Gastrointestinal (GI) involvement of IgA vasculitis (IgAV) has various clinical presentations from isolated abdominal pain to severe gastrointestinal bleeding. The aim of this study is to determine the incidence of GI involvement in children with IgAV and identify the predictors of severe GI involvement. Medical records of IgAV patients with GI involvement from 30 centers in Türkiye between 2014 and 2024 were retrospectively reviewed. Patients were classified into two groups according to the severity of GI presentations: Group 1 consisted of mild GI involvement, while Group 2 had severe GI involvement. Severe GI involvement was observed in 476 (42%) out of 1131 patients. A significant postpandemic (after March 2020) increase in GI involvement was observed (p < 0.001). Abdominal pain as an initial symptom, vomiting, purpuric rash on upper extremities and trunk, and kidney involvement were more frequent in Group 2 than in Group 1 (all p < 0.01). Leukocytosis, neutrophilia, thrombocytosis, increased C-reactive protein (CRP) level and neutrophil-to-lymphocyte ratio (NLR), and decreased serum total protein and albumin levels were detected more frequently in Group 2 (all p < 0.01). In multivariate regression analysis, thrombocytosis, elevated NLR and CRP, hypoalbuminemia, abdominal pain preceding rash, vomiting, and upper extremity rash were associated with severe GI involvement (all p < 0.05). ROC analyses identified the following optimal cut-off values for predicting severe GI involvement: WBC > 12.90 10^3/µL, ANS > 7.81 10[3]/µL, NLR > 3.09, PLT > 404 103/µL, CRP > 20 mg/L, plasma albumin ≤ 4 g/dL.Conclusion: Abdominal pain preceding rash, purpuric rash on upper extremities, vomiting, thrombocytosis, hypoalbuminemia, increased NLR, and high CRP may predict severe GI involvement in children with IgAV.

Background: Respiratory syncytial virus (RSV) is a serious disease in older adults and is associated with various comorbidities; however, comparative data across epidemic waves, both clinically and in terms of inflammatory profiles and their diagnostic and prognostic utility, remain limited. Methods: We conducted a retrospective study of adults hospitalized with RSV infection across two epidemic waves (2022-2023 and 2024-2025). Data on clinical characteristics, comorbidities, severity scores, and outcomes were collected, and serum interleukin-6 (IL-6), C-reactive protein (CRP), and hematological parameters were analyzed and compared with those in healthy controls. Results: A total of 152 patients were included in this study (81 in wave 1 and 71 in wave 2). Patients in wave 2 were older and had a higher burden of comorbidities, although ICU admission and in-hospital mortality were similar across waves. RSV induced a consistent systemic inflammatory response in both waves, characterized by elevated IL-6 and CRP levels, neutrophilia, lymphopenia, and increased neutrophil-to-lymphocyte ratios, with no relevant inter-wave differences. All biomarkers demonstrated good diagnostic performance. The neutrophil-to-lymphocyte ratio showed the highest accuracy, while IL-6 exhibited high rule-in capacity. However, none of the evaluated biomarkers were associated with disease severity or mortality. Conclusions: RSV infection in older adults is associated with a similar inflammatory profile across waves. Although biomarkers showed strong diagnostic utility, they did not show any significant prognostic discrimination in this cohort. We suggest that disease severity is primarily associated with host-related factors, particularly comorbidities, rather than with differences in the inflammatory response, highlighting the need for improved preventive and risk-stratification strategies in this population.

BackgroundChronic rhinosinusitis (CRS) comprises heterogeneous eosinophilic (type-2) and neutrophilic (type-1/3) endotypes, yet existing murine models rarely distinguish them or compare their therapeutic responsiveness.MethodsSeven-week-old female C57BL/6N mice received intranasal instillations three times weekly for 4 or 12 weeks with either (1) a clinically relevant airborne allergen cocktail (house dust mite [HDM], Aspergillus fumigatus, Alternaria alternata, and Staphylococcus aureus protease) to induce eosinophilic CRS (ECRS) or (2) an innate stimulus mixture (lipopolysaccharide, β-1,3-glucan, and S. aureus protease) to induce neutrophilic CRS (NCRS). A parallel cohort received weekly dexamethasone administration (2 mg/kg). Endpoints included flow cytometry, enzyme-linked immunosorbent assays, quantitative PCR, histology, and immunofluorescence assays.ResultsFour-week allergen exposure produced a pure ECRS phenotype characterized by robust tissue eosinophilia, type-2 cytokines, and marked responsiveness to dexamethasone. Extending allergen delivery to 12 weeks generated mixed CRS with superimposed neutrophilia, upregulation of Il1b/Tgfb1, mucus hypersecretion, and attenuated steroid efficacy. Innate stimulus treatment yielded a steroid-resistant NCRS phenotype dominated by neutrophils, elevated Ifng/Il17a expression, and minimal type-2 biomarkers. Systemic eotaxin and HDM-specific immunoglobulin E mirrored those found in local eosinophilia, whereas circulating granulocytes remained unchanged across groups.ConclusionsBy adjusting the stimulus type and duration, we established tunable murine models that recapitulate pure ECRS, mixed CRS, and steroid-resistant NCRS within a single genetic background. These paired models provide a versatile platform for dissecting endotype-specific mechanisms and evaluating tailored interventions, highlighting the potential importance of early, phenotype-directed CRS therapy.

Pseudomyxoma peritonei (PMP) is a rare peritoneal surface malignancy, most often of appendiceal origin. Diagnosis may be delayed when symptoms are indolent or when ascitic fluid studies suggest infection. A 65-year-old man presented with 1 year of progressive abdominal distension and 15 days of epigastric pain. He was haemodynamically stable and afebrile. Paracentesis showed cloudy exudative ascites with marked neutrophilia (17 900 cells/mm[3]; 52% neutrophils). Culture grew Escherichia coli and cytology was negative. Portal venous phase CT demonstrated complex hyperattenuating ascites, diffuse peritoneal implants with bulky omental caking, visceral scalloping and an abnormal enhancing appendix. Ultrasound-guided omental core biopsies confirmed high-grade mucinous carcinoma peritonei without signet-ring cells, supporting an appendiceal-type primary. The patient declined surgical exploration and died shortly after readmission with bowel perforation and abscess. This case underscores that characteristic CT findings should prompt tissue confirmation and explicit tumour grading even when ascites appears infectious.

Caspase-8 is essential for maintaining organismal integrity by preventing cell death and subsequent inflammation in specific epithelial and endothelial tissues. Here, we show that caspase-8 also controls a systemic, cell death-independent inflammatory pathway that is constitutively active during homeostasis. In vivo, selective caspase-8 inhibition produces, in the absence of other stimuli, marked neutrophilia driven by circulating proinflammatory and chemotactic cytokines and promotes bacterial clearance during infection. In vitro, caspase-8 inhibition triggers in neutrophils, but not in macrophages, a profound transcriptional response associated with the release of IL-1β and other cytokines. This process requires tonic TNF-α production by neutrophils, which acts autocrinally to sequentially activate RIPK1, RIPK3, MAPKs, and NF-κB. The IL-1β release induced by caspase-8 inhibition requires gasdermin D and neutrophil serine proteases, but not canonical inflammasome components. Our data uncover the mechanistic features of a neutrophil-centric, proinflammatory pathway that can be therapeutically targeted to augment host defenses against pathogens.

Neutrophil asthma is a severe, corticosteroid-resistant subtype characterized by airway neutrophilia and declining lung function. Su et al. identify a sirtuin 6-lactate dehydrogenase A-histone lactylation axis that links macrophage glycolysis to epigenetic chemokine regulation, offering mechanistic insight into neutrophil recruitment and highlighting potential therapeutic targets.

Drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome is a rare but potentially life-threatening drug-induced hypersensitivity reaction characterized by delayed onset and variable multi-organ involvement, which can complicate timely diagnosis. We report the case of a 75-year-old female who developed fever, generalized pruritic maculopapular rash, facial edema, lymphadenopathy, and acute kidney injury 10 days after completing a one-week course of amoxicillin-clavulanate for a respiratory infection. Laboratory evaluation revealed leukocytosis with neutrophilia, mild eosinophilia not meeting diagnostic threshold criteria, acute kidney injury with proteinuria and hematuria, and isolated cholestatic liver injury without significant ALT or AST elevation; atypical lymphocytosis was absent. Autoimmune serology and viral hepatitis screening were negative. Based on the RegiSCAR scoring system, the patient achieved a score of 7, consistent with a definite diagnosis of DRESS. Systemic corticosteroid therapy, alongside adjunctive topical treatment and antihistamines, led to progressive clinical and laboratory improvement. This case represents an atypical presentation of DRESS with predominantly renal involvement and isolated cholestatic liver injury, where the absence of typical hematologic manifestations posed a diagnostic challenge. Although viral reactivation, particularly HHV-6, is often implicated in DRESS pathogenesis, its role here remains unconfirmed due to the lack of virological testing. The case highlights the importance of considering DRESS in patients with delayed-onset cutaneous eruptions and unexplained acute kidney injury after drug exposure, even in the absence of classic hematologic features, as early recognition and appropriate management are crucial for favorable outcomes.