Summary Our study confirms an association between basophil histamine content and features of type IIb CSU. However, this biomarker is not suitable for predicting omalizumab treatment response or treatment course.

Chronic urticaria is a mast cell-driven inflammatory disease characterized by recurrent wheals, angioedema or both for more than 6 weeks, with substantial effects on sleep, quality of life, mental health and daily functioning. Type I autoallergic and type IIb autoimmune mechanisms represent major endotypes, but many patients show overlapping or mixed features, contributing to heterogeneous clinical courses and variable treatment responses. Current management relies on confirming the diagnosis, excluding differential diagnoses, identifying aggravating factors and comorbidities and monitoring disease activity and control using validated patient-reported outcome measures. A limited, clinically guided diagnostic workup is preferred, with extended investigations reserved for selected cases based on history, examination, red flags or isolated angioedema. Second-generation H1-antihistamines remain the first-line therapy, with up-dosing recommended in insufficient responders. Omalizumab has transformed the treatment of antihistamine-refractory disease, while newer options such as dupilumab and remibrutinib further expand the therapeutic landscape. Ciclosporin remains an effective option in selected patients, particularly those with severe or difficult-to-treat disease, but requires careful safety monitoring. In chronic inducible urticaria, provocation testing, threshold assessment, trigger counselling and individualized treatment are central to care. Despite recent advances, important unmet needs remain, including reliable biomarkers for endotyping, evidence-based selection among emerging therapies, better data in children and other special populations, standardized definitions of remission and relapse and disease-modifying strategies. Future management is expected to move towards biomarker-driven, personalized care, enabling more precise treatment selection and sustained disease control.

BACKGROUND:Chronic urticaria (CU) diagnosis includes the patient's clinical history and physical examination. However, atypical presentations or misdiagnosis can lead to diagnostic delay (DD). OBJECTIVE:The impact and contributing factors of DD in CU are unknown and were assessed in the present study. METHODS:We retrospectively analysed data from CU adult patients from the international, multicenter Chronic Urticaria Registry (CURE). RESULTS:Of 4332 CU patients, 61% had standalone chronic spontaneous urticaria (sCSU), 18% had ≥ 1 form of chronic inducible urticaria (CIndU), and 21% had a combination of both (CSU + CIndU). Diagnosis of CU was delayed in 24% of patients by at least 1 year. CIndU patients showed a longer DD compared to those with sCSU or CSU + CIndU (median, [IQR]: 4, [0-22] vs. 1, [0-6] vs. 2, [0-9] months, p < 0.001). Among CIndU patients, symptomatic dermographism (n = 264) and cholinergic urticaria (n = 103) patients had the longest DD compared to all other CIndU subgroups (median: 4 months, p = 0.005 for both). In CIndU patients, a longer DD was associated with having an additional CIndU (OR: 12.8, p = 0.03), younger age, comorbidities, lower disease control, and lack of second-generation H1-antihistamine treatment. In CSU patients, a DD of ≥ 6 months was associated with lower CSU activity (median weekly Urticaria Activity Score of 14 vs. 21, p = 0.02) compared to that of DD < 6 months. CONCLUSIONS:Diagnosis of CU is delayed in one out of four patients. Greater awareness of the guideline-recommended CU classification, clinical presentation, and diagnostic work-up can facilitate CU diagnosis.

BACKGROUND:Many patients with chronic spontaneous urticaria (CSU) remain symptomatic despite receiving second-generation H1-antihistamines (sgH1-AH). This data analysis from the Chronic Urticaria Registry (CURE) aimed to describe treatment patterns and identify unmet needs in real-world practice. METHODS:CURE is an international, prospective registry of patients with chronic urticaria. Treatment responses were categorized as Urticaria Control Test (UCT) changes from baseline (BL) to 6-month follow-up (FU). Complete response was defined as UCT = 16 with a ≥ 3-point increase. RESULTS:Data were available from 3995 adult patients with CSU at BL and 1288 at FU with evaluable UCT. After treatment escalation from BL to FU, 5.3% (no treatment to licensed-dose sgH1-AH), 6.0% (licensed-dose sgH1-AH to up-dosed sgH1-AH), and 28.4% (any dose sgH1-AH to omalizumab) achieved complete response. Factors associated with a lower probability of treatment escalation at FU were UCT ≥ 12 and omalizumab treatment at BL (both p < 0.0001). About one-third (28.6%) of patients clinically eligible for escalation at BL (UCT < 12) did not receive step-up treatment (18.0%) or were even stepped down (10.6%) and remained poorly controlled at FU. Factors associated with lack of escalation in this group included younger age (p = 0.014), shorter disease duration (p = 0.071), presence of wheals and angioedema (p = 0.002), better quality of life (p = 0.001), and treatment with up-dosed sgH1-AH (p = 0.031). CONCLUSION:Appropriate treatment escalation improves CSU control, although only about a quarter of patients achieve a complete response, indicating the need for novel treatments. Many patients with poorly controlled CSU do not receive guideline-recommended treatment escalation and remain symptomatic on their current treatments, which deserves further attention.

Chronic spontaneous urticaria (CSU) is a mast cell-driven inflammatory disease characterized by recurrent wheals and/or angioedema with an unpredictable course and substantial global prevalence. Beyond its visible skin manifestations, CSU may impose a profound and multifaceted burden on patients, families, healthcare systems, and society. This narrative review synthesizes current evidence on the overall burden of CSU, encompassing epidemiology, clinical manifestations, humanistic impact, cumulative life course impairment, and economic costs. CSU markedly disrupts quality of life through sleep disturbance, pruritus, emotional distress, psychiatric comorbidity, impaired social and occupational functioning, and stigma, with effects extending to children, caregivers, and family members. Disease burden is further amplified by angioedema, concomitant inducible urticaria, delayed diagnosis, suboptimal treatment, and persistent uncertainty regarding disease recurrence, even during periods of symptom control. Indirect and direct economic costs-including healthcare utilization, absenteeism, and presenteeism-are substantial and vary across regions, influenced by healthcare systems and access to effective therapies. The review highlights the importance of comprehensive, patient-centred burden assessment using validated patient-reported outcome measures, alongside disease activity evaluation, to inform individualized management strategies. Addressing the hidden and cumulative burden of CSU requires timely diagnosis, personalized and phenotype-based treatment, integration of psychosocial care, and improved access to effective therapies in order to meaningfully restore quality of life and long-term well-being.

We present the case of a 70-year-old woman with a 7-year history of widespread pruritic varioliform lesions recalcitrant to topical therapy.

BACKGROUND:A double-blind, randomized Phase 3 study (NCT04426890) confirmed that CT-P39 and European Union-approved reference omalizumab (ref-OMA) were comparable in terms of efficacy, quality of life (QoL), pharmacokinetics (PK), pharmacodynamics (PD), safety, and immunogenicity up to week 24. Here, we report results from the 16-week follow-up period. METHODS:The study included two 12-week treatment periods (TPs) and a 16-week off-treatment follow-up period. In TP1, 619 patients with chronic spontaneous urticaria (CSU) were randomized to CT-P39 300 mg, ref-OMA 300 mg, CT-P39 150 mg, or ref-OMA 150 mg. A total of 579 patients continued into TP2, in which patients treated with ref-OMA 300 mg were rerandomized to CT-P39 300 mg or to continue on ref-OMA 300 mg; patients initially randomized to CT-P39 300 mg continued this regimen; and patients initially randomized to CT-P39 or ref-OMA 150 mg increased their dose to 300 mg. Efficacy, PK, PD, QoL, safety, and immunogenicity were assessed during the follow-up period. RESULTS:Improvements in efficacy outcomes observed in the TPs gradually decreased during the follow-up period, but did not return to baseline values. Omalizumab serum concentrations that had increased during treatment subsequently decreased during the follow-up period. After completing treatment at week 24, total and free immunoglobulin E levels returned toward baseline levels. No clinically meaningful differences in QoL, safety, or immunogenicity outcomes were observed across the treatment groups. CONCLUSION:Follow-up results support the biosimilarity of CT-P39 and ref-OMA in terms of efficacy, PK, PD, QoL, safety, and immunogenicity in patients with CSU.

Mast cells develop from pluripotential cells in the bone marrow and populate tissues, including skin, by migration via the blood. Mastocytosis is characterised by clonal mast cell expansion. Accumulation of clonal mast cells leads to increased tissue burden and may result in clinical symptoms. Mastocytosis is usually suspected on the basis of persistent, pruritic skin lesions that urticate and confirmed by specialists. Patients presenting to allergists with anaphylaxis may have undiagnosed systemic mastocytosis, especially those without skin lesions who have bone marrow mastocytosis (BMM). An unwell adult may present directly with advanced haematological disease. Adults with low trauma fractures or vertebral collapse secondary to unexplained osteoporosis may have mastocytosis. Over 90% of adults have the common D816V mutation in exon 17 of KIT. Bone marrow is the richest source of mast cells, but PCR-assays with high sensitivity for detecting KIT mutations in blood, are now available in specialist clinical practice [1]. Other KIT mutations have been detected in skin of children [2] and blood in research studies although the implication of this on prognosis is unknown. Skin lesions are present in childhood mastocytosis and the majority of adults, but may be hard to recognise. Head to toe examination may be required to find localised maculopapular lesions. Adult patients presenting with anaphylaxis should undergo full skin examination, though the absence of skin lesions does not exclude mastocytosis, and have blood checked for tryptase as a biomarker of systemic mastocytosis (SM). The D816V KIT mutation should be looked for in blood, even with a normal tryptase, where the technology is available in hymenoptera venom-induced and idiopathic anaphylaxis. The WHO classification distinguishes subsets of cutaneous mastocytosis (CM) on clinical features and SM by bone marrow biopsy (or other extracutaneous tissue) (Table 1) [3]. Children presenting with skin lesions are assumed to have CM, even though some will have raised tryptase and many will have mutations in known hotspots of KIT (exons 8, 9, 17) on skin biopsy or in blood. Few adults have extensive maculopapular skin lesions with normal tryptase and no evidence of D816V KIT mutation. Others with confirmed SM may have no skin lesions (BMM). This blurring of boundaries is consistent with a concept of mastocytosis being a clinical spectrum due to mast cell clonality presenting in different patient populations with different clinical behaviours and possible co-morbidities. The term "mastocytosis in the skin" (MIS) is a useful terminology for patients with skin lesions, but no proof of systemic disease (without bone marrow biopsy). The term CM is usually understood to describe skin lesions with different subtypes defined by WHO without systemic disease, but MPCM and DCM may also present with systemic disease so the term CM should not be considered to exclude systemic involvement in children. In fact, an adult with MPCM will almost always have systemic involvement when fully investigated. Maculopapular cutaneous mastocytosis (MPCM) is the commonest presentation of mastocytosis in the skin. It is still widely known as urticaria pigmentosa (UP) since the lesions are usually, but not always, pigmented. They urticate rapidly after gentle rubbing and occasionally blister. Whealing of a lesion after minimal friction (Darier's sign) is almost 100% specific but not completely sensitive in children and less so in adults. Testing with a calibrated dermographometer (HTZ, East Grinstead, UK) at 20 and 36 g/mm2 is recommended when available, although in daily clinical practice, a wooden tongue spatula can be used. The response is reduced but not usually prevented by taking H1 antihistamines. It may be minimal in adult patients with long standing skin lesions. Polymorphic MPCM presenting with different sized macules, papules and plaques is primarily seen in children and may have a better prognosis for resolution than monomorphic MPCM [4]. The term 'telangiectasia macularis eruptiva perstans' (TMEP) has been used historically to describe persistent telangiectatic patches of CM in adults but is now merged with MPCM to reflect overlap with typical UP. Adult MPCM may be generalised but is often predominantly on the lower torso, buttocks and thighs with sparing of the face. It is associated with flushing, itching and localised swelling of visible lesions (and occasionally invisible marks that only show as hives after local mast cell activation, for instance with towelling after a shower). Mastocytomas are present at or shortly after birth. They are skin-coloured superficial nodules that are solitary or multiple (Table 1). Gentle friction will result in redness and swelling within the lesion that may progress to blistering and weeping. The urticarial reaction subsides over an hour or two. Loss of the blister roof results in superficial erosions that take a week or two to heal without scarring. The infant may become transiently flushed and distressed. Blistering recedes over two to three years as lesions regress. There is no adult counterpart. Diffuse cutaneous mastocytosis (DCM) starts early in life with generalised erythodermic or yellow-red (xanthelasmoid) thickened skin, which may be subtle or pronounced. The difference between DCM and extensive xanthelasmoid plaque-type UP may be subtle. Blistering with widespread erosions is common and may resemble staphylococcal impetigo or epidermolysis bullosa. The skin quality may remain subtly thickened in adult life but DCM is not primarily seen as an adult pattern of mastocytosis. Mastocytosis presenting with systemic features is more likely in adults with confirmed SM than children. The tryptase level or KIT D816V allele burden as an indicator of mast cell burden does not correlate well with clinical mediator related symptoms. Depression, fatigue and loss of concentration ('brain fog') may be reported by adults with and without skin lesions. Gastrointestinal tract symptoms include hyperacidity, bloating, pain and diarrhoea. Bone pain in adults may be due to fractures from osteoporosis, bone cysts or osteosclerosis of the spine and pelvis. Respiratory complaints are uncommon. Anaphylaxis is a serious complication of mastocytosis. Up to 50% of adults had grade I to IV anaphylaxis over the period of follow up [5]. Increased risk in children is only seen in those with extensive skin lesions or indolent systemic mastocytosis. Identifiable causes are primarily Hymenoptera stings and less commonly include, general anaesthesia, contrast media, drugs and foods, but anaphylaxis may remain unexplained after full evaluation. The REMA score using clinical criteria is useful to screen for underlying clonal mast cell disease in patients presenting with anaphylaxis but no skin lesions [6]. More severe reactions may occur when hereditary alpha tryptasaemia (HαT) is a co-morbidity. Diagnosis of mastocytosis in children is primarily clinical in combination with a positive Darier's sign. Lesional skin biopsy for mast cell enumeration is confirmatory. Criteria for making a pathological diagnosis of cutaneous lesions of mastocytosis have been published [7]. Finding KIT mutations in lesional skin biopsies is 100% specific and sensitive. Paired biopsies from adjacent normal appearing skin for comparative mast cell counts may be helpful when skin lesions are indistinct. All adults should be offered skin biopsy to confirm mastocytosis since the differential diagnosis includes inflammatory dyspigmentation and benign skin lesions [8]. Diagnostic criteria for skin and bone marrow biopsy are summarised in Table 2. Although baseline serum tryptase of 20 mcg/l is a minor criterion for diagnosing systemic mastocytosis, other reasons for persistent tryptasaemia include HαT. A correction factor for this is now applied when HαT is a co-morbidity of mastocytosis based on the copy number of TPSAB1 [9]. Tryptase is a useful measure of mast cell burden that can be followed longitudinally. Blood KIT D816V variant allele frequency (VAF) may also be useful to monitor disease progression. The morphology of skin lesions of mastocytosis varies and may overlap. Some patients present with very few lesions while others are widespread. Lesions in children often flatten with minimal discolouration as a prelude to clearing around puberty. MPCM often becomes more extensive after diagnosis in adults but also uncommonly can fade or resolve completely over decades. Clinicopathological correlation of skin biopsies is essential when mast cell numbers appear slightly increased in chronic inflammatory states, such as chronic spontaneous urticaria, and mast cell density varies by body region in normal skin. Increased baseline serum tryptase (BST) is often regarded as diagnostic for mastocytosis but is not specific because it may be a feature of HαT, renal failure or myeloproliferative neoplasms. A rise and fall within 6 h of an allergic event supports anaphylaxis. Mast cell activation syndrome (MCAS) is a term used for recurrent systemic mast cell activation, almost exclusively presenting with anaphylaxis. This may be allergic, idiopathic or associated with mastocytosis [10]. We firmly reject interpretations of chronic illness symptoms and unrelated co-morbidities. A different concept altogether is histamine intolerance secondary to reduced diamine oxidase with higher levels of dietary histamine leading to possible flushing, gastrointestinal symptoms and migraine. Recognition of mastocytosis is an important step for appropriate investigations on blood and tissue, including molecular genetics to confirm the diagnosis. Allergists have an important role in identifying patients presenting with anaphylaxis who were not aware of underlying mastocytosis and advising on how to manage risk in venom allergic patients, and those requiring medical interventions, including general anaesthesia. Adults with proven systemic disease require multidisciplinary follow up for recognised complications including loss of bone density and progression to advanced systemic disease (development of an associated haematological neoplasm or aggressive disease characterised by organ failure) and opportunities for clinical studies. C.G. wrote the first version and S.B.-O. and K.B. contributed to the writing of the final manuscript. The authors declare no conflicts of interest.

Background: Indolent systemic mastocytosis (ISM) is a rare clonal haematological neoplasm driven by KIT D816V mutation in 95% of cases leading to uncontrolled proliferation and accumulation of mast cells. It can be associated with debilitating mast cell mediator symptoms affecting skin, gastrointestinal (GI) tract, neurocognitive function, bone turnover and anaphylaxis which significantly impact quality of life. Treatment is limited to symptom management and there are no approved targeted therapies available in the UK. The ISM symptom assessment form (ISM-SAF ©; Taylor et al.[2021]) is a validated and effective symptom assessment tool developed specifically for ISM patients focusing on 11 symptoms over a 24-hour recall period: bone pain, abdominal pain, nausea, skin spots, itch, flushing, fatigue, dizziness, brain fog, headache and diarrhoea. Each symptom is scored on a scale from 0 (no symptom) to 10 (worst imaginable symptom). We present UK-wide data of 101 patients from four centres as a re-audit of a previous single-centre cohort of 76 patients by Veitch et al.[2023]. Methods: Adults with ISM diagnosed on a bone marrow biopsy and/or extracutaneous tissue as per World Health Organization classification were identified between June 2023 to July 2025 retrospectively. 101 patients participated across four centres in the UK [Guy′s and St Thomas' Hospital (68), University College London Hospital (14), St James University Hospital (10) and Nottingham University Hospital (9)]. Over a four-week period, patients were invited to complete the ISM SAF © by telephone or in person. Demographic, clinical data, anti-mediator therapy and anaphylaxis history were also collected. This study also focused on the impact of ISM on bone health, quality of life and working hours. All consultations were conducted by a haematology clinician in each institute. Results: Of the 101 patients, median age at diagnosis was 46 years (range 11-76) with female predominance (62.4%). Median time to ISM diagnosis was 4.1 years (range 0.1-55.6). Median latest serum tryptase was 37.5 mcg/L (range 7.9-196; n=99) and 2 patients had levels >200 mcg/L. 88 patients (87.1%) were noted to have the KIT D816V mutation (6.9% KIT D816V-negative, 4.9% not available and 0.99% equivocal). Bone marrow trephine mast cell infiltrate ranged between 2-70%. 30 patients (29.7%) had a history of anaphylaxis at least once in their lifetime and 6.6 % (n=2) reported using an adrenaline autoinjector within the last 12 months. The median total symptom score (TSS) was 31 (range 0-90). The highest scoring symptom was fatigue (mean score 5.1) followed by skin spots (mean score 4), flushing (mean score 3.7), brain fog (mean score 3.5) and itch (mean score 3.4). 55 patients (54.5%) had a TSS ≥28 and 35 patients (34.7%) had TSS of ≥42 indicating moderate and severe disease, respectively. 89 patients had a DEXA scan of which 16 patients (17.9%) had osteoporosis, 32 (35.9%) had osteopenia. 10 of 16 patients (62.5%) with osteoporosis were on bisphosphonate therapy. ISM is a recognised contributor to bone density loss and bone pain. Among patients with moderate disease (TSS ≥28), 41 patients (74.5%) were on ≥2 medications (needing combinations of up to 5 different classes of anti-mast cell mediator therapies). Medications included H1 antihistamines (n=89), H2 antihistamines (n=49), proton pump inhibitors (n=22), sodium cromoglicate (n=23), montelukast (n=12), oral corticosteroid (n=1) and omalizumab (n=3). 18 patients (17.8%) had to take time off their work in the last year due ISM related symptoms (range 1-90 days) and 11 patients (10.8%) reported reducing their working hours or retiring early because of ISM. Conclusion: Our re-audit highlights an additional 101 ISM patients across 4 centres in the UK with significant real-world symptom burden. This aligns with findings from the previous single-centre audit and the PRISM study (M. Triggiani et al. [2025]). This is the first UK audit to verify the impact of symptom burden on quality of life, 28.6% of patients having to adjust their working practice due to their ISM. A significant proportion of patients, 40.5% had TSS ≥28 and required two or more anti-mediator therapies. This compares to the original audit (36%), indicating a substantial unmet need in many patients receiving currently available standard therapies. These patients may benefit from treatment with tyrosine kinase inhibitors, presently accessible onlythrough clinical trials in the UK.

AimsTo demonstrate pharmacokinetic equivalence of CT-P39 administered via auto-injector (CT-P39 AI) and European Union-approved reference omalizumab via pre-filled syringe (EU-OMA PFS) in healthy Japanese adults.Participants & MethodsThis open-label, Phase 1 study randomized participants (1:1) to a single 150 mg/mL dose of CT-P39 AI or EU-OMA PFS. The primary endpoint was pharmacokinetic equivalence per area under the concentration-time curve from time zero to infinity (AUC0-inf) and maximum serum concentration (Cmax). Equivalence was concluded if the 90% confidence intervals (CIs) for the ratios of geometric least-squares means (gLSMs) were contained within the predefined 80-125% equivalence margin. Secondary endpoints comprised additional pharmacokinetics, pharmacodynamics, safety, and immunogenicity.ResultsOverall, 65 and 64 individuals were randomized to CT-P39 AI and EU-OMA PFS, respectively. Pharmacokinetic equivalence between CT-P39 AI and EU-OMA PFS was demonstrated for both AUC0-inf (ratio of gLSMs [90% CI] 101.66 [95.31-108.45]) and Cmax (93.91 [87.20-101.14]). Thirty-nine (60.0%; CT-P39 AI) and 32 (50.8%; EU-OMA PFS) participants experienced treatment-emergent adverse events (TEAEs) with no serious TEAEs. Secondary endpoints were comparable between groups.ConclusionsCT-P39 AI was pharmacokinetically equivalent to EU-OMA PFS following a single dose in healthy Japanese individuals; pharmacodynamics, safety, and immunogenicity were comparable.

BACKGROUND:Chronic spontaneous urticaria (CSU), a disease predominantly affecting females, has limited information available on its differences between females and males of varying ages. OBJECTIVES:To investigate sex differences in age groups regarding disease activity, comorbidities, quality of life (QoL) and treatment patterns in CSU patients. METHODS:We analysed Chronic Urticaria Registry (CURE) data, an international real-world registry for patients with chronic urticaria. Patients were recruited via an online platform using a standardized questionnaire. The data were analysed for demographics, age of onset, duration of urticaria, (Urticaria Activity Score [UAS], Urticaria Control Test [UCT], Chronic Urticaria Quality of Life Questionnaire [CU-Q2oL]), family history, systemic symptoms, aggravating factors, comorbidities, smoking and alcohol consumption, laboratory parameters, burden of disease, treatment distribution and response rates, compliance to treatment and adverse events. Comparisons were made among age groups <13, 13-17, 18-30, 31-50, 51-65 and >65 years. RESULTS:Across 4136 CSU patients (from 58 sites across 29 countries), 2994 (72.4%) were female. Statistically significant female predominance started at age 31 (<0.001). Compared with males, females showed higher rates of angioedema (59.6 vs. 51.7%; p < 0.001), systemic symptoms (34.6 vs. 25.4%; p < 0.001), sleep disturbance (38.9 vs. 32.5%; p < 0.001), QoL impairment (CU-Q2oL score 32 vs. 27.7; p < 0.001) and lower rates of urticaria control than males in all medication categories (p < 0.05 for all). Females had more concomitant diseases, including asthma, thyroid disease, obesity, autoimmune disease, gastrointestinal disease and depression (p < 0.05 for all). The disease was especially more burdensome and refractory in females aged 51-65 years than males, evidenced by more angioedema and systemic symptoms, worse QoL, lower UCT scores and more emergency visits (p < 0.05 for all). However, these differences were not prominent in the elderly females (>65 years). CONCLUSIONS:Compared with males, female CSU patients experience more burdensome disease, which gets worse in midlife. CLINICALTRIALS:gov (or equivalent) listing (if applicable None).

ABSTRACTBackgroundThis study compared the therapeutic equivalence of CT‐P39 (an omalizumab biosimilar) and EU‐approved reference omalizumab (ref‐OMA) in patients with chronic spontaneous urticaria.MethodsThis double‐blind, randomized, active‐controlled Phase 3 study (NCT04426890) included two 12‐week treatment periods (TPs). In TP1, patients received CT‐P39 300 mg, ref‐OMA 300 mg, CT‐P39 150 mg, or ref‐OMA 150 mg. In TP2, patients treated with ref‐OMA 300 mg were rerandomized to CT‐P39 300 mg or ref‐OMA 300 mg; patients initially randomized to CT‐P39 300 mg continued this regimen; and patients initially randomized to CT‐P39 or ref‐OMA 150 mg received 300 mg dosing with the same drug. The primary endpoint for the assessment of therapeutic equivalence of CT‐P39 300 mg and ref‐OMA 300 mg was change from baseline in weekly itch severity score (ISS7) at week 12.ResultsIn TP1, 619 patients were randomized (CT‐P39 300 mg, n = 204; ref‐OMA 300 mg, n = 205; CT‐P39 150 mg, n = 107; ref‐OMA 150 mg, n = 103). Equivalence was demonstrated between CT‐P39 300 mg and ref‐OMA 300 mg for mean change from baseline in ISS7 at week 12; confidence intervals (CIs) were within predefined equivalence margins: global analysis: treatment difference 0.77, 95% CI –0.37 to 1.90; US analysis: treatment difference 0.70, 90% CI –0.22 to 1.63. The proportion of patients experiencing ≥ 1 treatment‐related adverse event was comparable across groups. Secondary efficacy, quality of life, pharmacokinetic, safety, and immunogenicity outcomes were comparable between groups at a given dose level, with no evident impact of switching.ConclusionsEquivalent efficacy was observed between CT‐P39 and ref‐OMA, with comparable safety also evident.

BACKGROUND:Itch is the most bothersome symptom in chronic spontaneous urticaria (CSU) and severely affects quality of life. OBJECTIVE:To analyze factors associated with itch severity, and how itch is associated with quality of life and health care use in CSU. METHODS:We retrieved patient data from the Chronic Urticaria Registry. Patients were categorized by self-reported itch severity (recall period of 7 days). We used ordinal logistic regressions as well as negative binomial and gamma regressions with log link to investigate possible associations. RESULTS:A total of 3,045 patients, 74.3% female, mean age 44.4 years, with no, mild, moderate, or intense itch (16.4%, 25.2%, 32.5%, and 25.9%, respectively) were included. A higher itch rating was associated with symptomatic dermographism (odds ratio [OR] = 1.25; P = .027), malaise (OR = 1.43; P < .001), depression (OR = 1.46; P = .008), and laboratory signs of inflammation (ie, elevated erythrocyte sedimentation rate (OR = 1.57; P = .031) and leukocyte counts (OR = 2.37; P = .004)). Intense itch was associated with worse quality of life (Chronic Urticaria Quality of Life Questionnaire; P < .001) and more patients visiting a general practitioner, allergologist or dermatologist, and the emergency room (P < .001). CONCLUSIONS:Higher itch levels are associated with inflammation and depression and are linked to worse quality of life and increased health care demand. Addressing itch is crucial to reducing the humanistic and societal burden in CSU.

Niniejsza aktualizacja i rewizja międzynarodowych wytycznych dotyczących pokrzywki została opracowana zgodnie z metodami zalecanymi przez Cochrane i grupę roboczą Grading of Recommendations Assessment, Development and Evaluation (GRADE). Jest to wspólna inicjatywa Dermatology Section of the European Academy of Allergology and Clinical Immunology (EAACI), Global Allergy and Asthma European Network (GA2LEN) i jej Urticaria and Angioedema Centers of Reference and Excellence (UCAREs i ACAREs), European Dermatology Forum (EDF; EuroGuiDerm) oraz Asia Pacific Association of Allergy, Asthma and Clinical Immunology z udziałem 64 delegatów z 50 towarzystw krajowych i międzynarodowych z 31 krajów. Konferencja uzgodnieniowa odbyła się 3 grudnia 2020 r. Niniejsze wytyczne zostały uznane i zaakceptowane przez European Union of Medical Specialist s (UEMS). Pokrzywka jest częstą chorobą, w której pośredniczą komórki tuczne, objawiającą się bąblami, obrzękiem naczynioruchowym lub obydwoma tymi objawami. Częstość występowania ostrej pokrzywki w ciągu życia wynosi około 20%. Przewlekła pokrzywka spontaniczna lub indukowalna powoduje niesprawność, pogarsza jakość życia oraz wpływa na aktywność w pracy i w szkole. Ta zaktualizowana wersja międzynarodowych wytycznych dotyczących pokrzywki obejmuje definicję i klasyfikację pokrzywki oraz przedstawia opracowane przez ekspertów i oparte na dowodach metody diagnostyki i leczenia w przypadku różnych podtypów pokrzywki.