Helicobacter pylori cagA/vacAs1-m1 strain is associated with high risk of fibrosis in metabolic-dysfunction-associated steatotic liver disease.

INTRODUCTION AND OBJECTIVES: Recent studies have suggested an association between H. pylori and metabolic dysfunction associated steatotic liver disease (MASLD). We aim to evaluate the association of H. pylori virulence genes with non-invasive markers of liver injury and fibrosis in MASLD subjects. PATIENTS AND METHODS: A total of 362 dyspeptic patients who underwent gastroscopy were selected. Biochemical, clinical parameters, ultrasound, FIB-4 score, liver stiffness measurement (LSM) by vibration-controlled transient elastography (VCTE), gastric biopsies, and H. pylori virulence genes (cagA, vacA) were evaluated. RESULTS: A cohort comprised of 61 % women and 39 % men with a median age of 52 (40-60) years. MASLD was observed in 42 %, and H. pylori-positive in 45 %. No differences were observed regarding H. pylori status at co-morbid metabolic conditions. In MASLD cohort, H. pylori-positive was associated with higher AST, ALT, FIB-4 and LSM. Indeed, carriers of cagA/vacA-s1/m1-positive allelic combination were associated with higher AST, ALT, FIB-4 and LSM but not cagA/vacA-s1/m1-negative. The OR for high-risk of significant/advanced- fibrosis by VCTE (≥8 kPa) with H. pylori-positive was 2.56 (95 % CI, 1.2-5.75) and for cagA/vacA-s1/-m1-positive allelic carriers was 4.01 (95 % CI, 1.38-11.56), but non-significant association in cagA/vacA-s1/-m1-negative. After adjusting for age, gender, diabetes, BMI and hypertension the OR for VCTE ≥8 kPa with H. pylori-positive was 2.43 (95 % CI, 1.88-12.44), and cagA/vacA-s1/m1-positive allelic carriers was 4.06 (95 % CI, 1.22-14.49). CONCLUSIONS: In our cohort of functional dyspepsia (FD) patients with MASLD, H. pylori was associated with non-invasive markers of liver injury and fibrosis. Carriers of cagA/vacA-s1/m1-positive allelic combination showed an independent risk of significant/advanced fibrosis by VCTE.

Association between genetic polymorphisms of NOD1, Interleukin-1B, and cagA strain with low-grade duodenal eosinophilia in Helicobacter pylori-related dyspepsia.

BACKGROUND: Functional dyspepsia (FD) is a multifactorial disorder. Helicobacter pylori (H. pylori)-related dyspepsia (HpD) may be considered a separate entity. Duodenal eosinophilia is a potential pathogenic mechanism in FD. However, the impact of duodenal eosinophilia and host genetic polymorphism of innate and pro-inflammatory cascade, nucleotide-binding oligomerization domain 1 (NOD-1), and interleukin-1 beta (IL-1ß) in HpD was not explored. AIM: To evaluate the association of NOD1-796G>A and IL-1B-511C>T gene variants and low-grade duodenal eosinophilia in HpD. METHODS: A multicenter cross-sectional study was conducted. A total of 253 patients who met Rome-IV criteria were selected before upper endoscopy and 98 patients were included after unremarkable upper endoscopy and positive H. pylori in gastric biopsies were assessed. Clinical parameters, H. pylori cagA and duodenal histology, were evaluated. RESULTS: Sixty-four (65%) patients had epigastric pain syndrome (EPS), 24 (25%) postprandial distress syndrome (PDS), and 10 (10%) EPS/PDS overlap. FD subtypes were not associated with NOD1-796G>A and IL-1B-511C>T gene variants. Low-grade duodenal eosinophilia was significantly increased in NOD1-796 GG versus single A-allele, but not in IL-1B-511 single T-allele or CC-allele. This association is dependent of cagA infection, since harboring cagA strain was significantly associated with low-grade duodenal eosinophilia with isolated variants NOD1-796 GG and IL-1B-511 single T-allele, but not without cagA. When we performed combined polymorphism analysis with NOD1-796 GG/IL-1B-511 single T-allele, a synergistic effect on low-grade duodenal eosinophilia was found between these two loci irrespective of cagA strain status in HpD. CONCLUSION: Our findings suggest that low-grade duodenal eosinophilia is significantly associated with NOD1-796 GG allele specially in cagA strain and with allelic combination NOD1-796 GG/IL-1B-511 single T-allele independent of cagA strain infection in HpD patients.

Clinical Implications of Low-grade Duodenal Eosinophilia in Functional Dyspepsia: A Prospective Real-life Study.

BACKGROUND: Functional dyspepsia (FD) is a multifactorial disorder with no targeted therapy. Duodenal eosinophilia and low-grade inflammation are potential pathogenic mechanisms. However, the impact of duodenal eosinophils (D-EO) histologic evaluation in real-life clinical practice was not explored. AIM: To evaluate the clinical utility of D-EO and low-grade inflammation in FD in real-life practice. MATERIALS AND METHODS: A multicenter prospective study was conducted. A total of 636 patients who meet Rome-III criteria were selected before upper endoscopy and 516 patients were included after normal endoscopy were assessed. Clinical parameters, Helicobacter pylori ( H. pylori), and duodenal histology were evaluated. RESULTS: FD subtypes were 231 (45%) patients who had epigastric pain syndrome (EPS), 168 (33%) postprandial distress syndrome (PDS), and 117 (22%) EPS/PDS overlap. Two hundred fifty-nine (50.3%) patients were H. pylori+ . Histologic duodenal grading of chronic inflammation and intraepithelial lymphocytes showed no difference between FD subtypes. Increased in D-EO densities (>10 per high power field) was significant in PDS compared with EPS and EPS/PDS overlap subtypes. The odds ratio of PDS in subjects with duodenal eosinophilia densities was 2.28 (95% CI, 1.66-3.14; P <0.0001), adjusting for age, gender, H. pylori and nonsteroidal anti-inflammatory drug the odds ratio was 3.6 (95% CI, 2.45-5.28; P <0.0001). receiver operating characteristic curve analysis further demonstrated that low-grade duodenal eosinophilia, in particular H. pylori- , was highly accurate for PDS with the area under the curve 0.731 compared with H. pylori+ area under the curve 0.598. Furthermore, low-grade duodenal eosinophilia was significantly correlated with treatment response under 4 to 6 weeks of proton pump inhibitor therapy. CONCLUSION: Our findings suggest that low-grade duodenal eosinophilia is associated with PDS subtype non- H. pylori FD patients and could be a useful marker of treatment response.

Low-grade duodenal eosinophilia is associated with cagA in Helicobacter pylori-related dyspepsia.

BACKGROUND AND AIM: Functional dyspepsia (FD) is a multifactorial disorder. Helicobacter pylori (H. pylori)-related dyspepsia (HpD) may be considered a separate entity. Duodenal eosinophilia is a potential pathogenic mechanism in FD. However, the impact of duodenal eosinophilia and H. pylori virulence genes in HpD was not explored. We aim to evaluate the association of H. pylori virulence genes and low-grade duodenal eosinophilia in HpD. METHODS: A multi-center cross-sectional study was conducted. A total of 301 patients who meet Rome-III criteria were selected before upper endoscopy, and 95 patients were included after normal endoscopy and positive H. pylori in gastric biopsies were assessed. Clinical parameters, H. pylori virulence genes (cagA, oipA, and vacA) and duodenal histology were evaluated. RESULTS: Sixty-nine (72%) patients had epigastric pain syndrome (EPS), 17 (18%) post-prandial distress syndrome (PDS) and 9 (10%) EPS/PDS overlap. FD syndromes were not associated with cagA or oipA strains. A significantly trend of vacA s1/m1 (78%) and s1/m2 (80%) positive strains in EPS was observed. Histological duodenal grading of chronic inflammation, low-grade duodenal eosinophilia and intra-epithelial lymphocytes showed no difference in oipA and vacA strains. Low-grade duodenal eosinophilia was significant in cagA positive strain, and the OR for low-grade duodenal eosinophilia with H. pylori cagA positive strain was 4.2 (95% CI, 1.78-9.93). Adjusting for age, gender, smoking, diabetes, alcohol, PPI, and NSAID, the OR was 5.44 (1.989-14.902). CONCLUSION: Our findings suggest that low-grade duodenal eosinophilia is significantly associated with cagA strain in HpD.

The interplay between Helicobacter pylori infection and rs738409 PNPLA3 in metabolic dysfunction-associated steatotic liver disease.

BACKGROUND: Recent studies have suggested an association between H. pylori and metabolic-disfunction associated fatty liver disease (MASLD). However, epidemiologic studies have yielded inconsistent results. We aim to evaluate the association of H. pylori and G-allele PNPLA3 in MASLD diagnosis, and markers of severity. METHODS: A multi-center cross-sectional study was conducted. A total 224 functional dyspepsia (FD) patients cohort who underwent gastroscopy was selected. Biochemical, clinical parameters, ultrasound, FIB-4 score, LSM by VCTE, gastric biopsies, H. pylori status, and rs738409 PNPLA3 were evaluated. A second retrospective cohort of 86 patients with biopsy-proven MASLD who underwent gastroscopy with gastric biopsies was analyzed. RESULTS: In the FD cohort MASLD was observed in 52%, and H. pylori-positive in 51%. H. pylori infection was associated with MASLD prevalence, but in multivariate analyses adjusted for G-allele PNPLA3, it became not significant. Then in MASLD-only dyspeptic cohort, H. pylori infection was significantly linked to elevated serum AST levels and increased liver stiffness measurements, suggesting a potential role in liver injury and fibrosis. Histopathological analysis in biopsy-proven MASLD patients further supported these findings, showing a significant association between H. pylori infection and increased NAS score, fibrosis stage, and prevalence of MASH. Notably, the combination of H. pylori infection and G-allele PNPLA3 appeared to exacerbate MASLD severity beyond individual effects. CONCLUSIONS: Our results suggest that H. pylori infection may play a role in the progression of liver injury and fibrosis in patients with MASLD, especially in those with specific genetic predispositions.

[Distribution of vectors of visceral leishmaniasis in the Province of Corrientes, 2008]. / Distribución de vectores de leishmaniasis visceral en la Provincia de Corrientes, 2008.

Visceral leishmaniasis (VL) is a relevant parasitic disease in public health, produced by Leishmania infantum chagasi. Since the urbanization and emergence in Southern Brazil and Paraguay, the vector Lutzomyia longipalpis in Formosa, 2004, and the first human visceral leishmaniasis case in Misiones, 2006, have been reported in Argentina. Due to the reports of canine VL, a search of the vector in the Province of Corrientes, contiguous to Misiones, was performed during December 2008. Standarized trapping detected 376 Lu. longipalpis in Ituzaingó, Virasoro, Santo Tomé, Garruchos, Riachuelo, Corrientes and Monte Caseros localities. The risk of autochtonous vectorial transmission was then confirmed in the Province of Corrientes. The distribution of vectors in populated urban areas, with intense transit of canine reservoirs from localities with high transmission, and the existence of infected reservoirs, also implies epidemic risk.

Distribución de vectores de leishmaniasis visceral en la Provincia de Corrientes, 2008 / Distribution of vectors of visceral leishmaniasis in the Province of Corrientes, 2008

La leishmaniasis visceral es una parasitosis de importancia en salud pública, producida por Leishmania infantum chagasi. A partir de la urbanización y emergencia en el sur de Brasil y Paraguay, se notificó la presencia del insecto vector Lutzomyia longipalpis en la Argentina; en Formosa, 2004, y en Misiones el primer caso humano en 2006. La notificación de casos de reservorios caninos infectados en la provincia de Corrientes, contigua a Misiones, determinó la búsqueda del vector. Mediante trampeos estandarizados en diciembre del 2008 se capturaron 376 Lu. longipalpis en Ituzaingó, Virasoro, Santo Tomé, Garruchos, Riachuelo, Corrientes y Monte Caseros. Se confirma el riesgo de transmisión vectorial autóctona de leishmaniasis visceral en la provincia de Corrientes. La distribución de vectores en áreas urbanas densamente pobladas, con intenso tránsito de reservorios caninos desde zonas de alta transmisión, y la presencia de reservorios infectados, implica a su vez riesgo epidémico.

Visceral leishmaniasis (VL) is a relevant parasitic disease in public health, produced by Leishmania infantum chagasi. Since the urbanization and emergence in Southern Brazil and Paraguay, the vector Lutzomyia longipalpis in Formosa, 2004, and the first human visceral leishmaniasis case in Misiones, 2006, have been reported in Argentina. Due to the reports of canine VL, a search of the vector in the Province of Corrientes, contiguous to Misiones, was performed during December 2008. Standarized trapping detected 376 Lu. longipalpis in Ituzaingó, Virasoro, Santo Tomé, Garruchos, Riachuelo, Corrientes and Monte Caseros localities. The risk of autochtonous vectorial transmission was then confirmed in the Province of Corrientes. The distribution of vectors in populated urban areas, with intense transit of canine reservoirs from localities with high transmission, and the existence of infected reservoirs, also implies epidemic risk.

Bloqueo ductal pancreático : importancia de la cantidad de sustancia oclusiva empleada / Pancreatic ductal blockade : importance of quantity occlusive substance used

Serie de 16 perros que luego de provocarles pancreatitis aguda necrohemorrágica con ClCa al 20% en lóbulo izquierdo, se les ocluyó el sistema ductal con 2 cm.3 de adhesivo tisular(Tissucol). Dentro de las 24 hs. murieron 2 perros, los restantes evolucionaron satisfactoriamente y se los sacrificó a los 30, 40 y 120 días. La sobrevida(87,5%) demuestra que rellenando sólo el continente canalicular, se interrumpe el proceso necrohemorrágico, descartando la posible influencia terapéutica del excedente que pasa al intersticio. Estudios histopatológicos revelaron que con 2cm3 en lugar de 4 a 7 cm3 disminuye la secuela fibrótica.