RARE DISEASE
Solar urticaria
Solar urticaria
Solar urticaria
Drug discovery
2
drugs
With orphan designations
Overview
Solar urticaria is a rare IgE-mediated photodermatosis characterized by urticarial lesions within minutes of UV/visible light exposure, with potential systemic symptoms (e.g., anaphylaxis). It involves mast cell degranulation triggered by photoallergens, though the exact antigen remains unidentified. Chronic and often refractory to treatment, it requires phototesting for diagnosis and management [1][4][16].
Population
Therapies
1st-line: High-dose 2nd-gen H1 antihistamines (75.8% efficacy) ± H2 blockers (42.9% efficacy) [5][16].
2nd-line: UVA hardening therapy (88.9% efficacy for UVA-triggered cases) or omalizumab (80% response rate) [3][5][8][16].
Refractory cases: Immunosuppressants (cyclosporine), IVIG, plasmapheresis, or combination therapies [4][12][16].
Categories: rare skin diseases
Research Papers
234 drug discovery papers about Solar urticaria, with 1 first-in-class and 4 next-in-class emerging drug candidates forecasted to outperform the average preclinical success rate. Recent publications:
234 drug discovery papers about Solar urticaria, with 1 first-in-class and 4 next-in-class emerging drug candidates forecasted to outperform the average preclinical success rate. Recent publications:
2026-07-24 | Differential Effects of Dupilumab in a Patient With Localized Heat Urticaria, Delayed Solar Urticaria, and Symptomatic Dermographism.
Physical urticaria is a subtype of chronic inducible urticaria characterized by wheals and/or angioedema triggered by physical stimuli. We report a refractory case of combined localized heat urticaria, delayed solar urticaria, and symptomatic dermographism in a 16-year-old girl. Provocation testing showed erythematous and edematous lesions after thermal stimulation at 42°C and after the application of warm water at 40°C and 42°C. An intradermal test using the patient's serum heated to 42°C for 5 min yielded a positive result, leading to the diagnosis of localized heat urticaria. Visible light irradiation induced no immediate wheals; however, wheals developed at all irradiated sites 4.5 h later, accompanied by intense pruritus without burning sensation or pain, consistent with delayed solar urticaria. A FricTest provoked wheals, confirming symptomatic dermographism. Antihistamines were ineffective, and omalizumab, administered as a second-line treatment, improved only the symptomatic dermographism, with no effect on the heat or solar urticaria. Dupilumab was subsequently administered 12 times. Repeated provocation testing during treatment showed resolution of symptomatic dermographism, whereas localized heat urticaria persisted and delayed solar urticaria showed no meaningful improvement. The Urticaria Control Test score also did not improve. These findings suggest that the pathogenesis of symptomatic dermographism in this case may involve IgE- and IL-4/IL-13-mediated pathways, whereas localized heat urticaria and delayed solar urticaria may be driven by distinct mechanisms.
2026-04-22 | Refractory chronic spontaneous urticaria management in resource-poor settings: A critical appraisal
Urticaria is characterized by the occurrence of wheals, angioedema, or both. When urticaria duration is >6 weeks, it is known as chronic urticaria (CU). CU is classified as spontaneous (CSU) and inducible (CIndU). When the clinical course has no definite physical eliciting factor involved and shows a spontaneous course, it is described as CSU, and when a physical eliciting factor is present, it is called CIndU. CIndU is further subclassified as symptomatic dermographism, cold urticaria, delayed pressure urticaria, solar urticaria, heat urticaria, and vibratory angioedema, as well as cholinergic urticaria, contact urticaria, and aquagenic urticaria. CU patients can simultaneously present with more than one form of CU, especially CIndU. The management of CSU commences with the second-generation H1 anti-histamine. A few CSU patients do not respond to a single dose of 2 nd- generation anti-histamine; then, the dose is escalated to 4 fold the usual dose. About 10–50% patients do not respond to even 4-fold increased doses of which end up necessitating the repeated use of oral corticosteroids to control disease exacerbations is classified to have refractory CSU. Various drugs and biologics are in the armamentarium of dermatologists and allergologists; however, there are financial constraints in the developing world in resource-poor settings. Omalizumab, dupilumab, remibrutinib, and cyclosporine are the agents that are used in refractory urticaria. The financial burden of these agents restricts patients in poor settings to use for long-term therapy. The agents such as methotrexate, tofacitinib, and mycophenolate mofetil have been used with success anecdotally. However, azathioprine has shown a ray of hope in refractory urticaria patients, which may be an alternative in difficult-to-treat cases of CSU.
2026-04-10 | Omalizumab Therapy Results in Defined Behavioural Changes and Improvements in Quality of Life in Solar Urticaria.
Solar urticaria is a rare photodermatosis in which exquisite photosensitivity can require extreme behavioural adaptations, resulting in a substantial impact on quality of life (QoL). Omalizumab therapy has been demonstrated to improve several clinical outcome measures, but the impact on behavioural measures is poorly understood. Our objectives were to examine daylight exposure behaviours and QoL measures pre- and post-omalizumab therapy. Daylight exposure diaries were completed by n = 5 patients with solar urticaria and n = 7 healthy participants during different seasons in England, UK (51.1-53.5oN). These incorporated a range of measures, including time spent outdoors and clothing worn, and Dermatology Life Quality Index (DLQI) data were also collected. Prior to omalizumab, patients spent less time outdoors in sunny vs. non-sunny conditions in spring (mean 10 vs. 29 min/day, p < 0.05) and less than healthy volunteers (44 min in sunny conditions/day). On omalizumab, patients increased their time outdoors in sunny conditions, reaching similar levels to healthy volunteers in spring (45 min/day) and further increasing to 85 min/day in summer. This was accompanied by fewer days with symptoms (symptoms on 75% days in spring pre-omalizumab vs. 26% days in summer on omalizumab), an apparent doubling of skin surface area exposure and substantial improvement in patients' QoL (mean past-year DLQI pre-omalizumab vs. past-week summer on omalizumab 22 vs. 5, p < 0.001). Omalizumab therapy was associated with behavioural changes that increase daylight exposure, accompanied by improved QoL. This study highlights the importance of considering a range of outcome measures in assessing response to therapy.
2026-01-06 | O07 Solar urticaria is associated with novel rare missense variants in ACACA
Abstract Introduction and aims Solar urticaria (SU) is a rare, poorly understood photodermatosis characterized by inappropriate mast cell degranulation following cutaneous exposure to sunlight. Based on a lack of Mendelian inheritance in families and its onset in adulthood with limited impact on reproductive fitness, SU is likely a complex trait whose development is determined by genetic and environmental factors. Its rarity and unusual phenotype, which constitutes an extreme aberration of physiological responses to sunlight, imply that its genetic architecture may be underpinned by rare, highly penetrant and deleterious variants. To investigate this, we performed a case–control whole-exome sequencing gene association study in SU. Methods Forty-six patients of European ancestry with phototest-confirmed SU underwent whole-exome sequencing. Healthy control whole exomes (n = 971) were derived from the 1958 British Birth Cohort. Following quality control, joint variant calling and variant filtering to retain rare, high-impact variants, burden testing was performed. Sanger sequencing and bioinformatic resources were used to validate and explore identified genes/variants. Results Burden testing revealed exome-wide significant enrichment of rare, high-impact variants in ACACA among SU cases (P = 4.7 × 10−7). This gene encodes acetyl-coenzyme A carboxylase alpha, an enzyme that catalyses the rate-limiting step in de novo lipogenesis. Six of 46 SU cases carried rare, heterozygous missense variants in ACACA compared with 3 of 971 controls. Sanger sequencing validated the presence of these variants in ACACA. Structural analyses demonstrated that ACACA variants were predicted to decrease protein stability. Reanalysis of single-cell RNA sequencing data from skin confirmed ACACA expression in all cell types, including mast cells. Conclusions Enrichment of rare, deleterious ACACA variants among patients with SU suggests a role for altered lipid metabolism, potentially affecting mast cell function, in SU pathogenesis. Characterization of lipid-mediated disease mechanisms in SU should form the basis of future investigations.
2026-01-05 | Visible Light Protection Strategies for Diverse Populations.
Visible light (VL; 400-700 nm) constitutes nearly half of solar radiation and has distinct biological effects on human skin. High-energy visible light (HEVL), particularly blue light (400-490 nm), contributes to erythema, persistent pigmentation, and photoaging. Emerging data also demonstrate synergistic pigmentary interactions between VL and long-wavelength ultraviolet A1 (UVA1). Individuals with skin of colour (SOC) and patients with visible-light-sensitive dermatoses are particularly susceptible to the cutaneous effects of visible light. This review aims to provide an evidence-based overview of VL interactions with skin, the mechanisms driving VL-induced cutaneous changes, and current VL-directed photoprotection strategies, with emphasis on their relevance for SOC populations and visible-light-sensitive dermatoses. PubMed and Google Scholar were searched to identify studies addressing VL properties, cutaneous biological effects, and VL-specific photoprotection, including sunscreens, pigments, novel organic filters, antioxidants, and behavioural approaches. VL, especially blue light, induces oxidative stress, melanogenesis via opsin 3-mediated pathways, and degradation of dermal extracellular matrix. Tinted sunscreens containing iron oxides and pigmentary titanium dioxide provide the most effective and cosmetically acceptable VL protection, reducing HEVL transmission by up to 80-97% and improving clinical outcomes in melasma and other hyperpigmentation disorders. Novel organic UV filters such as TriAsorB™ expand absorbance into the VL spectrum, while adjunctive topical and oral antioxidants may attenuate VL-induced oxidative stress. VL may exacerbate photodermatoses, including autoimmune connective tissue diseases, porphyria, and solar urticaria. VL is a biologically active and clinically relevant component of sunlight with disproportionate effects in SOC and certain photosensitive dermatoses. Optimal photoprotection requires a multimodal approach integrating UV and VL protection through physical measures, tinted formulations, emerging broad-spectrum filters, antioxidants, and patient-centred photoeducation. Standardised VL-protection labelling and further clinical research are needed to guide future practice.
2026-07-24 | Differential Effects of Dupilumab in a Patient With Localized Heat Urticaria, Delayed Solar Urticaria, and Symptomatic Dermographism.
Physical urticaria is a subtype of chronic inducible urticaria characterized by wheals and/or angioedema triggered by physical stimuli. We report a refractory case of combined localized heat urticaria, delayed solar urticaria, and symptomatic dermographism in a 16-year-old girl. Provocation testing showed erythematous and edematous lesions after thermal stimulation at 42°C and after the application of warm water at 40°C and 42°C. An intradermal test using the patient's serum heated to 42°C for 5 min yielded a positive result, leading to the diagnosis of localized heat urticaria. Visible light irradiation induced no immediate wheals; however, wheals developed at all irradiated sites 4.5 h later, accompanied by intense pruritus without burning sensation or pain, consistent with delayed solar urticaria. A FricTest provoked wheals, confirming symptomatic dermographism. Antihistamines were ineffective, and omalizumab, administered as a second-line treatment, improved only the symptomatic dermographism, with no effect on the heat or solar urticaria. Dupilumab was subsequently administered 12 times. Repeated provocation testing during treatment showed resolution of symptomatic dermographism, whereas localized heat urticaria persisted and delayed solar urticaria showed no meaningful improvement. The Urticaria Control Test score also did not improve. These findings suggest that the pathogenesis of symptomatic dermographism in this case may involve IgE- and IL-4/IL-13-mediated pathways, whereas localized heat urticaria and delayed solar urticaria may be driven by distinct mechanisms.
2026-04-22 | Refractory chronic spontaneous urticaria management in resource-poor settings: A critical appraisal
Urticaria is characterized by the occurrence of wheals, angioedema, or both. When urticaria duration is >6 weeks, it is known as chronic urticaria (CU). CU is classified as spontaneous (CSU) and inducible (CIndU). When the clinical course has no definite physical eliciting factor involved and shows a spontaneous course, it is described as CSU, and when a physical eliciting factor is present, it is called CIndU. CIndU is further subclassified as symptomatic dermographism, cold urticaria, delayed pressure urticaria, solar urticaria, heat urticaria, and vibratory angioedema, as well as cholinergic urticaria, contact urticaria, and aquagenic urticaria. CU patients can simultaneously present with more than one form of CU, especially CIndU. The management of CSU commences with the second-generation H1 anti-histamine. A few CSU patients do not respond to a single dose of 2 nd- generation anti-histamine; then, the dose is escalated to 4 fold the usual dose. About 10–50% patients do not respond to even 4-fold increased doses of which end up necessitating the repeated use of oral corticosteroids to control disease exacerbations is classified to have refractory CSU. Various drugs and biologics are in the armamentarium of dermatologists and allergologists; however, there are financial constraints in the developing world in resource-poor settings. Omalizumab, dupilumab, remibrutinib, and cyclosporine are the agents that are used in refractory urticaria. The financial burden of these agents restricts patients in poor settings to use for long-term therapy. The agents such as methotrexate, tofacitinib, and mycophenolate mofetil have been used with success anecdotally. However, azathioprine has shown a ray of hope in refractory urticaria patients, which may be an alternative in difficult-to-treat cases of CSU.
2026-04-10 | Omalizumab Therapy Results in Defined Behavioural Changes and Improvements in Quality of Life in Solar Urticaria.
Solar urticaria is a rare photodermatosis in which exquisite photosensitivity can require extreme behavioural adaptations, resulting in a substantial impact on quality of life (QoL). Omalizumab therapy has been demonstrated to improve several clinical outcome measures, but the impact on behavioural measures is poorly understood. Our objectives were to examine daylight exposure behaviours and QoL measures pre- and post-omalizumab therapy. Daylight exposure diaries were completed by n = 5 patients with solar urticaria and n = 7 healthy participants during different seasons in England, UK (51.1-53.5oN). These incorporated a range of measures, including time spent outdoors and clothing worn, and Dermatology Life Quality Index (DLQI) data were also collected. Prior to omalizumab, patients spent less time outdoors in sunny vs. non-sunny conditions in spring (mean 10 vs. 29 min/day, p < 0.05) and less than healthy volunteers (44 min in sunny conditions/day). On omalizumab, patients increased their time outdoors in sunny conditions, reaching similar levels to healthy volunteers in spring (45 min/day) and further increasing to 85 min/day in summer. This was accompanied by fewer days with symptoms (symptoms on 75% days in spring pre-omalizumab vs. 26% days in summer on omalizumab), an apparent doubling of skin surface area exposure and substantial improvement in patients' QoL (mean past-year DLQI pre-omalizumab vs. past-week summer on omalizumab 22 vs. 5, p < 0.001). Omalizumab therapy was associated with behavioural changes that increase daylight exposure, accompanied by improved QoL. This study highlights the importance of considering a range of outcome measures in assessing response to therapy.
2026-01-06 | O07 Solar urticaria is associated with novel rare missense variants in ACACA
Abstract Introduction and aims Solar urticaria (SU) is a rare, poorly understood photodermatosis characterized by inappropriate mast cell degranulation following cutaneous exposure to sunlight. Based on a lack of Mendelian inheritance in families and its onset in adulthood with limited impact on reproductive fitness, SU is likely a complex trait whose development is determined by genetic and environmental factors. Its rarity and unusual phenotype, which constitutes an extreme aberration of physiological responses to sunlight, imply that its genetic architecture may be underpinned by rare, highly penetrant and deleterious variants. To investigate this, we performed a case–control whole-exome sequencing gene association study in SU. Methods Forty-six patients of European ancestry with phototest-confirmed SU underwent whole-exome sequencing. Healthy control whole exomes (n = 971) were derived from the 1958 British Birth Cohort. Following quality control, joint variant calling and variant filtering to retain rare, high-impact variants, burden testing was performed. Sanger sequencing and bioinformatic resources were used to validate and explore identified genes/variants. Results Burden testing revealed exome-wide significant enrichment of rare, high-impact variants in ACACA among SU cases (P = 4.7 × 10−7). This gene encodes acetyl-coenzyme A carboxylase alpha, an enzyme that catalyses the rate-limiting step in de novo lipogenesis. Six of 46 SU cases carried rare, heterozygous missense variants in ACACA compared with 3 of 971 controls. Sanger sequencing validated the presence of these variants in ACACA. Structural analyses demonstrated that ACACA variants were predicted to decrease protein stability. Reanalysis of single-cell RNA sequencing data from skin confirmed ACACA expression in all cell types, including mast cells. Conclusions Enrichment of rare, deleterious ACACA variants among patients with SU suggests a role for altered lipid metabolism, potentially affecting mast cell function, in SU pathogenesis. Characterization of lipid-mediated disease mechanisms in SU should form the basis of future investigations.
2026-01-05 | Visible Light Protection Strategies for Diverse Populations.
Visible light (VL; 400-700 nm) constitutes nearly half of solar radiation and has distinct biological effects on human skin. High-energy visible light (HEVL), particularly blue light (400-490 nm), contributes to erythema, persistent pigmentation, and photoaging. Emerging data also demonstrate synergistic pigmentary interactions between VL and long-wavelength ultraviolet A1 (UVA1). Individuals with skin of colour (SOC) and patients with visible-light-sensitive dermatoses are particularly susceptible to the cutaneous effects of visible light. This review aims to provide an evidence-based overview of VL interactions with skin, the mechanisms driving VL-induced cutaneous changes, and current VL-directed photoprotection strategies, with emphasis on their relevance for SOC populations and visible-light-sensitive dermatoses. PubMed and Google Scholar were searched to identify studies addressing VL properties, cutaneous biological effects, and VL-specific photoprotection, including sunscreens, pigments, novel organic filters, antioxidants, and behavioural approaches. VL, especially blue light, induces oxidative stress, melanogenesis via opsin 3-mediated pathways, and degradation of dermal extracellular matrix. Tinted sunscreens containing iron oxides and pigmentary titanium dioxide provide the most effective and cosmetically acceptable VL protection, reducing HEVL transmission by up to 80-97% and improving clinical outcomes in melasma and other hyperpigmentation disorders. Novel organic UV filters such as TriAsorB™ expand absorbance into the VL spectrum, while adjunctive topical and oral antioxidants may attenuate VL-induced oxidative stress. VL may exacerbate photodermatoses, including autoimmune connective tissue diseases, porphyria, and solar urticaria. VL is a biologically active and clinically relevant component of sunlight with disproportionate effects in SOC and certain photosensitive dermatoses. Optimal photoprotection requires a multimodal approach integrating UV and VL protection through physical measures, tinted formulations, emerging broad-spectrum filters, antioxidants, and patient-centred photoeducation. Standardised VL-protection labelling and further clinical research are needed to guide future practice.
Access all drug discovery papers and probability of success in trials forecasts:
Access all drug discovery papers and probability of success in trials forecasts:
Drug Discovery Landscape
2 orphan drug designations for Solar urticaria.
2 orphan drug designations for Solar urticaria.
Drug | Therapy type | Regulator | Orphan designation | Approval | Sponsor |
|---|---|---|---|---|---|
afamelanotide | peptides | FDA | 2009-12-11 | — | Clinuvel, Inc. |
Afamelanotide | small molecules | EMA | 2009-07-24 | — | Clinuvel Europe Limited |
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