Helicobacter pylori infection is a severe global health problem that is closely associated with acid-related diseases and gastric malignancies. Eradicating H. pylori is strongly recommended for lowering peptic ulcer recurrence and preventing gastric cancer. The current approved H. pylori eradication regimen combines a proton pump inhibitor (PPI) with two antibiotics. Unfortunately, this regimen failed to meet expectations mostly due to antibiotic resistance and insufficient gastric acid suppression. Vonoprazan, a novel potassium-competitive acid blocker, showed promising results as a PPI replacement. Vonoprazan inhibits gastric acid secretion by acting as a reversible competitive inhibitor against potassium ions and forming disulfide bonds with the cysteine molecule of H+/K+-ATPase. Vonoprazan has superior pharmacological characteristics over PPI, such as no requirement for acid activation, stability in acidic conditions, shorter optimum acid suppression period, and resistance to cytochrome P (CYP)2C19 polymorphism. Several comparative randomized controlled trials and meta-analyses revealed the superiority of vonoprazan in eradicating H. pylori, notably the resistant strains. The adverse effect caused by vonoprazan is long-term acid suppression that may induce elevated gastrin serum, hypochlorhydria, and malabsorption. All vonoprazan studies have only been conducted in Japan. Further studies outside Japan are necessary for universally conclusive results.

Background: Gastroesophageal reflux disease (GERD) and Helicobacter pylori infection are globally prevalent diseases. Recent studies suggested that GERD is associated with increased lung cancer risk although the results were still inconclusive. Previous studies also suggested that lung cancer is an extra-gastric manifestation of H. pylori infection although the results were inconsistent. This study aims to measure the lung cancer risk in the GERD and H. pylori infection patients. Methods: We did comprehensive searching in online databases of Pubmed, EMBASE, ScienceDirect, and The Cochrane Library, to include all relevant studies from January 2000 until January 2021. We included all observational studies particularly cohort studies, that access the lung cancer risk in GERD and H. pylori infection patients. Bias risk was accessed with The Newcastle-Ottawa Scale for observational studies. Analysis was performed to provide pooled risk ratios (RR) with 95% confidence interval (CI) using random-effect heterogeneity test. Results: We included 5 cohort and 4 cross-sectional studies met our inclusion criteria. Analysis of 3 GERD cohort studies suggests that GERD increase lung cancer risk significantly (pooled RR = 1.47, 95% CI 1.13-1.91, p = 0.004, I 2 = 70%). Significant incremental lung cancer risk in H. pylori infection was shown in both cohort ( pooled RR = 1.55, 95% CI 1.10-2.18, p = 0.01, I 2 = 39%) and non-cohort (pooled RR = 2.06, 95% CI 1.22-3.46, p = 0.006, I 2 = 62%) studies analysis, thus the overall analysis also suggests significantly increased lung cancer risk in H. pylori infection patients (pooled RR = 1.74, 95% CI 1.30-2.33, p = 0.0002, I 2 = 50%). Conclusions: Gastroesophageal reflux disease and Helicobacter pylori infection increase lung cancer risks. However, further studies are needed to establish the causalities.Legal entity responsible for the study: The authors. Funding: Has not received any funding. Disclosure: All authors have declared no conflicts of interest.

BACKGROUND AND AIMS Chronic kidney disease (CKD) is a worldwide health problem whose incremental prevalence. Early detection and proper monitoring of renal dysfunction can decrease morbidity and mortality among CKD patients. Estimated glomerular filtration rate (eGFR) and albuminuria have been used for monitoring CKD progression. Unfortunately, substantial CKD patients’ proportion might undergo CKD progression through non-proteinuric pathways. Dickkopf-3 (DKK3), stress-induced renal tubular epithelial-derived glycoprotein, is a key driver of tubulointerstitial fibrosis through the canonical Wnt/β-catenin signaling pathway. This study aims to evaluate the role of DKK3 in detecting and monitoring renal dysfunction and CKD progression. METHOD Comprehensive literature searching was performed through the online databases of PubMed, EMBASE, ScienceDirect and The Cochrane Library. This study followed the PRISMA guidelines. The inclusion criteria are all cohort studies that assess the correlation and clinical implications of increased urinary DKK3 with CKD progression. The quality of included studies was accessed by using the Newcastle–Ottawa Scale. RESULTS Six cohort studies matched the inclusion criteria. Urinary DKK3-to-creatinine >4000 pg/mg was independently associated with annual eGFR decline among early CKD stages. A multivariate analysis study suggested that 24-h urinary DKK3 was independently associated with the annual Kt/V decline among peritoneal dialysis patients. Increased urinary DKK3 was associated with a significant eGFR decline in 6 months among IgA nephropathy patients. A cohort study suggested that populations with microalbuminuria were significantly susceptible to prevalent cardiovascular diseases, prevalent CKD, and new-onset CKD risks. Urinary DKK3 was associated with significant incremental risks for declining eGFR and proteinuria as well as CKD progression risks in chronic obstructive pulmonary disease (COPD) patients. In a study, involving CKD patients who underwent coronary angiography, the baseline urinary DKK3-to-creatinine ratio was superior to serum cystatin-C and serum and urinary neutrophil gelatinase-associated lipocalin (NGAL), predicting both acute kidney injury (AKI) and persistent renal dysfunction. A cardiac surgery study showed that high urinary DKK3-to-creatinine ratio >471 pg/mg was significantly associated with AKI, persistent renal dysfunction and dialysis dependency. CONCLUSION Dickkopf-3 shows promising prospective roles for detecting early renal dysfunction and monitoring CKD progression. Nevertheless, further studies are warranted to confirm its promising prospective role.

Gene BM at diagnosis EGFR (n = 53)19 (36%) MET (n = 14) 3 (21%) ALK (n = 12) 4 (33%) ERBB2 (n = 8) 1 (13%) BRAF (n = 7) 3 (43%) ROS (n = 2) 0 (0%) RET (n = 2) 2 (100%)Conclusions: In the analyzed cohort of patients, we note that patients with NSCLC with driver mutations have a high incidence of BM at diagnosis. Contrary to historical controls, these patients with molecular alterations have favorable outcomes despite development of BM. This could be due to the availability of potent active targeted drugs with good CNS penetration.

In both patients with NDD-CKD and DD-CKD, roxadustat facilitated iron transport and utilization resulting in increases in both serum iron and TIBC, likely driven by reduced hepcidin. Overall, despite the observed greater Hb increase from BL with roxadustat, IV iron use was reduced with roxadustat in both the NDD-CKD and DD-CKD populations.