Background/Objectives: Chronic spontaneous urticaria (CSU) is characterized by almost daily wheals or angioedema lasting for more than six weeks and not attributable to a defined inducing factor. CSU reportedly affects 1-2% of the general population and may lead to a substantial impairment in patients' quality of life. Thus, developing methods that enable early diagnosis and assessment of disease activity is a major objective for scientists and clinicians. Methods: A significant proportion of CSU cases appears to be associated with autoimmune mechanisms, which mainly involve IgE autoantibodies (type I CSU), IgG autoantibodies (type IIb CSU), or both (type I and type IIb overlap). To this end, detection of specific IgE and/or IgG autoantibodies in CSU patients using biological or immunochemical assays can offer valuable information and enable further investigation and better management of the disease. Results: This review focuses on and presents various immunochemical assays, mainly ELISAs, for determining specific IgE and/or IgG autoantibodies, along with immunochemical methods for quantifying total IgE levels as an additional biomarker in CSU patients; the development and/or application of these assays has been reported in several papers published in the last decade on CSU. Conclusions: The methods presented have recently been applied and have substantially contributed to CSU diagnosis, endotyping and prediction of response to various treatments. Further validation of the existing immunochemical assays along with the development of reliable assays for novel autoantibodies and/or autoantigens will deepen our understanding of CSU pathogenesis and support the clinical diagnosis and treatment of CSU.

Background: Reliable biomarkers that predict delayed treatment-free remission with omalizumab in chronic spontaneous urticaria (CSU) remain unclear. Objective: The objective was to identify independent predictors of delayed treatment-free remission with omalizumab by comparing patients who achieved treatment-free remission with ≤ 12 doses with those who required > 12 doses. Methods: This single-center retrospective study included 163 adult patients with antihistamine-refractory CSU who were treated with omalizumab (300 mg every 4 weeks) between January 2018 and October 2025. Treatment discontinuation was considered only after at least six consecutive doses and complete disease control, defined as a urticaria control test (UCT) score of 16 with no wheals or angioedema. Treatment-free remission was defined as a symptom-free period of at least 6 months without pharmacotherapy after discontinuation. Patients were classified as having early remission (≤12 doses) or delayed remission (>12 doses). Demographic, clinical, and laboratory variables were compared, and multivariable logistic regression was performed. Results: Of the 163 patients (median age, 41 years; 60.1% women), 99 (60.7%) had delayed remission and 64 (39.3%) had early remission. Delayed remission was associated with a higher prevalence of autoimmune disease in the delayed remission group than in the early remission group (27.3% versus 12.5%; p = 0.025) longer symptom duration before omalizumab initiation (p < 0.001), and higher baseline total immunoglobulin E (IgE) levels (p < 0.001). In multivariable analysis, longer pretreatment symptom duration (odds ratio [OR] 1.023 [95% confidence interval {CI}, 1.009-1.038]; p = 0.002) and autoimmune disease (OR 2.984 [95% CI, 1.130-7.882]; p = 0.027) independently predicted delayed remission, whereas the total IgE value did not (p = 0.070). Conclusion: Longer pretreatment symptom duration and coexisting autoimmune disease were the strongest independent predictors of delayed treatment-free remission with omalizumab in CSU.

Background: Hereditary angioedema (HAE) is a rare, potentially life-threatening bradykinin-mediated disorder with limited pediatric treatment options and little comparative evidence. Icatibant, a bradykinin B2 receptor antagonist, has demonstrated efficacy in adults and has emerging evidence in children. Objective: To evaluate and synthesize clinical evidence on the efficacy and safety of icatibant for acute HAE attacks in pediatric patients. Methods: A literature search was performed by using medical literature data bases, clinical trial and research registries, and key journals through January 2026. The primary outcome was the time to onset of symptom relief. Secondary outcomes included the time to minimum symptoms, pain scores, adverse events, and feasibility of self- or caregiver administration. All included studies were nonrandomized, single-arm trials with heterogeneous designs and outcomes definitions; therefore, a meta-analysis was not performed, and all studies were descriptively evaluated. Results: This systematic review identified three clinical studies of icatibant for acute HAE attacks in children ages 0 to 17 years. Three open-label, phase III studies, which included 43 pediatric patients were reviewed. Icatibant demonstrated rapid symptom relief, with a median onset at ∼1 hour and minimum symptoms within 2 hours, although repeated dosing showed variability. Icatibant was well tolerated, with injection-site reactions as the most common adverse events and no serious treatment-related events. Self- or caregiver administration was feasible and effective in adolescents. Conclusion: Icatibant was safe and effective in the pediatric studies, providing rapid symptoms relief and a favorable tolerability profile. Despite limitations from small sample sizes and lack of comparator trials, current evidence supports icatibant as a targeted, practical option for treating acute HAE attacks in children.

In 169 hospitalized adults with penicillin allergy histories, either through interview or listed in the electronic medical record of urticaria, angioedema, anaphylaxis, and/or shortness of breath at least 10 years ago, 94.1% tolerated a direct oral amoxicillin challenge led by a non-allergy specialist and were delabeled. Mild reactions occurred in 5.9%, with no severe events. This safe, effective approach may improve antibiotic stewardship, reduce costs, and support broader implementation over penicillin skin testing.

Mastocytosis is a neoplasm characterised by clonal proliferation of mast cells (MCs) in the skin and other organs, including the heart, and symptoms produced by MC-derived mediators. MC activation syndrome (MCAS) relates to increased and inappropriate activation of MCs without clonal proliferation. Mast cells are tissue-resident immune cells strategically located in different cardiac sites, e.g., myocardium, pericardium, aortic valve, and close to nerves, and in atherosclerotic plaques. The mediators (e.g., histamine, tryptase, chymase, cytokines, and chemokines) have roles in inflammation, angiogenesis, tissue remodelling, and fibrosis. They activate different cardiac resident immune cells (e.g., macrophages) and structural cells (e.g., fibroblasts and endothelial cells). MCs participate in atherosclerosis and several cardiovascular diseases (CVD), comprising allergic angina, coronary syndromes, and arrhythmias, by destabilizing and promoting atherosclerotic plaque rupture with its attendant dire consequences. Furthermore, MCs stimulate fibrosis after a myocardial infarction. MCAS is increasingly appreciated as it affects many patients previously noted to have various apparently idiopathic chronic multisystem inflammatory and/or allergic diseases or dystrophisms. Symptoms resulting from mediator release comprise flushing, hypotension, urticaria, angioedema, headache, vomiting, and diarrhea. Diagnosis is rendered by skin and/or bone marrow biopsy. Considering the increasing incidence and prevalence of MC-related diseases, guidance is needed for clinicians or researchers to select efficacious MC stabilizers that could block external stimulus signals into cells, inhibit intracellular signalling pathways, and disrupt degranulation. These novel therapies may soon find their way into the clinical arena. All relevant data and important advances in this recently recognized clinical entity are herein reviewed.

Hereditary angioedema (HAE) is a rare genetic disorder characterized by recurrent episodes of vascular leakage and tissue swelling. Although excessive bradykinin generation has long been considered the central pathogenic mechanism, increasing evidence indicates that endothelial cells play a decisive role in determining when and where vascular permeability occurs. This Review summarizes recent advances in endothelial biology relevant to HAE, highlighting how intercellular junctions, the endothelial glycocalyx, and dynamic endothelial activation states cooperatively regulate barrier integrity. Newly identified HAE subtypes caused by pathogenic variants that directly affect endothelial regulatory pathways further support endothelial dysfunction as a key disease mechanism beyond bradykinin excess. By integrating bradykinin-dependent and bradykinin-independent processes within an endothelial-centered framework, this Review proposes a revised conceptual model for HAE pathogenesis and discusses its implications for biomarker discovery and therapeutic strategies aimed at stabilizing the endothelial barrier.

We present a Mexican multigenerational family series of type I hereditary angioedema (HAE) with predominant abdominal involvement, including three affected adult sisters and a child identified through family screening. The index case was a 44-year-old woman with recurrent abdominal attacks, chronic diarrhea, multiple hospitalizations, and previous abdominopelvic interventions with no conclusive findings. During her clinical course, she developed non-urticarial lip edema, and abdominal CT showed segmental thickening of jejunal loops and mesenteric edema, findings consistent with bowel wall edema during an abdominal attack. The diagnosis was confirmed by low C4, decreased C1-INH functional activity, and low C1-INH antigenic levels. Family evaluation identified additional cases compatible with type I HAE, supporting a pattern of vertical transmission. After diagnosis, the index case received on-demand icatibant and initiated long-term prophylaxis with lanadelumab, remaining asymptomatic at the most recent follow-up. This series highlights the importance of considering HAE in patients with unexplained recurrent abdominal pain, edema without urticaria, and a suggestive family history, particularly when imaging suggests reversible small-bowel involvement, in order to reduce diagnostic delay and prevent potentially avoidable interventions.