MF Imunologijos ir alergologijos klinika (04.21)

Background Major depressive disorder (MDD) lacks established biological markers, although immune dysregulation and gut-derived inflammation have been implicated in a subset of patients; however, their diagnostic utility across levels of depression severity and impact of psychotropic treatment remain unclear. Methods This cross-sectional study examined circulating lipopolysaccharide (LPS) and cytokines (TNF-α, IL-6, IL-10, IFN-γ) in 95 patients with MDD and 51 healthy controls (HC), evaluating their diagnostic utility across depression severity and the influence of psychotropic medication. Depression severity was assessed using the Montgomery–Åsberg Depression Rating Scale, with patients stratified into mild-to-moderate and severe groups. Results Compared with HC, patients with MDD showed elevated LPS and TNF-α levels and reduced IL-10, while IL-6 and IFN-γ did not differ. LPS elevation was specific to mild-to-moderate MDD, whereas TNF-α was consistently elevated across all severity levels. A combined model including LPS, TNF-α, and IL-10 demonstrated the highest diagnostic accuracy for MDD (AUC = 0.778) and mild-to-moderate MDD (AUC = 0.818). TNF-α alone was the strongest predictor of severe MDD (AUC = 0.677), while LPS alone distinguished mild-to-moderate from severe MDD (AUC = 0.679). These associations remained significant after adjusting for age, sex, BMI, smoking status, and psychotropic medication use. LPS levels were higher in mild-to-moderate MDD during antidepressant monotherapy and lower with combination therapy regardless of severity. Conclusions Mild-to-moderate MDD is associated with elevated LPS, reflecting gut-derived inflammation and a distinct subtype, whereas severe MDD is linked to TNF-α. These biomarkers may aid in distinguishing MDD subtypes and inform targeted therapeutic strategies.

Background and Aims: Due to limited evidence linking lipid-related biomarkers (Lp(a), ApoB, oxLDL) with endothelial injuury and extracellular matrix glycoproteins (ECM) markers (endocan, vimentin, thrombospondin-1 (TSP-1), thrombospondin-2 (TSP-2)) in atherosclerosis, this study investigated their correlation with coronary atherosclerosis degree. Methods: This cross-sectional pilot study included 93 patients with stable angina pectoris (SAP). All participants underwent invasive coronary angiography (ICA), coronary computed tomography angiography (CCTA), or both, to evaluate coronary artery disease severity. Serum levels of oxLDL, ECM glycoproteins (TSP-1, TSP-2), vimentin, and endocan were measured using commercial ELISA kits. Each patient underwent echocardiography, carotid ultrasound for intima-media thickness (IMT) and plaque assessment, anklebrachial index (ABI) testing for peripheral artery disease (PAD) risk, and evaluation of arterial stiffness using cardio-ankle vascular index (CAVI) and pulse wave velocity (PWV). Results: Coronary artery disease (CAD) was diagnosed in 76.3% of patients (n = 71). OxLDL showed the strongest significant correlation with CAD severity (Figure 1). OxLDL serum levels correlations with selected clinical characteristics and indicators of atherosclerosis severity are presented in Tables 1 and 2. Serum vimentin levels were significantly correlated with many indicators of CAD severity (Table 3). In contrast,serum endocan levels did not differsignificantly betweenCADand nonCAD patients and showed no correlation with CAD severity, except for a weak inverse association with oxLDL. No significant differences in TSP-1 or TSP-2 levels were observed regarding CAD presence or severity; however, TSP-2 correlated positively with serum vimentin level, smoking status, and dyslipidemia Conclusions: OxLDL and vimentin significantly correlated with each other and with CAD severity. Vimentin also correlated with hsCRP. These results suggest their potential as biomarkers of atherosclerosis degree and supplement knowledge about relationship between oxLDL, endothelium damage and inflammation in the atherosclerosis pathogenesis. Endocan, TSP-1, and TSP-2 showed no independent correlations. Larger studies are warranted to confirm these findings.

Hereditary angioedema (HAE) is a rare genetic disorder characterized by recurrent episodes of severe, non-pitting edema, most commonly caused by a deficiency or dysfunction of C1 esterase inhibitor (C1-INH), resulting in excessive bradykinin production. HAE subtypes differ according to C1-INH levels, functional activity, underlying genetic variants, and increasingly recognized molecular mechanisms. Awareness of HAE outside specialized medical fields remains limited, and recurrent angioedema may arise through different pathophysiological mechanisms, which together contribute to frequent misdiagnosis, particularly in patients without a positive family history. Consequently, many patients experience significant diagnostic delays and inappropriate interventions. Rapid advances in endotype-based classification, molecular diagnostics, and targeted therapies have substantially changed the understanding and management of HAE, highlighting the need for an updated clinical overview. This review provides a comprehensive overview of HAE classification, clinical presentation, genetic background, diagnosis, and current management. Particular attention is given to advances in diagnostic biomarkers and genetic testing, newly approved targeted therapies, and oral on-demand treatment. Together, these advances are moving HAE management toward earlier diagnosis, more individualized treatment, and more patient-centered care.

Background and Objectives: Tobacco smoking is associated with an increased risk of depression and anxiety symptoms, but it remains unclear whether this relationship differs according to the type of nicotine product used. The increasing popularity of heated tobacco products has created a need to better understand their association with mental health, particularly in comparison with combustible cigarettes. Therefore, this study aimed to compare the prevalence of depression and anxiety symptoms among combustible cigarette (CC) users, heated tobacco product (HTP) users, and non-smokers. Materials and Methods: A cross-sectional study was conducted among 497 adults. Participants were classified into three groups according to their tobacco-use status: combustible cigarette smokers, heated tobacco users, and non-smokers. Depressive symptoms were assessed using the Patient Health Questionnaire-9 (PHQ-9), and anxiety symptoms were assessed using the Generalized Anxiety Disorder-7 (GAD-7). Group differences were evaluated using hierarchical linear regression analyses adjusted for sociodemographic, health, and lifestyle factors. Results: Tobacco-use group significantly improved the model fit for PHQ-9 (ΔR2 = 0.0575, p < 0.001) and GAD-7 (ΔR2 = 0.0764, p < 0.001). In non-smokers, scores of depression were 3.48 lower than in CC users and 1.42 lower than in the HTP users’ group. In HTP users, these scores were 2.06 lower than in the CC users’ group. Anxiety scores were 3.71 lower in non-smokers than in CC users, and 1.29 lower than in the HTP users’ group. In the HTP users’ group, this score was 2.42 lower than in the CC users’ group. HC3 robust standard errors with 5000-sample BCa bootstrap confidence intervals and reduced-adjustment sensitivity analyses confirmed the primary pattern. Conclusions: Our study results showed that combustible cigarette users had the highest adjusted depression and anxiety scores, HTP users had intermediate scores, and non-smokers had the lowest. In both tobacco-using groups, greater product-specific nicotine dependence was associated with higher PHQ-9 and GAD-7 scores. Further interdisciplinary studies incorporating biomarkers of nicotine exposure, HPA axis function, inflammation, and oxidative stress are needed to clarify whether the observed differences reflect the characteristics of individuals who choose specific tobacco products or are partly attributable to product-specific effects.

Allergic Rhinitis and its Impact on Asthma (ARIA) was, up until 2017, a guideline using the best evidence (Grading of Recommendations, Assessment, Development and Evaluation, GRADE) and developed as a change management strategy. A second change management strategy-in collaboration with the European Academy of Allergy and Clinical Immunology (ARIA-EAACI)-was developed as a person-centred, digitally enabled, artificial intelligence-assisted care (person-centred care) with strong political involvement. The digital tools of ARIA are mainly based on MASK-air, an Organisation for Economic Co-operation and Development (OECD) Best Practice for integrated care for chronic diseases. Artificial intelligence was used, in particular, to approach the patients' views and expectations. The current paper describes the steps to build and achieve a new change management strategy. The future of the Change Management strategy is (i) a collaboration between ARIA and EAACI, (ii) the development of ARIA 2024-2025 guidelines, (iii) the new ARIA-MeDALL classification of multimorbid airway diseases and (iv) embedding MASK-air in a registry for severe allergic diseases. The ultimate goals of the ARIA-EAACI change management strategy will be (i) the transformation of health and care in rhinitis and asthma multimorbidity and (ii) the development of novel guidelines and policies in a cost-effective manner, improving shared-decision-making.

Background: Inflammatory mechanisms contribute to major depressive disorder (MDD) in a subset of patients. Lipopolysaccharide (LPS), a potent inflammatory endotoxin, can induce depressive-like symptoms, but its relationship with specific depressive symptom profiles remains unclear. Methods: In total, 95 adults with MDD (mean age was 44 ± 14 years) were recruited from psychiatric inpatient and outpatient services. Depressive symptom severity was assessed using the Montgomery–Åsberg Depression Rating Scale (MADRS). Serum concentrations of LPS, IL-10, TNF-α, IL-6, and IFN-γ were measured by ELISA. Associations between inflammatory markers and depressive symptoms were examined using group comparisons, correlation analyses, multivariable linear regression, quantile regression, and mediation analyses adjusted for demographic and clinical covariates. Results: Patients with severe depression exhibited significantly lower circulating LPS levels than those with mild-to-moderate depression (95.6 vs. 165.2 pg/mL, p = 0.007), despite no significant differences in cytokine concentrations. LPS levels were inversely associated with depression severity, anhedonia factor score, and MADRS item 8 (“inability to feel”). Lower LPS concentrations were independently predicted by higher inability to feel, reduced appetite and combined pharmacotherapy use. Quantile regression demonstrated heterogeneity across the LPS distribution, with symptom–LPS associations evident among patients with higher LPS concentrations. Higher LPS levels were associated with greater apparent sadness, concentration difficulties, and reduced sleep, but lower levels of anhedonia, less reduced appetite, less lassitude, lower inner tension, and lower suicidality. Mediation analyses indicated that anhedonia mediated the association between LPS levels and depression severity. Conclusions: Higher circulating LPS may characterize a biologically distinct subgroup of MDD patients with lower symptom severity and less anhedonia, supporting biological heterogeneity within MDD.

Atopic dermatitis is a chronic inflammatory skin disease influenced by genetic predisposition, immune dysregulation, and environmental factors, as well as skin and gut microbiota. This review summarises the key mechanisms involved in this disease development, including disturbances in innate and adaptive immune responses, ethnic differences in immune pathways, and the contribution of microbial imbalance to skin barrier dysfunction. Special attention is given to salivary biomarkers-such as cortisol, melatonin, alpha-amylase, chromogranin A, C-reactive protein, and immunoglobulin A-which offer a non-invasive method for monitoring stress, sleep quality, and disease severity in patients with atopic dermatitis. Understanding the complexity of these factors may support earlier diagnosis and different treatment strategies and improve long-term disease management in a better way.

LF hypertrophy contributes to the narrowing and compression of neural structures, impairing limb function. It is a leading cause of spinal stenosis, particularly in the lumbar region. About 20% of those over 60 show lumbar stenosis on imaging, but over 80% have no symptoms. Surgery is the main treatment option and is only recommended for symptomatic cases. The exact cause of LF hypertrophy remains unclear, though chronic inflammation, fibrosis and oxidative stress are implicated. Research consistently shows that increased cytokines and growth factors drive extracellular matrix remodeling, immune cell infiltration, and fibroblast and osteoblast activation. The aim of this article is to briefly review the role of the main immune markers that are involved in the pathogenesis of LF hypertrophy. This narrative review is based on a PubMed literature search and includes 23 original articles published between 2019 and 2026.