Allergologia et immunopathologia最新文献

Background: Proton pump inhibitors (PPIs) are identified to cause immediate hypersensitivity reactions and cross-reactivity among them. In this study, we aimed to describe the clinical features of immediate-type hypersensitivity reactions caused by PPIs, the results of drug tests performed with PPIs, and the cross-reactivity between PPIs. There are immediate hypersensitivity reactions with PPIs and there may be cross-reactivity between PPIs. In this study, we aimed to describe the clinical features of immediate-type hypersensitivity reactions caused by PPIs, the results of drug tests performed with PPIs and the cross-reactivity between PPIs.

Methods: Adult patients who described an immediate hypersensitivity reaction to PPIs between March 1, 2017 and March 1, 2023 were evaluated.

Results: Of the 47 patients included in the study, 89.4% were females, and the suspected PPI in 68% of the patients was lansoprazole. Anaphylaxis accounted for 72.3% of reactions, and the most common reaction was grade 2 (42.6%) according to Ring Messmer. Those who had two or more reactions to the same or different PPI were 51.1% of patients. A positivity rate of 43.8% was observed in the skin prick test with the suspected drug, 33.3% in the intradermal test, and 100% in the provocation test. There is varying potential for cross-reactivity among five different PPIs.

Conclusions: İmmediate hypersensitivity reactions are observed among PPIs, particularly to lansoprazole, with the majority of reactions being anaphylaxis. Multiple life-threatening reactions can be prevented by increasing awareness of allergies to PPIs. Cross-reactivities among PPIs are variable, and further studies are needed to elucidate cross-reactivity with PPIs.

Drug-induced fixed urticaria (DIFU) is a rare skin reaction, characteri zed by pruritic hives that reappear in the same location after exposure to the triggering drug. In the few cases reported in the literature, it is considered as an atypical variant of fixed drug eruption (FDE). We present the case of a 10-year-old girl with allergic rhinoconjunctivitis, who had experienced three episodes of localized urticaria on the dorsal surface of both arms, 1 hour after taking ibuprofen. These manifestations did not appear when taking paracetamol, which she tolerated. Her father suffers from generalized urticaria to NSAIDs. An oral provocation test (OPT) was performed with ibuprofen, acetylsalicylic acid, and metamizole, which also caused the same fixed-location wheals and subsequent spontaneous resolution. She, however, tolerated an OPT with meloxicam. This case is notable because of the rarity of the DIFU and the familial aggregation of hypersensitivity to NSAIDs. In this case, as in those of DIFU described in the literature, the hives appeared shortly after the drug was administered and resolved rapidly. This feature distinguishes it from FDE, and it resembles acute drug urticaria, as in the patient's father, which raises questions concerning the pathophysiology of DIFU.

Background: Several inflammatory diseases, including colitis, are treated via probiotics but still the mechanism is not clear.

Objective: This study aimed to restore normal functioning of the gut and ameliorate inflammation in dextran sulfate sodium (DSS)-induced colitis mice via the probiotic intervention of Pediococcus acidilactici (P. acidilactici) BCB1H and Lactiplantibacillus plantarum (L. plantarum) HMX2.

Material and methods: L. plantarum HMX2 and P. acidilactici BCB1H showed a remarkable reduction in the symptoms of DSS-induced colitis, including weight loss, shortening and damage of the colon, decreased tight junction protein, and pro-inflammatory cytokines in the blood of mice. Two treatment groups were administered with probiotic strains based on animal weight for a duration of 28 days; however, prior to this, DSS was induced.

Results: After consuming both probiotics, the levels of inflammatory markers, such as tumour necrosis factor alpha (TNF-α) and interleukins (IL-1β) exhibited a noticeable decline, indicating a reduction in inflammation. The Disease Activity indices for both probiotic-treated groups (P. acidilactici BCB1H- and L. plantarum HMX2-treated groups) were significantly lower (1±0.45, 1±0.36, 3±0.08, 1±0.18, respectively) than that for the DSS-treated group. Both these treatment strains significantly affected the markers of oxidative stress and inflammation (i.e., malondialdehyde [MDA], superoxide dismutase [SOD], and myeloperoxidase [MPO], compared to the intoxicated group. Similarly, the BCB1H- and HMX2-treated groups showed partial recovery, with improved hepatocyte structure and reduced inflammatory cell infiltration, compared to the intoxicated group. Polymerase chain reaction results of gel analysis showed crucial indicators that measure both colonic integrity and inflammation across four experimental groups of colitis-induced mice. Pro-inflammatory cytokines (TNF-α and IL-1β), E-cadherin, and MUC2 mucin served as evaluated markers across experimental groups.

Conclusion: Increased expression of these genes suggests that both probiotic strains successfully enhanced and restored normal functions of the gut and suppressed inflammation. This could be attributed to the combined immunomodulatory action of probiotics.

Following bee stings, multiple case reports have described the onset of autoimmune-related conditions, including myasthenia gravis, nephrotic syndrome, Henoch-Schönlein purpura, myocardial infarction, cerebrovascular events, and localized alopecia, typically within a few days, indicating that bee venom may play a role in triggering autoimmunity. We report a rare case of total alopecia occurring within ten days after a bee sting. While the literature includes one prior case of total alopecia following bee sting-induced anaphylaxis, our case is distinct in that the patient developed total alopecia in the absence of any hypersensitivity reactions, suggesting a potential immunomodulatory or exacerbating effect of the bee sting on the immune system.

Rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) are chronic autoimmune diseases characterized by persistent inflammation and progressive tissue damage, posing significant challenges to effective treatment. To gain deeper insights into their shared molecular mechanisms, we performed an integrative bioinformatics investigation aimed at uncovering common pathways and therapeutic targets. Using a cutoff of p-value < 0.05 and Log2 FC > 1, differential gene expression analysis identified 1178 DEGs in RA and 7783 DEGs in SLE, with 358 genes common to both diseases. Construction of a protein-protein interaction network revealed several hub genes, including PDE4A, H1-10, H4C6, and PIP, which were highly interconnected and clustered into functional modules. Molecular docking analysis demonstrated that alpha linolenic acid (ALA) exhibited strong binding affinity toward these key proteins, with binding energies ranging from -8.3 to -9.4 kcal/mol. Toxicity profiling further suggested that ALA possesses a favorable safety profile, showing minimal risks of hepatotoxicity, neurotoxicity, and related adverse outcomes. Functional enrichment pointed to the involvement of common signaling cascades, particularly the cAMP and TGF-β pathways, as potential therapeutic avenues. Collectively, our findings highlight ALA as a promising therapeutic candidate capable of modulating shared molecular drivers in RA and SLE. Further in vitro and in vivo validation is essential to confirm its mechanistic effects and therapeutic potential for clinical translation.

Background: Anaphylaxis is a severe, potentially fatal, systemic hypersensitivity reaction induced by various triggers.

Objective: Only a few studies have examined the clinical manifestations of childhood anaphylaxis across different age groups. We aimed to evaluate, according to age group and trigger, the clinical features of anaphylaxis in pediatric patients.

Methods: We retrospectively evaluated 130 children diagnosed with anaphylaxis over 11 years.

Results: The median age of the patients was 10 years (min-max: 0.5-17.8), and 83 (63.8%) were male. Regarding age groups, 23 (17.7%) of the patients were infants, 26 (20%) were preschoolers, 31 (23.8%) were school-age children, and 50 (38.5%) were adolescents. Among the causes with known triggers, the most prevalent trigger was identified as food- affecting 44 (33.8%) cases-followed by drugs (34 cases, 26.2%) and venoms (18 cases, 13.8%). There was a statistically significant relationship between age groups and triggers (p < 0.001). The triggering role of drugs and venoms was found to be low in infants. Also, the infant group had significantly lower risks of venom-induced and drug-induced anaphylaxis compared to the adolescent group. The top three triggers identified in our patients were compared according to the system involved, and a statistically significant relationship was found between triggers and cardiovascular findings (p = 0.006).

Conclusion: The etiology of anaphylaxis may vary by age group. Depending on the trigger, it may also have different clinical manifestations.

Abemaciclib, a cyclin-dependent kinase 4/6 (CDK4/6) inhibitor, is an effective targeted therapy for hormone receptor-positive (HR+), HER2-negative, advanced or metastatic breast cancer. While nonimmediate hypersensitivity reactions (NIHRs) have been reported, no immediate hypersensitivity reactions (IHRs) to abemaciclib have been documented to date. Here, we report the first successful desensitization protocol for a patient who developed IHR to abemaciclib. A 75-year-old female with stage II breast cancer underwent a partial mastectomy followed by chemotherapy. Abemaciclib was initiated as part of adjuvant treatment. One hour after the third dose, she presented to the emergency department with lip swelling and urticaria. Symptoms resolved following the administration of intravenous methylprednisolone (0.5 mg/kg) and maleate pheniramine (45.5 mg/mL). Skin prick testing with abemaciclib was negative; however, a drug provocation test led to recurrence of urticaria at a cumulative dose of 150 mg. Given the clinical necessity of abemaciclib and the lack of alternatives, a 12-step desensitization protocol was implemented using 300 mg of abemaciclib dissolved in 100 mL of distilled water. The protocol was completed over 4 h, with no complications observed during the procedure or in the subsequent 3-month follow-up. The patient continued abemaciclib at 300 mg/day without recurrence of symptoms. This case highlights the importance of drug desensitization in oncology, particularly in patients for whom no alternative therapies are available.

Introduction: Molecular characterization of house dust mite (HDM) and storage mite allergens provides valuable insights into sensitization patterns; however, relationships among different mite allergens and their clinical implications remain unclear.

Methods: A total of 100 patients with allergic rhinitis sensitized to Dermatophagoides pteronyssinus were analyzed. Specific IgE (sIgE) levels were measured using singleplex and multiplex assays. Correlations among mite allergens and their associations with clinical and demographic variables were evaluated.

Results: The median sIgE level to Der p was 15.8 kU/L (IQR: 50.25); no relevant Dermatophagoides spp. sensitization was found below 2 kU/L. Among patients with Der p >10 kU/L, 59 of 60 had significant sIgE to at least one major HDM allergen. The highest prevalence was for Der p 1 (92%), though its median level was low (3.19 kU/L, IQR: 8.18). Conversely, Der f 2 had the highest median sIgE (23.4 kU/L, IQR: 33.74). Multivariate analysis revealed that most allergen levels were predictable from clusters of other mite allergens (R²=0.27-0.98). Mite allergen sIgE (Aca s, Blo t 5/10/21, Der f 1/2, Der p 1/2/5/7) correlated positively with sensitization number. sIgE levels negatively correlated with age and positively correlated with atopic dermatitis (Der p 1/2/23, Der f 1/2), asthma (Aca s, Der p 21), food allergy (Aca s, Der f 1, Der p 1), and rural residence (Der p 7).

Conclusion: Der p source allergen reliably excludes clinically relevant sIgE to HDM components. The correlations among mite allergens highlight challenges in clinical relevance assessment, emphasizing the need for component-resolved diagnostics to optimize immunotherapy responses.

Introduction: Immunoglobulin G (IgG) subclass deficiencies are among the most common primary immunodeficiencies in children and are associated with increased susceptibility to infections. This study aimed to investigate the clinical features, associated immunological conditions, and treatment outcomes in affected pediatric patients.

Methods: A retrospective analysis was conducted on 43 patients diagnosed with IgG subclass deficiency at the Allergy and Immunology Clinic of Fırat University between January 2019 and July 2024. Clinical records were reviewed for demographic data, immunoglobulin levels, and history of infections. The impact of prophylactic treatments-including intravenous immunoglobulin (IVIG), oral bacterial lysates, and antibiotics-on the frequency of infection was evaluated.

Results: Among the 43 patients, 32 (74.4%) were male and 11 (25.6%) were female, with a mean age at diagnosis of 6.77 ± 2.30 years. The most common clinical presentation was recurrent upper respiratory tract infections, reported in 23 patients (53.5%). Isolated IgG3 deficiency was identified in 34 patients (79.1%). During follow-up, normalization of IgG levels was achieved in 39 patients (90.7%), with a mean time to normalization of 2.1 ± 1.19 years. Prophylactic interventions significantly reduced the annual infection rate from 18.12 ± 10.37 to 3.09 ± 2.40 (p < 0.001).

Conclusion: IgG subclass deficiencies represent a significant health concern in children because of their association with recurrent infections. Early diagnosis and the implementation of appropriate prophylactic treatment strategies are crucial in reducing infection frequency and improving the quality of life. However, the retrospective nature of the study and the relatively small sample size may have limited the evaluation of clinical outcomes and treatment responses, potentially affecting the generalizability of the results. Despite these limitations, the findings highlight the potential benefits of prophylactic interventions in managing infections among children with IgG subclass deficiencies and emphasize the need for larger, prospective studies to inform evidence-based therapeutic strategies for this population.

Background: Rheumatoid arthritis (RA) is a chronic systemic autoimmune disorder that causes joint pain and significantly impairs patients' quality of life. Fucoxanthin, a naturally occurring carotenoid found in seaweeds and diatoms, has been reported to exert various therapeutic effects in multiple pathological conditions. However, its regulatory role in the pathogenesis of RA remains largely undefined.

Methods: Cell viability was assessed using the cell counting kit-8 (CCK-8) assay, while cell migration and invasion were evaluated through the wound healing and Transwell assays, respectively. Angiogenic potential was determined by the tube formation assay. The levels of pro-inflammatory cytokines, including interleukin (IL)-6, IL-1β, and IL-8, were measured using enzyme-linked-immunosorbent serologic assay. Intracellular reactive oxygen species (ROS) levels were analyzed via DCFH-DA staining, and protein expression was evaluated by Western blot analysis.

Results: Fucoxanthin significantly suppressed tumor necrosis factor-α (TNF-α)-induced proliferation of MH7A synovial cells. Additionally, TNF-α stimulation enhanced cell migration and invasion, whereas these effects were reversed with fucoxanthin treatment. TNF-α also promoted angiogenesis, as evidenced by an increased number of tube formations, which were markedly reduced by fucoxanthin in a dose-dependent manner (control; TNF-α; TNF-α + fucoxanthin [2 μM]; and TNF-α + fucoxanthin [4 μM], with respective values of 1.33 ± 0.58; 26 ± 3.61; 17 ± 2.65; and 8.33 ± 1.53; P < 0.001). Moreover, fucoxanthin alleviated TNF-α-induced inflammatory cytokine release and oxidative stress. Mechanistically, fucoxanthin was found to regulate the PPAR-γ/CTGF signaling pathway.

Conclusion: Fucoxanthin may attenuate inflammation and angiogenesis in RA by modulating the PPAR-γ/CTGF pathway, suggesting its potential as a therapeutic agent for managing RA.