Prescribing of the glucagon-like peptide 1 receptor agonists (GLP-1RA) is rapidly increasing as their efficacy for multiple indications becomes apparent. A better understanding of their cutaneous adverse effect profile is crucial, particularly as they are suggested for use in inflammatory dermatoses. We describe two patients who developed novel cutaneous reactions associated with initiation of a GLP-1RA. Patient 1 developed multiple tender subcutaneous nodules on the trunk and limbs 4 weeks after the initiation of semaglutide. Histology demonstrated a noncaseating granulomatous dermatitis, and serum -angiotensin-converting enzyme was elevated. A diagnosis of cutaneous (and likely drug-induced) sarcoidosis was made once systemic involvement had been excluded. On cessation of semaglutide, all lesions resolved without additional treatment. The Naranjo score indicated a probable drug reaction. Patient 2 presented with a recurrence of solar urticaria, confirmed on phototesting, 5 days after commencement of liraglutide, having previously been in remission for over 20 years. Her course was recalcitrant, despite cessation of liraglutide and a broad range of therapies. The Naranjo score suggested a probable association. These cases represent the first descriptions of cutaneous sarcoidosis and solar urticaria associated with GLP-1RA -therapy. While further work is required to define possible underlying mechanisms, we report these cases due to the convincing temporal relationship, high Naranjo scores and the large patient population now currently exposed to this drug class. Dermatologists should be aware of the possible cutaneous adverse or exacerbatory effects, as well as the potential significant benefits, of these increasingly commonly used medications.

Primary familial gastrointestinal stromal tumors (GIST) are characterized by the presence of typically multifocal GIST that most often involve the stomach. Additional gastrointestinal (GI) manifestations can include inflammatory fibroid polyps most often in the stomach or small bowel and interstitial cell of Cajal hyperplasia occurring throughout the GI tract. Skin hyperpigmentation typically involving the neck, face, axillae, groin, and perineum that appears in childhood or adolescence is common. Additional integument findings can include increased nevi, lentigines, and multiple café au lait macules. Less common features include urticaria pigmentosa, cutaneous mastocytosis, and systemic mastocytosis.

The stem cell factor (SCF)/KIT signaling axis regulates the survival, proliferation, differentiation, and migration of hematopoietic stem and progenitor cells, mast cells, interstitial cells of Cajal, germ cells, and melanocytes through multiple downstream pathways, including PI3K/AKT and RAS/MAPK. Its biological and pathological effects are determined by cell lineage, ligand presentation, and mutational context. At the pathway level, SCF expression and processing, KIT abundance, and activating mutations determine signal initiation and intensity, whereas CBL-mediated receptor degradation and SHP-1-mediated dephosphorylation limit signal duration. This narrative review critically examines representative multisystem diseases for which SCF/KIT involvement is supported by genetic, functional, or therapeutic evidence and distinguishes established treatments from investigational approaches. Activating KIT mutations drive gastrointestinal stromal tumors (GISTs) and systemic mastocytosis. Clinically established KIT-directed tyrosine kinase inhibitors, including imatinib for mutation-sensitive GIST and midostaurin or avapritinib for advanced systemic mastocytosis, have transformed disease management. By contrast, increased local SCF availability and KIT-dependent mast cell persistence may amplify inflammatory diseases, whereas impaired signaling is associated with gastrointestinal dysmotility, reproductive dysfunction, and pigmentary abnormalities. Emerging anti-KIT antibodies are being investigated as a strategy to deplete mast cells in chronic urticaria, whereas recombinant SCF-based mobilization has largely historical clinical relevance and regenerative applications remain experimental. Mutation-dependent drug sensitivity, polyclonal secondary resistance, multikinase-related toxicity, and on-target effects in normal KIT-dependent tissues remain major challenges. A disease-, genotype-, and cell-specific framework is therefore essential for translating SCF/KIT biology into safe and effective precision therapies.

Chronic spontaneous urticaria (CSU) is a mast cell-driven inflammatory disease frequently accompanied by anxiety, depression, sleep disturbance, fatigue, and impaired quality of life. Pruritus, disturbed sleep, psychosocial burden, and treatment-related effects are established contributors to this neuropsychiatric and functional burden. Whether immune-to-brain signalling provides an additional mechanism in a susceptible subgroup remains unknown. This hypothesis-driven narrative review examines the blood-brain barrier (BBB) as one potential interface linking CSU-associated inflammation to central effects. CSU studies report systemic inflammatory, vascular, and neuroimmune signals, including cytokine signatures, circulating matrix metalloproteinase-9, and substance P-MRGPRX2-related findings. Their potential neurovascular relevance is inferred from experimental or other disease settings rather than demonstrated in CSU per se. Our targeted search identified no human CSU studies assessing regional BBB permeability with dynamic contrast-enhanced magnetic resonance imaging or tracer methods, blood-cerebrospinal fluid barrier function with the albumin quotient, serum S100B, or brain endothelial tight-junction integrity, including claudin-5 or occludin. Structural and functional neuroimaging findings in CSU do not establish barrier dysfunction. Systemic mastocytosis provides comparative evidence for mast-cell-related neuropsychiatric manifestations, although barrier involvement remains unproven. We therefore propose neurovascular alteration as a testable, non-exclusive risk modifier whose relevance to CSU pathophysiology and psychiatric symptoms remains to be established.

We report a case of acute hemorrhagic edema in a four-month-old boy, which occurred following a viral respiratory infection seven days prior to his admission. The clinical presentation began with the appearance of erythematous macules initially localized to both feet, which then spread to both thighs. All of this occurred against a background of a fever of 38.5 °C, while the child's general condition remained stable. Initially treated as purpura fulminans, but given the child's stable general condition and normal laboratory findings, the diagnosis was revised to acute hemorrhagic edema of infancy, characterized by fever and large, coin-shaped purpuric skin lesions, often associated with edema. The differential diagnosis includes hemorrhagic urticaria, other non-infectious vasculitides, erythema multiforme, Kawasaki disease, infectious eczema, and sepsis (meningococcal or otherwise). Some of these conditions carry a risk of mortality. Management is based primarily on symptomatic treatment, with a favorable prognosis.

Chronic idiopathic urticaria (CIU) is a dermatologic condition characterized by recurrent wheals, angioedema, or both for more than six weeks in the absence of an identifiable trigger. It is driven by spontaneous mast cell activation and the release of inflammatory mediators in the skin. Given its poorly understood pathogenesis, significant morbidity, and limitations of available treatment modalities, studies have suggested a link between diet and CIU. The primary objective of this study was to evaluate the literature published from 2015 to 2025 on this link, with an emphasis on dietary interventions, patient-reported outcomes, and gaps in the existing knowledge base. We conducted a scoping review following PRISMA guidelines, utilizing databases such as EMBASE, OVID Medline, and Web of Science. Search terms related to urticaria included "chronic idiopathic urticaria," "chronic spontaneous urticaria," "chronic idiopathic/spontaneous urticaria," "CIU/CSU," "CSU/CIU," "spontaneous chronic urticaria," and "idiopathic chronic urticaria," combined with terms related to diet, including "diet," "diet influence," "diet regimen," and "dietary effect." The initial database search identified 121 records, of which nine met the eligibility criteria and eight were included after critical appraisal. The eight included studies examined the Mediterranean diet, a low-pseudoallergen diet, a pseudoallergen-free diet, a histamine-free, low-pseudoallergen diet, and a low-histamine diet, as well as micronutrient levels and inflammatory markers. The dietary interventions lasted from seven to slightly more than 39 days. The studies evaluated the effects of these diets on CIU disease activity, disease control, and quality of life using measures such as the Urticarial Activity Score, Urticarial Control Test, and Chronic Urticaria Quality of Life score. Outcomes tended to improve in the short term following the implementation of these diets, particularly in studies of diets limiting histamine and pseudoallergen intake. Additional findings included an association between CIU and a higher BMI. One study also reported higher vitamin D levels and lower vitamin B12 levels in patients with CIU than in the general population. The current body of literature is limited by small sample sizes, short intervention durations, and limited immunologic exploration. However, the consistency of patient-reported improvements across diverse geographic and dietary contexts underscores the potential role of diet as an adjunctive approach to CIU management. Future research should prioritize larger sample sizes, more balanced representation of the sexes, longer-term trials, and better control of participant-level confounding variables.

A 6-year-old child with complicated necrotizing pneumonia developed acute ataxia, urticarial rash and urinary incontinence on the third day of levofloxacin therapy. No structural abnormalities were found on imaging. The antibiotic was discontinued, and corticosteroids with antihistamines were initiated, leading to complete symptom resolution without sequelae. This pediatric case underscores the need for vigilance regarding levofloxacin-induced movement disorders, even with short-term use.

In the article "Safety and Efficacy of Remibrutinib for Chronic Spontaneous Urticaria: A Systematic Review and Meta-Analysis" [Int Arch Allergy Immunol. 2026;187(6):635-646. https://doi.org/10.1159/000548302] by Muhammad Burhan et al., online supplementary Figure 11 has been corrected.Following publication, the authors reviewed their data and found that an error occurred during the compilation of their forest plot of online supplementary Figure 11. This error arose from an internal data entry oversight during the analysis phase.The corrected online supplementary Figure 11 has been provided here. In addition, the corrected Results sentence in the manuscript text is as follows:"Three studies examined nasopharyngitis cases in both groups. The pooled analysis, as depicted in online supplementary Figure 11, demonstrated a statistically significant increase in the risk of nasopharyngitis in the remibrutinib group compared with placebo (RR: 1.88, 95% CI: 1.11-3.19, I[2] = 0%, p = 0.02)."

Spironolactone is a widely used mineralocorticoid receptor antagonist with a well-established adverse-effect profile; however, angioedema is uncommon and a poorly recognized adverse reaction. We report a case of suspected isolated lip angioedema associated with spironolactone therapy in a 74-year-old woman. The patient presented with a two-week history of persistent upper-lip swelling and facial heaviness without urticaria, pruritus, tongue or oropharyngeal involvement, or symptoms of airway compromise. Although spironolactone had been prescribed approximately one year earlier, the patient had been poorly adherent and had resumed consistent daily use approximately one month before the onset of symptoms. She continued spironolactone despite the development of swelling. Clinical evaluation and laboratory investigations did not identify an alternative cause, and serum complement C4 was within the normal range. C1-esterase inhibitor antigenic and functional assays were unavailable. Spironolactone was discontinued, resulting in substantial improvement by Day 7 and complete resolution by Day 14 without recurrence. The Naranjo Adverse Drug Reaction Probability Scale yielded a score of 6, consistent with a probable adverse drug reaction. This case highlights isolated lip angioedema as a potential, although rare, adverse reaction to spironolactone and underscores the importance of establishing actual medication exposure when assessing suspected drug-related reactions. Recognition of uncommon medication triggers may facilitate timely withdrawal of the offending agent and prevent potentially more severe recurrence.