Fluoxetine is a widely prescribed selective serotonin reuptake inhibitor in children and adolescents. Hypersensitivity reactions are rare and poorly characterized in this population. We report the case of a 17-year-old female who developed acute throat tightness with perceived oropharyngeal swelling and respiratory symptoms within 30 minutes of the first dose of fluoxetine, in the absence of cutaneous manifestations. Symptoms improved with bronchodilator therapy. Basophil activation testing demonstrated drug-induced activation, and an oral drug provocation test reproduced symptoms, confirming hypersensitivity. Previously reported pediatric cases included delayed urticaria, angioedema, and drug rash with eosinophilia and systemic symptoms. In contrast, this case highlights an immediate reaction predominantly affecting the airway. This report expands the known clinical spectrum of fluoxetine hypersensitivity reactions and emphasizes that the absence of cutaneous manifestations does not exclude drug allergy.

BACKGROUND Angioedema is a rare manifestation of systemic lupus erythematosus (SLE) that can lead to life-threatening complications, including airway compromise. Acquired angioedema is classically associated with C1 esterase inhibitor (C1-INH) deficiency caused either by increased consumption of C1-INH or the development of autoantibodies against C1-INH. However, emerging reports describe patients with active SLE who develop recurrent angioedema despite preserved C1-INH levels and function, suggesting a possible complement-mediated or bradykinin-associated inflammatory phenotype that remains incompletely characterized. CASE REPORT We report the case of a woman in her early 20s with SLE and lupus nephritis who presented with a urinary tract infection and unilateral periorbital edema. Initial laboratory evaluation revealed anemia, thrombocytopenia, and acute-on-chronic kidney injury. She was treated with antibiotics for presumed urinary tract infection and preseptal cellulitis. During hospitalization, she developed laryngeal edema requiring prompt treatment with intravenous dexamethasone, with rapid clinical improvement. Further evaluation demonstrated low C4 and C1q complement levels, elevated C1q complement binding levels, elevated anti-C1q antibodies, and preserved C1-INH antigen and functional levels, raising suspicion for complement-mediated angioedema occurring in the setting of active SLE. Over the ensuing 6 months, she experienced recurrent episodes of angioedema with progressive renal dysfunction and concern for evolving macrophage activation syndrome or severe hyperinflammatory immune activation. CONCLUSIONS This case highlights a rare presentation of recurrent angioedema associated with active SLE and complement activation despite preserved C1-INH levels and function. The case underscores the importance of early recognition of airway involvement in patients with lupus and illustrates the diagnostic challenges surrounding complement-mediated angioedema phenotypes in autoimmune disease.

Botulinum toxin (BoNT) type A is widely used in aesthetic and functional medicine and is generally considered safe when administered at appropriate doses and using proper techniques. However, rare and unusual complications may occur, even in patients with no previous neurological or allergic history. The author reports the case of a 24-year-old female who developed an unexpected neuromuscular complication characterized by progressive weakness of the forearm flexor muscles following a nonstandard intradermal sensitivity test of BoNT performed on the volar aspect of the forearm. The procedure was carried out by a nonspecialist practitioner. The patient subsequently developed reduced grip strength and functional limitation of hand movements within days, without systemic symptoms or clinical evidence of an allergic reaction. Clinical evaluation suggested a pharmacological neuromuscular effect rather than an immunologically mediated hypersensitivity reaction. No cutaneous signs of allergy, such as urticaria or angioedema, were observed. The temporal relationship and anatomical distribution of weakness were consistent with possible local toxin diffusion or unintended neuromuscular junction blockade. The patient was managed conservatively; a gradual improvement in muscle strength was observed over time. This case highlights a rare and atypical complication associated with the nonstandard use of BoNT and emphasizes the importance of adherence to evidence-based injection protocols performed by qualified specialists. It also raises concerns regarding the practice of intradermal "sensitivity testing," which lacks scientific validation and may lead to unintended neuromuscular effects, particularly when performed by nonspecialists. Further studies are needed to clarify the safety implications of nonstandard applications and to distinguish true hypersensitivity reactions from pharmacologic diffusion-related effects. Level of Evidence: 5 (Therapeutic) For image description, please refer to the figure legend and surrounding text.

Hereditary angioedema (HAE) is a rare genetic disorder, characterized by unpredictable, potentially life-threatening edema attacks. Treatment options include on-demand treatment (ODT) and long-term prophylactic (LTP) therapy. This study describes the HAE treatment landscape in Sweden, focusing on the uptake of recently reimbursed modern LTP therapies and patterns of ODT dispensation as an indirect proxy for breakthrough attacks.

Henoch-Schönlein purpura (HSP) is a small vessel immunoglobulin A (IgA) vasculitis that primarily affects children. Characteristic manifestations include purpuric rash, abdominal pain, renal insult and arthralgia. Non-classical manifestations, such as angioedema, may mimic signs and symptoms associated with differential diagnoses including hereditary angioedema, anaphylaxis and urticarial vasculitis. We present the case of a girl in middle childhood who presented with angioedema with a known history of HSP. Familiarity with atypical manifestations of HSP may mitigate the need for invasive diagnostics such as renal or skin biopsy.

Chronic spontaneous urticaria (CSU) and hereditary angioedema caused by C1 inhibitor (C1-INH) deficiency are mechanistically distinct disorders. When persistent wheals coexist with recurrent throat or abdominal symptoms, however, assigning individual episodes to mast-cell- or bradykinin-mediated pathways can be difficult.

Hereditary angioedema (HAE) is a rare genetic disease characterized by unpredictable, painful cutaneous and/or subcutaneous swelling attacks; laryngeal attacks can be fatal. For many patients, long-term prophylaxis (LTP) is critical for disease control and quality of life.Lanadelumab, a plasma kallikrein inhibitor, was approved for HAE LTP for adults and adolescents in 2018 and for children aged ≥ 2 years in 2023; it is currently one of the guideline-recommended, first-line LTP options. By integrating 7 years of cumulative clinical trial and real-world data, this narrative review summarizes lanadelumab long-term effectiveness and safety in adult, adolescent, and pediatric HAE populations. Outcomes in 41 peer-reviewed publications were evaluated, including 5 clinical trials involving 262 lanadelumab-treated patients and 28 real-world studies comprising ~ 700 patients. Across clinical trials, lanadelumab reduced attack rates by up to 100%, with an average of 24.9-27.3 patient-reported attack-free days per 28-day period. These findings were largely corroborated by real-world data, including 2 large observational studies with > 100 patients each. Patient-reported disease control and health-related quality of life improved consistently across both settings. The main treatment-related adverse events across studies were injection site reactions. Treatment persistence was generally high in clinical practice. Unmet needs remain for specific populations, including pregnant or lactating patients and those without access to guideline-recommended LTP. Future research should address real-world outcomes in pediatric patients, extended dosing intervals in well-controlled disease, transitions from other LTP therapies, and cost-effectiveness. Overall, sustained effectiveness, safety, and quality-of-life benefits of lanadelumab reinforce its role as a cornerstone of HAE management.

Chronic urticaria is a common mast-cell-driven inflammatory disorder characterized by recurrent wheals, angioedema, or both. Angioedema is associated with higher disease burden, impaired quality of life, and greater difficulty in clinical assessment, yet the overall research structure of chronic urticaria in the context of angioedema has not been systematically mapped. Publications were retrieved from the Web of Science Core Collection on July 14, 2026. English-language Articles and Reviews published between 1947 and 2026 were included after independent screening by two researchers, with disagreements resolved by a third researcher. Bibliometrix, VOSviewer, CiteSpace, Scimago Graphica, and GraphPad Prism were used to analyze annual output, countries, institutions, authors, journals, co-cited references, and keyword evolution. A total of 881 publications were included. Annual output increased over time, with faster growth after 2014. The United States ranked first in productivity, Germany had the highest citation count and total link strength, and Charité - Universitätsmedizin Berlin was the leading institution. The knowledge base was concentrated in mast cell biology, autoimmune mechanisms, anti-IgE therapy, and patient-reported outcomes. Keyword analysis showed a shift from early immune plausibility and idiopathic descriptions toward disease standardization, quality of life, and targeted therapy, including omalizumab and newer targeted treatments. Angioedema remained a high-frequency term and was repeatedly linked to disease burden, assessment, and treatment. The literature addressing both chronic urticaria and angioedema showed increasing emphasis on structured clinical assessment, mast-cell and autoimmune mechanisms, patient-reported outcomes, biomarker-oriented stratification, and targeted treatment. Future research should broaden international participation and evaluate clinically useful biomarkers and patient-centered outcomes across diverse populations.

A 12-year-old premenarchal female patient presented with right iliac fossa pain, perianal pruritus, urticaria, angioedema, arthralgia, peripheral eosinophilia, and an initially undetectable C-reactive protein. Serial ultrasonography demonstrated increasing intra-abdominal free fluid. Diagnostic laparoscopy demonstrated appendiceal serosal injection, turbid pelvic fluid, and mesenteric lymphadenopathy, prompting appendectomy. Histopathology identified Enterobius vermicularis (EV) within the appendiceal lumen, with reactive lymphoid hyperplasia but no acute suppurative inflammation. Symptoms resolved following surgery and mebendazole treatment. A descriptive updated systematic review of appendectomy specimens containing EV was performed. Seventy-six studies comprising 196,138 appendectomy specimens were included. EV was identified in 3,913 specimens, corresponding to a crude proportion among appendectomy specimens of 2.00% (95% CI: 1.93-2.06%). Among 11 newly identified studies reporting histological subclassification, 247 of 694 EV-positive specimens (35.6%) demonstrated histological acute appendicitis, whereas most showed non-suppurative or reactive pathology. This case and review suggest that appendiceal enterobiasis may present as an appendicitis-like illness, particularly when abdominal pain occurs alongside atypical features such as perianal pruritus, eosinophilia, urticaria, or angioedema. Recognition of enterobiasis may guide anthelmintic therapy and consideration of household treatment; however, a causal relationship between EV and systemic hypersensitivity features cannot be established from a single case. Importantly, clinical deterioration should continue to prompt urgent surgical assessment.

Chronic spontaneous urticaria (CSU) is marked by repeated episodes of wheals and/or angioedema lasting more than six weeks and occasionally coexists with autoimmune thyroid disease. Autoimmune thyroid disease may contribute to CSU in a subset of patients, and symptoms can be refractory to conventional antihistamine and corticosteroid therapy. A 33-year-old woman with a history of asthma presented with recurrent widespread urticaria and periorbital angioedema, often triggered by food, resulting in repeated acute care visits. Symptoms were minimally responsive to high-dose antihistamines and systemic corticosteroids. She underwent evaluation for mast cell disorders and neuroendocrine tumors, which were excluded through normal serum tryptase, urinary 5-hydroxyindoleacetic acid, and plasma metanephrine levels. Biochemical testing revealed suppressed thyroid-stimulating hormone (TSH) and elevated free thyroid hormones, with positive TSH receptor antibodies, consistent with autoimmune thyroid disease. Medical management with antithyroid therapy, beta-blockers, and antihistamines achieved biochemical control of hyperthyroidism but did not improve urticaria. Thyroid ultrasound demonstrated diffuse hypervascular enlargement. Given persistent severe CSU and refractory hyperthyroidism, the patient underwent total thyroidectomy. Histopathological examination confirmed autoimmune thyroid disease. Following surgery, urticaria and angioedema resolved completely, with no recurrence at follow-up. This case illustrates a severe autoimmune CSU phenotype likely mediated by overlapping IgE- and IgG-driven mechanisms sustained by active thyroid autoimmunity. The complete resolution of urticaria following thyroidectomy suggests a direct causal relationship. Early recognition of thyroid dysfunction in patients with recurrent or refractory CSU can guide targeted management, prevent repeated hospital visits, and, in select cases, may enable definitive thyroid ablation as a curative approach. Multidisciplinary evaluation and individualized treatment planning are essential for patients presenting with severe autoimmune CSU unresponsive to conventional therapy.

Angioedema is defined as transient swelling of the skin and/or mucous membranes. Based on the underlying mediator, angioedema is essentially classified as either mast cell-mediated or bradykinin-mediated. In general, mast cell-mediated angioedema is of shorter duration (1-3 days) and responds to antihistamines, corticosteroids and adrenaline, whereas swelling associated with bradykinin-mediated angioedema typically persists longer and does not respond to histamine-targeted drugs. Mast cell-mediated angioedema includes swelling occurring as part of allergic (IgE-mediated) or pseudoallergic (non-IgE-mediated) reactions, such as those observed in anaphylaxis or intolerance to analgesics. The diagnostic evaluation comprises a detailed medical history, measurement of specific IgE antibodies and/or skin prick testing, as well as provocation testing when indicated. Mast cell-mediated angioedema frequently occurs in association with chronic spontaneous urticaria (CSU), in which approximately 10% of patients can present with isolated angioedema without wheals as well as with chronic inducible urticaria (CIndU). The diagnostic work-up follows current recommendations for chronic urticaria and includes a thorough medical history, physical examination (potentially supported by review of photographic documentation) and basic laboratory investigations, including a differential blood count, C‑reactive protein (CRP), total IgE, and IgG anti-thyroid peroxidase (anti-TPO) antibodies. In the routine clinical practice, in both emergency settings and during the elective evaluation of patients with angioedema, it is essential to be familiar with the characteristic clinical features, differential diagnoses and diagnostic approaches of the various forms of mast cell-mediated angioedema.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are a well-known cause of systemic hypersensitivity (urticaria, angioedema, and bronchospasm). Ocular involvement is usually described as merely a component of a systemic reaction. It should be distinguished from the local toxicity of topical ocular NSAIDs. To our knowledge, very few cases of isolated allergic conjunctivitis induced by oral NSAIDs have been reported. We report the case of a 24-year-old woman with no history of atopy, who had presented for the past 7 months with recurrent bilateral asymmetric allergic conjunctivitis, predominantly affecting the right eye and strictly coinciding with her menstrual cycle. Examination revealed reduced visual acuity due to conjunctival chemosis and tearing, at 20/25 (LogMAR 0.10) in the right eye and 20/22 (LogMAR 0.05) in the left eye. Allergy testing, including prick tests and eosinophil counts, did not identify a relevant causative allergen explaining the clinical presentation. A detailed medication history revealed a temporal correlation with oral ibuprofen used for severe dysmenorrhea, without any accompanying cutaneous, respiratory, or systemic symptoms. Upon discontinuation of ibuprofen and its replacement with paracetamol and codeine, no recurrence was observed for four consecutive months, and an oral provocation test performed in the fifth month was positive, with mild conjunctivitis confirming the diagnosis. We report a case of isolated allergic conjunctivitis induced by oral NSAIDs and confirmed by an oral provocation test, which highlights the importance of a systematic review of medication history in all cases of recurrent conjunctivitis and that oral NSAIDs should be considered in the diagnosis of recurrent conjunctivitis.