Helicobacter pylori (H. pylori) represents an independent risk factor for Gastric Cancer (GC). First Degree Relatives (FDR) of GC subjects and Autoimmune Gastritis (AG) patients are both at increased risk for GC. H. pylori genetic heterogeneity within the gastric niche of FDR and AG individuals has been little explored. To understand whether they exploit an increased H. pylori stability and virulence, 14 AG, 25 FDR, 39 GC and 13 dyspeptic patients (D) were investigated by a cultural PCR-based approach characterizing single colonies-forming-units. We chose three loci within the Cytotoxin-associated gene-A Pathogenicity Island (CagPAI) (cagA,cagE,virB11), vacA, homA and homB as markers of virulence with reported association to GC. Inflammatory/precancerous lesions were staged according to Sydney System. When compared to D, FDR, similarly to GC patients, were associated to higher atrophy (OR = 6.29; 95% CI:1.23–31.96 in FDR; OR = 7.50; 95% CI:1.67–33.72 in GC) and a lower frequency of mixed infections (OR = 0.16; 95% CI:0.03–0.81 in FDR; OR = 0.10; 95% CI:0.02–0.48 in GC). FDR presented also an increased neutrophil infiltration (OR = 7.19; 95% CI:1.16–44.65). Both FDR and GC carried a higher proportion of CagPAI⁺vacAs1i1mx⁺homB⁺ profiles (OR = 2.71; 95% CI: 1.66–4.41 and OR = 3.43; 95% CI: 2.16–5.44, respectively). Conversely, AG patients presented a lower frequency of subtypes carrying a stable CagPAI and vacAs1i1mx. These results underline different H. pylori plasticity in FDR and AG individuals, and thus, a different host-bacterium interaction capacity that should be considered in the context of eradication therapies.

Acute infectious diseases are some of the most common reasons for receiving medical care, and analysis of the host immune response is an attractive approach for their diagnosis. The present study aimed to evaluate the potential usefulness of CD169 expression on peripheral monocytes (mCD169) as a marker of viral-associated host immune response. In a large mono-institutional cohort of 4,025 patients evaluated for SARS-CoV-2 (CoV2) and other viral infections, mCD169 analysis was performed by rapid flow cytometry assay. Increased mCD169 values (median, 17.50; IQR, 8.40-25.72) were found in 1,631 patients with CoV2+ acute infection compared to 2,394 in CoV2– patients (median, 2.35; IQR, 2.0-3.25) (odds ratio [OR], 21.84; 95% CI ,17.53-27.21; P < .001). Among CoV2– patients, 1,484 (62.0%) were assessed for other viral infections, and viral etiology was laboratory confirmed in 428 patients (CoV2– Vir+), with RNA viruses most frequently detected (94.6%). Higher levels of mCD169 were also confirmed in CoV2– Vir+ compared to CoV2– Vir– patients (OR, 10.05; 95% CI, 7.35-13.74; P < .001). mCD169 analysis by rapid flow cytometry assay may be a sensitive broad marker useful for the rapid triage of patients with suspected acute viral infections and could potentially be directly applied to eventual new emergent viral outbreaks.

Objectives: Mid-regional pro-adrenomedullin (MR-proADM) and monocyte CD169 (CD169) are valuable prognostic indicators of severe COVID-19. Methods: We assessed the predictive ability of a single measurement of MR-proADM and CD169 at emergency department (ED) admission to forecast in-hospital and 60-day mortality in adult COVID-19 patients. We analyzed clinical and laboratory data, with in-hospital mortality as the primary endpoint and 60-day mortality as the secondary endpoint. We examined associations with clinical and laboratory variables through univariate and multivariate analyses. Results: Data from 382 patients over 14 months were analyzed. Significant predictors of in-hospital mortality included age ⩾ 70 years (hazard ratio [HR] 8.1; 95% confidence interval [CI] 2.2-29.5), CD169 ratio ⩾ 20 (HR: 2.4; 95%CI: 1.6-5.6), MR-proADM ⩾ 1.1 mmol/L (HR: 5.1; 95%CI: 1.7-15.6), the need for invasive mechanical ventilation (HR: 6.8; 95%CI: 2.4-19.1), and active cancer (HR: 5.2; 95%CI: 1.8-15.2). For 60-day mortality, only elevated MR-proADM levels showed predictive value (HR: 6.7; 95%CI: 1.7-25.0), while high serologic titer was protective (HR: 0.4; 95%CI: 0.1-0.9). Conclusion: A single MR-proADM and CD169 measurement upon ED admission has prognostic value for in-hospital mortality, with MR-proADM also predicting 60-day mortality.

Refractoriness to standard first-line therapy in immune thrombocytopenia (ITP) should foster additional diagnostic work-up to exclude hematological clonal disease, mostly myelodysplatic syndrome (MDS) or clonal cytopenia of unknown significance (CCUS), which may present with isolated thrombocytopenia of immune or non-immune origin. We herein report on a patient who showed a transient leukoerythroblastic reaction (LEB) associated with bone marrow myelofibrosis upon rompilostim treatment, challenging a diagnosis of primary ITP and requiring additional investigations. RUNX-1-mutated myelodysplastic syndrome was eventually diagnosed. Even though LEB and marrow fibrosis have already been rarely reported during romiplostim treatment for ITP, this is the first case to our knowledge in which a background clonal hematopoiesis was diagnosed and deemed potentially involved in the abnormal response to this thrombopoietin receptor agonist (TPO-RA).

Kikuchi–Fujimoto disease (KFD) is a rare, benign lymphoproliferative disease of uncertain origin that can mimic other inflammatory or clonal lymphoproliferative disorders. Given the lack of available blood biomarkers, diagnosis is based on the biopsy of an affected lymph node. In recent years, evidence has been mounting that a dysregulated type I INF innate immune response plays a pivotal role in the pathogenesis of the disease and might be a future therapeutic target. Nonetheless, laboratory assays measuring the expression of interferon alpha (INFα) and INF-stimulated genes (ISGs) are cumbersome and not widely available, limiting their use in clinical and translational research and encouraging the use of more convenient surrogate markers. In this study, a rapid flow cytometry assay detected increased levels of expression of CD169 (Siglec-1), an INFα-induced surface protein involved in innate immunity regulation, on circulating monocytes from two patients with KFD. Our results are in line with previous experiences and set the stage for a more extended investigation into the use of this assay in exploring the pathophysiology of KFD.