Background: Fixed drug eruption (FDE) is a non-immediate, CD8+ T cell–mediated hypersensitivity reaction characterized by well-demarcated erythematous–violaceous plaques that recur at the same site after re-exposure to the causative drug. Although NSAIDs and antibiotics are the most common triggers, various other medications may induce FDE, and genetic susceptibility has been linked to specific HLA alleles. Methods: We conducted a clinical evaluation supported by patch testing, oral drug provocation, and assessment of therapeutic alternatives to identify the causative agent and confirm delayed-type hypersensitivity. Results: We report the case of a 53-year-old woman with essential hypertension, autoimmune thyroiditis, and renal lithiasis who developed well-demarcated erythematous plaques with central vesiculation and moderate pruritus on the dorsal hand and posterior calf approximately 8 h after ingestion of a 60 mg etoricoxib tablet. Patch testing was negative, while oral challenge confirmed etoricoxib-induced FDE; celecoxib was subsequently evaluated as a potential safe alternative. Conclusions: This case underscores the importance of an integrated diagnostic approach—including careful history, clinical examination, and confirmatory testing—to accurately diagnose delayed cutaneous drug reactions and to identify safe therapeutic options for patients.

Background/Objectives: Leptin is a pleiotropic adipokine linking energy metabolism with innate and adaptive immunity. Its relationship with clinical severity across distinct airway disease phenotypes remains insufficiently characterized. This study examined serum leptin concentrations in adults with allergic rhinitis, non-allergic asthma, and allergic asthma associated with allergic rhinitis. Methods: This single-center retrospective observational study analyzed fully anonymized clinical and laboratory data from 88 adults: patients with allergic rhinitis (n = 31), non-allergic asthma (n = 15), or allergic asthma with allergic rhinitis (n = 22) and healthy controls (n = 20). Serum leptin was measured using a quantitative sandwich enzyme-linked immunosorbent assay. Disease severity was classified using the Allergic Rhinitis and its Impact on Asthma and Global Initiative for Asthma frameworks applicable during the study period. Statistical analyses were performed using IBM SPSS Statistics, version 26.0 (IBM Corp., Armonk, NY, USA), and available original statistical outputs were summarized using retained t statistics and two-sided p values. Results: Stage-specific mean serum leptin concentrations were heterogeneous and non-monotonic. Statistically significant relationships between leptin concentration and disease stage were reported for allergic rhinitis (t = 2.844; p = 0.008), non-allergic asthma (t = 4.240; p = 0.001), and allergic asthma with allergic rhinitis (t = 2.700; p = 0.013). In the allergic rhinitis subgroup, 64.5% of participants had normal weight, 32.3% were overweight, and 3.2% had grade II obesity; weight category was not significantly related to rhinitis stage. Conclusions: The retained analyses indicate statistically significant relationships between serum leptin concentration and clinical disease stage across the investigated airway phenotypes. However, the stage-specific descriptive means were heterogeneous and non-monotonic and therefore do not support a uniform progressive increase in leptin with increasing disease severity. Because complete model outputs and covariate-adjusted estimates were unavailable, these findings should be regarded as exploratory and require prospective validation with appropriate adjustment for adiposity and other relevant metabolic confounders.

Interleukin-11 (IL-11) is implicated in epithelial dysfunction, fibroblast activation, tissue remodeling, and chronic inflammatory responses; however, the clinical value of circulating IL-11 in airway disease remains uncertain. This single-center retrospective exploratory observational study included 88 adults: 31 with allergic rhinitis, 15 with non-allergic asthma, 22 with allergic asthma associated with allergic rhinitis, and 20 healthy controls. Serum IL-11 concentrations were measured using a quantitative sandwich enzyme-linked immunosorbent assay. Between-group differences were assessed using the Kruskal–Wallis test followed by Holm-adjusted pairwise Mann–Whitney U tests. Associations with disease-specific ordinal clinical categories were evaluated using Spearman rank correlation, with GINA treatment Steps used for asthma phenotypes and ARIA severity categories for allergic rhinitis. Median IL-11 concentrations were 62.01 pg/mL in non-allergic asthma, 78.87 pg/mL in allergic rhinitis, 61.92 pg/mL in allergic asthma associated with allergic rhinitis, and 95.46 pg/mL in healthy controls. The primary global comparison was not statistically significant (H = 5.667, p = 0.129), and no pairwise comparison remained significant after Holm correction. Six measurements (6.8%) were below the assay detection limit; replacing these values with 4.0 pg/mL in a sensitivity analysis did not materially alter the global result (H = 5.671, p = 0.129). Serum IL-11 was not significantly associated with GINA treatment step in non-allergic asthma (rho = −0.170, p = 0.544) or allergic asthma associated with allergic rhinitis (rho = 0.052, p = 0.818), nor with ARIA severity category in allergic rhinitis (rho = 0.046, p = 0.805). In an exploratory analysis adjusted for age, sex, body-mass category, and current smoking status, IL-11 concentrations were lower in each clinical phenotype relative to healthy controls; given the modest group sizes and baseline imbalance, this finding was considered hypothesis-generating. Overall, the primary analysis did not demonstrate significant differences in circulating IL-11 across study groups, and serum IL-11 was not associated with disease-specific ordinal clinical categories. These findings do not support the use of a single serum IL-11 measurement as a stand-alone biomarker of airway disease phenotype or clinical category in this cohort and warrant confirmation in larger, prospectively characterized cohorts.

Background: Interleukin-17 (IL-17) contributes to persistent airway inflammation, neutrophil recruitment, and inflammatory pathways extending beyond classical type 2 immunity. However, the distribution of circulating IL-17 across clinically distinct upper- and lower-airway disease phenotypes remains incompletely characterized. This study compared serum IL-17 concentrations in allergic rhinitis, non-allergic asthma, allergic asthma associated with allergic rhinitis, and healthy controls. Methods: This retrospective single-center observational study included 88 adults: allergic rhinitis (n = 31), non-allergic asthma (n = 15), allergic asthma associated with allergic rhinitis (n = 22), and healthy controls (n = 20). Serum IL-17 concentrations were measured using a quantitative sandwich enzyme-linked immunosorbent assay. Overall group differences were assessed using the Kruskal–Wallis test, followed by Holm-adjusted pairwise Mann–Whitney U tests. Results: Serum IL-17 concentrations differed significantly across the four groups (Kruskal–Wallis H = 12.981, p = 0.0047). Median IL-17 concentrations were 126.21 pg/mL in non-allergic asthma, 50.97 pg/mL in allergic rhinitis, 54.72 pg/mL in allergic asthma associated with allergic rhinitis, and 0.00 pg/mL in healthy controls. Each disease group had significantly higher IL-17 than controls after Holm correction (adjusted p = 0.0103, 0.0172, and 0.0196, respectively), whereas the three disease phenotypes did not differ significantly from one another. Conclusions: Circulating IL-17 concentrations were higher in allergic rhinitis, non-allergic asthma, and allergic asthma associated with allergic rhinitis than in healthy controls. However, the substantial overlap among disease phenotypes and the absence of statistically significant between-phenotype differences should not be interpreted as evidence of equivalence or a shared biological mechanism. These findings should be considered exploratory and require confirmation in larger, prospectively characterized cohorts.

Background: Alcohol-related macrocytic anemia remains insufficiently characterized, particularly regarding molecular correlates of disease severity and treatment response. We evaluated the hepatic, inflammatory and microRNA profile of patients with alcohol-related macrocytic anemia and explored predictors of hematologic improvement. Methods: This prospective single-center observational study included 60 adults with alcohol-related macrocytic anemia. Patients were stratified by baseline severity (mild, n = 21; moderate, n = 17; severe, n = 22) and by treatment response (no change, n = 18; improved, n = 42). Hematologic, iron, nutritional, inflammatory, hepatic and miRNA (miR-21, miR-34a, miR-451a) data were analyzed using non-parametric tests, Spearman correlations and exploratory logistic regression. Results: Greater anemia severity was associated with longer alcohol exposure, higher weekly alcohol intake, higher GGT, more frequent chronic liver disease and higher expression of all three miRNAs. Hemoglobin and hematocrit decreased across severity groups, whereas MCV increased. Vitamin B12, folate, iron indices, CRP and IL-6 did not differ significantly by severity. No variable significantly distinguished patients who improved from those without hematologic change. All three miRNAs correlated inversely with hemoglobin and positively with MCV, GGT and alcohol-consumption measures. Conclusions: Alcohol-related macrocytic anemia shows a severity gradient linked to alcohol burden, hepatic involvement and distinct miRNA dysregulation. Predictors of treatment response were weak, supporting larger validation studies.

Chia seed (Salvia hispanica L.) is increasingly incorporated into contemporary foods, yet its allergenic potential remains poorly characterized. Published clinical evidence is limited to a small number of case reports, conference reports, and one case series describing immediate IgE-mediated reactions, cutaneous manifestations, and anaphylaxis. Molecular studies have identified candidate allergenic protein families, including 2S albumins, 7S vicilin-like globulins, 11S legumin-like globulins, and oleosins, and have demonstrated IgE recognition and potential cross-reactivity, particularly with sesame. However, molecular cross-recognition does not establish clinically relevant cross-allergy. This structured narrative review synthesizes the available clinical and molecular evidence regarding chia seed allergy, with emphasis on clinical manifestations, candidate allergens, chia–sesame cross-reactivity, diagnosis, and major knowledge gaps. Current evidence supports chia as a potential emerging food allergen but is insufficient to determine prevalence, natural history, reaction thresholds, or individual risk. Standardized diagnostic extracts, validated specific IgE thresholds, component-resolved diagnostics, and chia-specific oral food challenge protocols are currently lacking. Prospective clinical studies and further molecular characterization are required to establish the true clinical significance of chia seed allergy.