls. H. pylori infection was confirmed by western blot. Plasma IgA1 and galactose-deficient IgA1 (Gd-IgA1) levels were detected by specific enzyme-linked immunosorbent assay. Total H. pylori infection rates showed no statistical differences between IgAN patients and healthy controls, but the infection rates of type I H. pylori in IgAN patients were significantly higher than those in healthy controls (44.4 vs. 28.3%, p = 0.040). Compared with uninfected patients, the systolic blood pressure, 24-h proteinuria, and blood urea nitrogen levels were significantly higher in patients with H. pylori infection (126.0 ± 15.5 vs. 119.6 ± 14.5 mmHg, p = 0.010; 1.8 ± 2.7 vs. 1.2 ± 1.4 g/24h, p = 0.013; 7.9 ± 5.4 vs. 6.7 ± 3.9 μmol/L, p = 0.042), especially in patients with type I infection (126.5 ± 15.4 vs. 119.6 ± 14.5 mmHg, p = 0.002; 1.9 ± 2.9 vs. 1.2 ± 1.4 g/24 h, p = 0.033; 8.1 ± 5.6 vs. 6.7 ± 3.9 μmol/L, p = 0.041). Similarly, patients with IgAN and type I H. pylori infection showed higher plasma Gd-IgA1 levels than uninfected patients (5.5 ± 2.2 vs. 4.5 ± 2.2 μg/mL, p = 0.037). Virulent type I H. pylori infection is more common in patients with IgAN. Patients with IgAN and type I H. pylori infection showed lower renal function and higher underglycosylation of plasma IgA1.

Helicobacter pylori (Hp)-related gastropathies are accompanied by alterations in gastric secretion function, but the effects of infection of different Hp strains on gastric function are not yet well-elucidated. Our cross-sectional clinical study aim to research the effects of infection with different Hp types on gastric function. We analyzed 525 patients' serum cytotoxin-associated protein gene A (CagA), vacuolating cytotoxin-associated protein gene A (VacA), urease (Ure), Gastrin-17 (G-17), Pepsinogen I (PGI), Pepsinogen II (PGII) and PGI/PGII ratio (PGR). The PGII levels (8.19 ± 5.44 5.98 ± 10.75, = 0.013) were higher in the Hp infected group than in the uninfected, while the PGR levels (16.81 ± 8.22 23.23 ± 8.36, < 0.001) were lower. The PGR levels were higher in the uninfected group (23.23 ± 8.36, < 0.001) than in Hp-I (16.47 ± 7.45) and Hp-II infected groups (17.39 ± 8.98). In the uninfected group, the G-17 level was positively correlated with the levels of PGI (Pearson coefficient = 0.177, = 0.001), PGII (Pearson coefficient = 0.140, = 0.008) and age (Pearson coefficient = 0.121, = 0.022), negatively with the PGR levels (Pearson coefficient = -0.201, < 0.001). In the Hp-I (Pearson coefficient = -0.003, = 0.975) and Hp-II (Pearson coefficient = 0.018, = 0.161) infected groups, the G-17 levels were not correlated with age. Hp-I with CagA and/or VacA positive and Hp-II without cytotoxicity can reduce gastric secretion function regardless of age and sex. Gastric function in patients with Hp eradication was similar to that in those without Hp infection. G-17 rises physiologically with age, but infection with Hp will affect it.