Article

Key clinical point: Patients with atopic dermatitis (AD) treated with dupilumab have an increased risk for cutaneous T-cell lymphoma (CTCL) compared with those not treated with dupilumab.

Major finding: Patients with AD who did vs did not receive dupilumab had a significantly higher risk of developing CTCL (odds ratio [OR] 4.1003; 95% CI 2.055-8.192). The risk for CTCL persisted in those with no prior exposure to disease-modifying antirheumatic drugs (OR 3.202; 95% CI 1.573-6.514).

Study details: This retrospective cohort study included patients with AD who did (n = 22,888) or did not (n = 22,871) receive dupilumab treatment and did not have a preexisting diagnosis for CTCL, Hodgkin lymphoma, non-Hodgkin lymphoma, nonfollicular lymphoma, leukemia, malignant melanoma, squamous cell carcinoma, or basal cell carcinoma.

Disclosures: This study did not receive any funding. The authors declared no conflicts of interest.

Source: Hasan I, Parsons L, Duran S, Zinn Z. Dupilumab therapy for atopic dermatitis is associated with increased risk of cutaneous T cell lymphoma: A retrospective cohort study. J Am Acad Dermatol. 2024 (Apr 6). doi: 10.1016/j.jaad.2024.03.039 Source

Key clinical point: Patients with atopic dermatitis (AD) treated with dupilumab have an increased risk for cutaneous T-cell lymphoma (CTCL) compared with those not treated with dupilumab.

Major finding: Patients with AD who did vs did not receive dupilumab had a significantly higher risk of developing CTCL (odds ratio [OR] 4.1003; 95% CI 2.055-8.192). The risk for CTCL persisted in those with no prior exposure to disease-modifying antirheumatic drugs (OR 3.202; 95% CI 1.573-6.514).

Study details: This retrospective cohort study included patients with AD who did (n = 22,888) or did not (n = 22,871) receive dupilumab treatment and did not have a preexisting diagnosis for CTCL, Hodgkin lymphoma, non-Hodgkin lymphoma, nonfollicular lymphoma, leukemia, malignant melanoma, squamous cell carcinoma, or basal cell carcinoma.

Disclosures: This study did not receive any funding. The authors declared no conflicts of interest.

Source: Hasan I, Parsons L, Duran S, Zinn Z. Dupilumab therapy for atopic dermatitis is associated with increased risk of cutaneous T cell lymphoma: A retrospective cohort study. J Am Acad Dermatol. 2024 (Apr 6). doi: 10.1016/j.jaad.2024.03.039 Source

Key clinical point: Patients with atopic dermatitis (AD) treated with dupilumab have an increased risk for cutaneous T-cell lymphoma (CTCL) compared with those not treated with dupilumab.

Major finding: Patients with AD who did vs did not receive dupilumab had a significantly higher risk of developing CTCL (odds ratio [OR] 4.1003; 95% CI 2.055-8.192). The risk for CTCL persisted in those with no prior exposure to disease-modifying antirheumatic drugs (OR 3.202; 95% CI 1.573-6.514).

Study details: This retrospective cohort study included patients with AD who did (n = 22,888) or did not (n = 22,871) receive dupilumab treatment and did not have a preexisting diagnosis for CTCL, Hodgkin lymphoma, non-Hodgkin lymphoma, nonfollicular lymphoma, leukemia, malignant melanoma, squamous cell carcinoma, or basal cell carcinoma.

Disclosures: This study did not receive any funding. The authors declared no conflicts of interest.

Source: Hasan I, Parsons L, Duran S, Zinn Z. Dupilumab therapy for atopic dermatitis is associated with increased risk of cutaneous T cell lymphoma: A retrospective cohort study. J Am Acad Dermatol. 2024 (Apr 6). doi: 10.1016/j.jaad.2024.03.039 Source

Key clinical point: Established and new atopic dermatitis (AD)-associated filaggrin loss-of-function variants are associated with increased risks for clinical AD outcomes and disruption of skin barrier integrity in lesional and nonlesional skin of children with AD.

Major finding: Twenty variants were identified, including one novel variant. The presence of one or more variants was associated with a higher risk for moderate or severe AD vs mild AD (odds ratio 2.00; corrected P = .0394), a higher Scoring AD score (corrected P = .0394), and transepidermal water loss in both lesional (P = .018) and nonlesional (P = .015) skin.

Study details: This study included 438 children with AD (age ≤ 2 years; gestation period ≥ 36 weeks) from the early-life Mechanisms of Progression of Atopic Dermatitis to Asthma in Children cohort without a comorbid lung condition or dependence on immunosuppression or oral steroids for a condition except asthma.

Disclosures: This study was funded by the US National Institutes of Health. Matthew S. Hestand declared being an employee and shareholder of Pacific Biosciences. The other authors declared no conflicts of interest.

Source: Virolainen SJ, Satish L, Biagini JM, et al. Filaggrin loss-of-function variants are associated with atopic dermatitis phenotypes in a diverse, early life prospective cohort. JCI Insight. 2024 (Apr 2). doi: 10.1172/jci.insight.178258 Source

Key clinical point: Established and new atopic dermatitis (AD)-associated filaggrin loss-of-function variants are associated with increased risks for clinical AD outcomes and disruption of skin barrier integrity in lesional and nonlesional skin of children with AD.

Major finding: Twenty variants were identified, including one novel variant. The presence of one or more variants was associated with a higher risk for moderate or severe AD vs mild AD (odds ratio 2.00; corrected P = .0394), a higher Scoring AD score (corrected P = .0394), and transepidermal water loss in both lesional (P = .018) and nonlesional (P = .015) skin.

Study details: This study included 438 children with AD (age ≤ 2 years; gestation period ≥ 36 weeks) from the early-life Mechanisms of Progression of Atopic Dermatitis to Asthma in Children cohort without a comorbid lung condition or dependence on immunosuppression or oral steroids for a condition except asthma.

Disclosures: This study was funded by the US National Institutes of Health. Matthew S. Hestand declared being an employee and shareholder of Pacific Biosciences. The other authors declared no conflicts of interest.

Source: Virolainen SJ, Satish L, Biagini JM, et al. Filaggrin loss-of-function variants are associated with atopic dermatitis phenotypes in a diverse, early life prospective cohort. JCI Insight. 2024 (Apr 2). doi: 10.1172/jci.insight.178258 Source

Key clinical point: Established and new atopic dermatitis (AD)-associated filaggrin loss-of-function variants are associated with increased risks for clinical AD outcomes and disruption of skin barrier integrity in lesional and nonlesional skin of children with AD.

Major finding: Twenty variants were identified, including one novel variant. The presence of one or more variants was associated with a higher risk for moderate or severe AD vs mild AD (odds ratio 2.00; corrected P = .0394), a higher Scoring AD score (corrected P = .0394), and transepidermal water loss in both lesional (P = .018) and nonlesional (P = .015) skin.

Study details: This study included 438 children with AD (age ≤ 2 years; gestation period ≥ 36 weeks) from the early-life Mechanisms of Progression of Atopic Dermatitis to Asthma in Children cohort without a comorbid lung condition or dependence on immunosuppression or oral steroids for a condition except asthma.

Disclosures: This study was funded by the US National Institutes of Health. Matthew S. Hestand declared being an employee and shareholder of Pacific Biosciences. The other authors declared no conflicts of interest.

Source: Virolainen SJ, Satish L, Biagini JM, et al. Filaggrin loss-of-function variants are associated with atopic dermatitis phenotypes in a diverse, early life prospective cohort. JCI Insight. 2024 (Apr 2). doi: 10.1172/jci.insight.178258 Source

Key clinical point: Baricitinib treatment was effective and well-tolerated in patients with moderate to severe atopic dermatitis (AD) who were followed-up for 3 months in real-world settings.

Major finding: Baricitinib led to a significant reduction in the Eczema Area Severity Index (21.5 ± 13.2 vs 9.3 ± 9.0) and objective Scoring AD (45.9 ± 12.3 vs 28.2 ± 15.5) scores at 3 months vs start visit (both P < .001). The treatment discontinuation rate was 16.7%, with two patients discontinuing baricitinib due to adverse events.

Study details: This was an interim analysis of the TREATgermany registry that included 81 adult patients with moderate to severe AD who received baricitinib and concomitant topical treatment, of whom 49 had initiated baricitinib at a registry visit; 26 of these did not switch from a previous systemic drug and had their first follow-up visit at 3 months.

Disclosures: TREATgermany is supported by AbbVie Deutschland GmbH & Co. KG, Galderma S.A., and others. Six authors declared serving as consultants, lecturers, etc., for or having other ties with various organizations, including the sponsors of TREATgermany. The other authors declared no conflicts of interest.

Source: Traidl S, Heinrich L, Siegels D, et al, and the TREATgermany study group. Treatment of moderate-to-severe atopic dermatitis with baricitinib: Results from an interim analysis of the TREATgermany registry. J Eur Acad Dermatol Venereol. 2024 (Mar 28). doi: 10.1111/jdv.19979 Source

Key clinical point: Baricitinib treatment was effective and well-tolerated in patients with moderate to severe atopic dermatitis (AD) who were followed-up for 3 months in real-world settings.

Major finding: Baricitinib led to a significant reduction in the Eczema Area Severity Index (21.5 ± 13.2 vs 9.3 ± 9.0) and objective Scoring AD (45.9 ± 12.3 vs 28.2 ± 15.5) scores at 3 months vs start visit (both P < .001). The treatment discontinuation rate was 16.7%, with two patients discontinuing baricitinib due to adverse events.

Study details: This was an interim analysis of the TREATgermany registry that included 81 adult patients with moderate to severe AD who received baricitinib and concomitant topical treatment, of whom 49 had initiated baricitinib at a registry visit; 26 of these did not switch from a previous systemic drug and had their first follow-up visit at 3 months.

Disclosures: TREATgermany is supported by AbbVie Deutschland GmbH & Co. KG, Galderma S.A., and others. Six authors declared serving as consultants, lecturers, etc., for or having other ties with various organizations, including the sponsors of TREATgermany. The other authors declared no conflicts of interest.

Source: Traidl S, Heinrich L, Siegels D, et al, and the TREATgermany study group. Treatment of moderate-to-severe atopic dermatitis with baricitinib: Results from an interim analysis of the TREATgermany registry. J Eur Acad Dermatol Venereol. 2024 (Mar 28). doi: 10.1111/jdv.19979 Source

Key clinical point: Baricitinib treatment was effective and well-tolerated in patients with moderate to severe atopic dermatitis (AD) who were followed-up for 3 months in real-world settings.

Major finding: Baricitinib led to a significant reduction in the Eczema Area Severity Index (21.5 ± 13.2 vs 9.3 ± 9.0) and objective Scoring AD (45.9 ± 12.3 vs 28.2 ± 15.5) scores at 3 months vs start visit (both P < .001). The treatment discontinuation rate was 16.7%, with two patients discontinuing baricitinib due to adverse events.

Study details: This was an interim analysis of the TREATgermany registry that included 81 adult patients with moderate to severe AD who received baricitinib and concomitant topical treatment, of whom 49 had initiated baricitinib at a registry visit; 26 of these did not switch from a previous systemic drug and had their first follow-up visit at 3 months.

Disclosures: TREATgermany is supported by AbbVie Deutschland GmbH & Co. KG, Galderma S.A., and others. Six authors declared serving as consultants, lecturers, etc., for or having other ties with various organizations, including the sponsors of TREATgermany. The other authors declared no conflicts of interest.

Source: Traidl S, Heinrich L, Siegels D, et al, and the TREATgermany study group. Treatment of moderate-to-severe atopic dermatitis with baricitinib: Results from an interim analysis of the TREATgermany registry. J Eur Acad Dermatol Venereol. 2024 (Mar 28). doi: 10.1111/jdv.19979 Source

Key clinical point: Patients with atopic dermatitis (AD) have a significantly increased risk of developing lymphoma.

Major finding: Patients with AD vs control individuals showed a significantly increased likelihood of developing noncutaneous T-cell lymphoma (odds ratio [OR] 2.52; 95% CI 1.37-4.62), with similar outcomes for the peripheral T-cell lymphoma subtype (OR 4.00; 95% CI 1.50-10.66).

Study details: Findings are from a nested case-control study including 6425 adult patients with AD and 25,700 matched control individuals without AD from electronic health records.

Disclosures: This study did not receive any funding. Benjamin Ungar reported being an employee of Mount Sinai and receiving research funds from and serving as a consultant for various organizations.

Source: Powers CM, Piontkowski AJ, Orloff J, et al. Risk of lymphoma in patients with atopic dermatitis: A case-control study in the All of Us database. J Am Acad Dermatol. 2024 (Apr 4). doi: 10.1016/j.jaad.2024.03.038 Source

Key clinical point: Patients with atopic dermatitis (AD) have a significantly increased risk of developing lymphoma.

Major finding: Patients with AD vs control individuals showed a significantly increased likelihood of developing noncutaneous T-cell lymphoma (odds ratio [OR] 2.52; 95% CI 1.37-4.62), with similar outcomes for the peripheral T-cell lymphoma subtype (OR 4.00; 95% CI 1.50-10.66).

Study details: Findings are from a nested case-control study including 6425 adult patients with AD and 25,700 matched control individuals without AD from electronic health records.

Disclosures: This study did not receive any funding. Benjamin Ungar reported being an employee of Mount Sinai and receiving research funds from and serving as a consultant for various organizations.

Source: Powers CM, Piontkowski AJ, Orloff J, et al. Risk of lymphoma in patients with atopic dermatitis: A case-control study in the All of Us database. J Am Acad Dermatol. 2024 (Apr 4). doi: 10.1016/j.jaad.2024.03.038 Source

Key clinical point: Patients with atopic dermatitis (AD) have a significantly increased risk of developing lymphoma.

Major finding: Patients with AD vs control individuals showed a significantly increased likelihood of developing noncutaneous T-cell lymphoma (odds ratio [OR] 2.52; 95% CI 1.37-4.62), with similar outcomes for the peripheral T-cell lymphoma subtype (OR 4.00; 95% CI 1.50-10.66).

Study details: Findings are from a nested case-control study including 6425 adult patients with AD and 25,700 matched control individuals without AD from electronic health records.

Disclosures: This study did not receive any funding. Benjamin Ungar reported being an employee of Mount Sinai and receiving research funds from and serving as a consultant for various organizations.

Source: Powers CM, Piontkowski AJ, Orloff J, et al. Risk of lymphoma in patients with atopic dermatitis: A case-control study in the All of Us database. J Am Acad Dermatol. 2024 (Apr 4). doi: 10.1016/j.jaad.2024.03.038 Source

Key clinical point: Passive smoking during pregnancy is associated with an increased risk for atopic dermatitis (AD) in offspring; however, the association between active smoking during pregnancy and AD in offspring remains unestablished.

Major finding: Passive smoking during pregnancy led to a higher risk for AD in offspring (odds ratio [OR] 1.52; 95% CI 1.36-1.70); however, active smoking during pregnancy did not increase the risk for AD in offspring (OR 0.96; 95% CI 0.86-1.07).

Study details: This meta-analysis of 15 observational studies included children or mother-child pairs who underwent either questionnaire-based or physician assessment for AD diagnosis and questionnaire-based assessment or cotinine level measurement for evaluating exposure to active or passive smoking.

Disclosures: This study was supported by the Key Scientific and Technological Research Projects of Henan Province and the Key Scientific Research Projects in Universities of Henan Province, China. The authors declared no conflicts of interest.

Source: Chao L, Liang W, Zhao X, et al. Maternal tobacco exposure during pregnancy and atopic dermatitis in offspring: A systematic review and meta-analysis. J Eur Acad Dermatol Venereol. 2024 (Ma 14). doi: 10.1111/jdv.19958 Source

Key clinical point: Passive smoking during pregnancy is associated with an increased risk for atopic dermatitis (AD) in offspring; however, the association between active smoking during pregnancy and AD in offspring remains unestablished.

Major finding: Passive smoking during pregnancy led to a higher risk for AD in offspring (odds ratio [OR] 1.52; 95% CI 1.36-1.70); however, active smoking during pregnancy did not increase the risk for AD in offspring (OR 0.96; 95% CI 0.86-1.07).

Study details: This meta-analysis of 15 observational studies included children or mother-child pairs who underwent either questionnaire-based or physician assessment for AD diagnosis and questionnaire-based assessment or cotinine level measurement for evaluating exposure to active or passive smoking.

Disclosures: This study was supported by the Key Scientific and Technological Research Projects of Henan Province and the Key Scientific Research Projects in Universities of Henan Province, China. The authors declared no conflicts of interest.

Source: Chao L, Liang W, Zhao X, et al. Maternal tobacco exposure during pregnancy and atopic dermatitis in offspring: A systematic review and meta-analysis. J Eur Acad Dermatol Venereol. 2024 (Ma 14). doi: 10.1111/jdv.19958 Source

Key clinical point: Passive smoking during pregnancy is associated with an increased risk for atopic dermatitis (AD) in offspring; however, the association between active smoking during pregnancy and AD in offspring remains unestablished.

Major finding: Passive smoking during pregnancy led to a higher risk for AD in offspring (odds ratio [OR] 1.52; 95% CI 1.36-1.70); however, active smoking during pregnancy did not increase the risk for AD in offspring (OR 0.96; 95% CI 0.86-1.07).

Study details: This meta-analysis of 15 observational studies included children or mother-child pairs who underwent either questionnaire-based or physician assessment for AD diagnosis and questionnaire-based assessment or cotinine level measurement for evaluating exposure to active or passive smoking.

Disclosures: This study was supported by the Key Scientific and Technological Research Projects of Henan Province and the Key Scientific Research Projects in Universities of Henan Province, China. The authors declared no conflicts of interest.

Source: Chao L, Liang W, Zhao X, et al. Maternal tobacco exposure during pregnancy and atopic dermatitis in offspring: A systematic review and meta-analysis. J Eur Acad Dermatol Venereol. 2024 (Ma 14). doi: 10.1111/jdv.19958 Source

Key clinical point: In children with atopic dermatitis (AD), weekly vitamin D3 (VD3) supplementation vs placebo for 6 weeks failed to decrease the clinical severity of AD or alter type 2 immunity biomarkers.

Major finding: At 6 weeks, the change in the Severity Scoring of AD (SCORAD) index was similar in the VD3 (−5.3 ± 11.6) and placebo (−5.5 ± 9.9; P = .91) groups. No significant between-group differences were observed for change in type 2 immunity blood biomarkers, such as eosinophil counts, total immunoglobulin E (IgE), and specific IgE against staphylococcal enterotoxin A and B (all P > .05).

Study details: This randomized controlled trial included 101 children with AD (age 2-17 years) who were randomly assigned to receive weekly oral VD3 (8000, 12,000, and 16,000 IU for ages 2-5.9, 6-11.9, and 12-17.9 years, respectively; n = 53) or placebo (n = 48) for 6 weeks.

Disclosures: This study was funded by Fondo de Desarrollo Científico y Tecnológico, Chile. The authors declared no conflicts of interest.

Source: Borzutzky A, Iturriaga C, Pérez-Mateluna G, et al. Effect of weekly vitamin D supplementation on the severity of atopic dermatitis and type 2 immunity biomarkers in children: A randomized controlled trial. J Eur Acad Dermatol Venereol. 2024 (Mar 14). doi: 10.1111/jdv.19959 Source

Key clinical point: In children with atopic dermatitis (AD), weekly vitamin D3 (VD3) supplementation vs placebo for 6 weeks failed to decrease the clinical severity of AD or alter type 2 immunity biomarkers.

Major finding: At 6 weeks, the change in the Severity Scoring of AD (SCORAD) index was similar in the VD3 (−5.3 ± 11.6) and placebo (−5.5 ± 9.9; P = .91) groups. No significant between-group differences were observed for change in type 2 immunity blood biomarkers, such as eosinophil counts, total immunoglobulin E (IgE), and specific IgE against staphylococcal enterotoxin A and B (all P > .05).

Study details: This randomized controlled trial included 101 children with AD (age 2-17 years) who were randomly assigned to receive weekly oral VD3 (8000, 12,000, and 16,000 IU for ages 2-5.9, 6-11.9, and 12-17.9 years, respectively; n = 53) or placebo (n = 48) for 6 weeks.

Disclosures: This study was funded by Fondo de Desarrollo Científico y Tecnológico, Chile. The authors declared no conflicts of interest.

Source: Borzutzky A, Iturriaga C, Pérez-Mateluna G, et al. Effect of weekly vitamin D supplementation on the severity of atopic dermatitis and type 2 immunity biomarkers in children: A randomized controlled trial. J Eur Acad Dermatol Venereol. 2024 (Mar 14). doi: 10.1111/jdv.19959 Source

Key clinical point: In children with atopic dermatitis (AD), weekly vitamin D3 (VD3) supplementation vs placebo for 6 weeks failed to decrease the clinical severity of AD or alter type 2 immunity biomarkers.

Major finding: At 6 weeks, the change in the Severity Scoring of AD (SCORAD) index was similar in the VD3 (−5.3 ± 11.6) and placebo (−5.5 ± 9.9; P = .91) groups. No significant between-group differences were observed for change in type 2 immunity blood biomarkers, such as eosinophil counts, total immunoglobulin E (IgE), and specific IgE against staphylococcal enterotoxin A and B (all P > .05).

Study details: This randomized controlled trial included 101 children with AD (age 2-17 years) who were randomly assigned to receive weekly oral VD3 (8000, 12,000, and 16,000 IU for ages 2-5.9, 6-11.9, and 12-17.9 years, respectively; n = 53) or placebo (n = 48) for 6 weeks.

Disclosures: This study was funded by Fondo de Desarrollo Científico y Tecnológico, Chile. The authors declared no conflicts of interest.

Source: Borzutzky A, Iturriaga C, Pérez-Mateluna G, et al. Effect of weekly vitamin D supplementation on the severity of atopic dermatitis and type 2 immunity biomarkers in children: A randomized controlled trial. J Eur Acad Dermatol Venereol. 2024 (Mar 14). doi: 10.1111/jdv.19959 Source

Key clinical point: Tralokinumab-mediated inhibition of interleukin (IL)-13 improved epidermal pathology and reduced the expression of key atopic dermatitis (AD) biomarkers in the serum of patients with moderate to severe AD.

Major finding: At week 16, tralokinumab vs placebo led to a significantly greater decrease from baseline in serum levels of type 2 biomarkers (CCL17/TARC, periostin, immunoglobulin E, and IL-22; all P < .05), a greater mean percentage change in the Eczema Area Severity Index score (−55.6 vs −36.7), and improved expression of genes dysregulated in AD (46.6% vs 16.4%; P < .001).

Study details: This study involved the collection of blood samples from 802 patients with moderate to severe AD randomized in the ECZTRA 1 and ECZTEND trials, followed by the selection of a subset of 299 patients with relevant samples available who had received tralokinumab (n = 223) or placebo (n = 76).

Disclosures: LEO Pharma A/S funded both ECZTRA 1 and the ongoing ECZTEND trial. Six authors declared being employees or shareholders of LEO Pharma. Several authors declared receiving research grants from or having other ties with various sources, including LEO Pharma.

Source: Guttman-Yassky E, Kabashima K, Staumont-Salle D, et al. Targeting IL-13 with tralokinumab normalizes type 2 inflammation in atopic dermatitis both early and at 2 years. Allergy. 2024 (Apr 2). doi: 10.1111/all.16108 Source

Key clinical point: Tralokinumab-mediated inhibition of interleukin (IL)-13 improved epidermal pathology and reduced the expression of key atopic dermatitis (AD) biomarkers in the serum of patients with moderate to severe AD.

Major finding: At week 16, tralokinumab vs placebo led to a significantly greater decrease from baseline in serum levels of type 2 biomarkers (CCL17/TARC, periostin, immunoglobulin E, and IL-22; all P < .05), a greater mean percentage change in the Eczema Area Severity Index score (−55.6 vs −36.7), and improved expression of genes dysregulated in AD (46.6% vs 16.4%; P < .001).

Study details: This study involved the collection of blood samples from 802 patients with moderate to severe AD randomized in the ECZTRA 1 and ECZTEND trials, followed by the selection of a subset of 299 patients with relevant samples available who had received tralokinumab (n = 223) or placebo (n = 76).

Disclosures: LEO Pharma A/S funded both ECZTRA 1 and the ongoing ECZTEND trial. Six authors declared being employees or shareholders of LEO Pharma. Several authors declared receiving research grants from or having other ties with various sources, including LEO Pharma.

Source: Guttman-Yassky E, Kabashima K, Staumont-Salle D, et al. Targeting IL-13 with tralokinumab normalizes type 2 inflammation in atopic dermatitis both early and at 2 years. Allergy. 2024 (Apr 2). doi: 10.1111/all.16108 Source

Key clinical point: Tralokinumab-mediated inhibition of interleukin (IL)-13 improved epidermal pathology and reduced the expression of key atopic dermatitis (AD) biomarkers in the serum of patients with moderate to severe AD.

Major finding: At week 16, tralokinumab vs placebo led to a significantly greater decrease from baseline in serum levels of type 2 biomarkers (CCL17/TARC, periostin, immunoglobulin E, and IL-22; all P < .05), a greater mean percentage change in the Eczema Area Severity Index score (−55.6 vs −36.7), and improved expression of genes dysregulated in AD (46.6% vs 16.4%; P < .001).

Study details: This study involved the collection of blood samples from 802 patients with moderate to severe AD randomized in the ECZTRA 1 and ECZTEND trials, followed by the selection of a subset of 299 patients with relevant samples available who had received tralokinumab (n = 223) or placebo (n = 76).

Disclosures: LEO Pharma A/S funded both ECZTRA 1 and the ongoing ECZTEND trial. Six authors declared being employees or shareholders of LEO Pharma. Several authors declared receiving research grants from or having other ties with various sources, including LEO Pharma.

Source: Guttman-Yassky E, Kabashima K, Staumont-Salle D, et al. Targeting IL-13 with tralokinumab normalizes type 2 inflammation in atopic dermatitis both early and at 2 years. Allergy. 2024 (Apr 2). doi: 10.1111/all.16108 Source

Key clinical point: Children with atopic dermatitis (AD) at age 3 years showed an increased subsequent risk of developing inflammatory bowel disease (IBD), Crohn's disease (CD), and ulcerative colitis (UC); however, atopic manifestations were not associated with IBD.

Major finding: The presence of AD at age 3 years significantly increased the risk for IBD (pooled adjusted hazard ratio [aHR] 1.46; 95% CI 1.13-1.88), CD (pooled aHR 1.53; 95% CI 1.04-2.26), and UC (pooled aHR 1.78; 95% CI 1.15-2.75) later in life. Any atopic manifestation by age 3 years was not associated with IBD (pooled aHR 1.20; 95% CI 0.95-1.52).

Study details: This study included 83,311 children from the All Babies in Southeast Sweden (1997-1999) and the Norwegian Mother, Father, and Child (1999-2008) birth cohorts with questionnaire-based prospectively collected parent-reported information on asthma, AD, etc., developed by 3 years of age who were followed up from birth until 2021 or a diagnosis of IBD.

Disclosure: This study was supported by The Swedish Research Council and others. The authors declared no conflicts of interest.

Source: Lerchova T, Størdal K, Andersson B, Ludvigsson J, Mårild K. Atopic dermatitis in early childhood and risk of inflammatory bowel disease: A Scandinavian birth cohort study. J Pediatr. 2024;270:14027 (Mar21). doi: 10.1016/j.jpeds.2024.114027. Source

Key clinical point: Children with atopic dermatitis (AD) at age 3 years showed an increased subsequent risk of developing inflammatory bowel disease (IBD), Crohn's disease (CD), and ulcerative colitis (UC); however, atopic manifestations were not associated with IBD.

Major finding: The presence of AD at age 3 years significantly increased the risk for IBD (pooled adjusted hazard ratio [aHR] 1.46; 95% CI 1.13-1.88), CD (pooled aHR 1.53; 95% CI 1.04-2.26), and UC (pooled aHR 1.78; 95% CI 1.15-2.75) later in life. Any atopic manifestation by age 3 years was not associated with IBD (pooled aHR 1.20; 95% CI 0.95-1.52).

Study details: This study included 83,311 children from the All Babies in Southeast Sweden (1997-1999) and the Norwegian Mother, Father, and Child (1999-2008) birth cohorts with questionnaire-based prospectively collected parent-reported information on asthma, AD, etc., developed by 3 years of age who were followed up from birth until 2021 or a diagnosis of IBD.

Disclosure: This study was supported by The Swedish Research Council and others. The authors declared no conflicts of interest.

Source: Lerchova T, Størdal K, Andersson B, Ludvigsson J, Mårild K. Atopic dermatitis in early childhood and risk of inflammatory bowel disease: A Scandinavian birth cohort study. J Pediatr. 2024;270:14027 (Mar21). doi: 10.1016/j.jpeds.2024.114027. Source

Key clinical point: Children with atopic dermatitis (AD) at age 3 years showed an increased subsequent risk of developing inflammatory bowel disease (IBD), Crohn's disease (CD), and ulcerative colitis (UC); however, atopic manifestations were not associated with IBD.

Major finding: The presence of AD at age 3 years significantly increased the risk for IBD (pooled adjusted hazard ratio [aHR] 1.46; 95% CI 1.13-1.88), CD (pooled aHR 1.53; 95% CI 1.04-2.26), and UC (pooled aHR 1.78; 95% CI 1.15-2.75) later in life. Any atopic manifestation by age 3 years was not associated with IBD (pooled aHR 1.20; 95% CI 0.95-1.52).

Study details: This study included 83,311 children from the All Babies in Southeast Sweden (1997-1999) and the Norwegian Mother, Father, and Child (1999-2008) birth cohorts with questionnaire-based prospectively collected parent-reported information on asthma, AD, etc., developed by 3 years of age who were followed up from birth until 2021 or a diagnosis of IBD.

Disclosure: This study was supported by The Swedish Research Council and others. The authors declared no conflicts of interest.

Source: Lerchova T, Størdal K, Andersson B, Ludvigsson J, Mårild K. Atopic dermatitis in early childhood and risk of inflammatory bowel disease: A Scandinavian birth cohort study. J Pediatr. 2024;270:14027 (Mar21). doi: 10.1016/j.jpeds.2024.114027. Source

The Diagnosis: Subcutaneous Fat Necrosis

Histopathology revealed lobular panniculitis with lymphohistiocytic inflammation, lipid crystals, and calcifications in our patient (Figure). Subcutaneous fat necrosis (SCFN) was diagnosed based on these characteristic histopathologic findings. No further treatment was pursued.

Subcutaneous fat necrosis is a rare, self-limiting panniculitis that typically resolves within several weeks to months without scarring. It manifests as red or violaceous subcutaneous nodules or plaques most commonly on the buttocks, trunk, proximal arms and legs, and cheeks.¹ Histopathology reveals lobular panniculitis with dense granulomatous infiltrates of histiocytes, eosinophils, and multinucleated giant cells with needle-shaped crystals. Focal areas of fat necrosis with calcification also can be seen.²

The epidemiology of SCFN is unknown. Most cases occur in healthy full-term to postterm neonates who experience hypoxia, other prenatal stressors, or therapeutic hypothermia for the treatment of hypoxic-ischemic encephalopathy.³ Although the etiology is unclear, certain inciting factors such as local tissue hypoxia, cold exposure, meconium aspiration, maternal diabetes, preeclampsia, and mechanical pressure have been proposed. Our patient underwent hypothermic cooling protocol, and it has been suggested that the increased saturated to unsaturated fat concentration in the skin of newborns increases the melting point, thus predisposing them to fat crystalization.⁴ Cases of SCFN involving the scalp are rare; therefore, any newborns receiving hypothermic therapy for hypoxic-ischemic encephalopathy should have a thorough skin examination with possible biopsy of lesions that are characteristic of SCFN, such as red or violaceous subcutaneous nodules or plaques, for specific disease identification.

The main complication of SCFN is hypercalcemia, which occurs in approximately 50% of cases. Other serum abnormalities include hyperglycemia, hypertriglyceridemia, and thrombocytopenia, though these findings are not as well associated.⁴ Patients with associated hypercalcemia may be asymptomatic, as in our patient, but other presentations include irritability, weakness, anorexia, vomiting, renal failure, failure to thrive, and encephalopathy. Nephrocalcinosis is a common complication of severe hypercalcemia; however, there is little evidence of associated major renal dysfunction.⁵ The exact mechanism of hypercalcemia is poorly understood. A widely accepted theory postulates that a granulomatous inflammatory infiltrate upregulates 1-α-hydroxylase activity, which enzymatically converts 25-hydroxyvitamin D to its active form, 1,25-dihydroxycholecalciferol, which increases bone resorption and calcium absorption through the gastrointestinal tract and renal systems. Treatments for hypercalcemia include hyperhydration, calcium-wasting diuretics, and low calcium intake.⁶ Furthermore, calcium levels should be obtained at the time of diagnosis and 30, 45, and 60 days after the lesions resolve.⁴

Subcutaneous fat necrosis needs to be differentiated from the more severe panniculitis, sclerema neonatorum (SN), which typically affects critically ill, preterm, and small-for-gestational-age newborns. It is associated with a high mortality rate and is characterized by skin and subadjacent tissue structures. The process typically begins in the thighs, buttocks, or trunk and spreads diffusely, sparing the fat-free palms, soles, and genitalia.⁷ Although our patient was born preterm, the physical characteristics of the nodule and the lack of severe illness placed SN lower on our differential. Histopathologic differences between SCFN and SN involve the extent of tissue fibrosis and presence of inflammatory cells. Sclerema neonatorum typically manifests with thickened connective tissue with a sparse inflammatory infiltrate, including lymphocytes, histiocytes, and multinucleated giant cells.⁷ Conversely, SCFN manifests with fat necrosis with an extensive inflammatory infiltrate. It is important to be able to distinguish between these 2 conditions, as both have vastly different prognoses.

Cold panniculitis, sometimes called “popsicle panniculitis,” is a phenomenon in which cold contact with the skin causes eruption of firm, erythematous, indurated plaques at the site of exposure. This self-limiting condition typically appears hours to days after cold exposure and spontaneously resolves in a few weeks.⁸ Therapeutic hypothermic protocol treatment involves using cooling devices to lower the body temperature for a short duration. The temperature typically is lowered to approximately 32 °C to 36 °C. These temperatures are not low enough to induce cold panniculitis, which is more commonly seen in facial ice applications when managing supraventricular tachycardia in neonates.

Cephalohematoma is a birthing injury that causes blood accumulation within the subperiosteal space. During parturition, the compressive and sheering forces on the calvarium rupture the vessels passing through the periosteum, causing blood to pool slowly into the subperiostium; thus, a cephalohematoma usually manifests later at 1 to 3 days of life as localized head swelling.⁹ The bleeding typically does not cross suture lines and is primarily found in the occipital or parietal regions. The incidence has been reported to be 0.4% to 2.5% of all live births.¹⁰ Although the location of the nodule in our patient was in the occipital region, imaging and biopsy results did not show hemorrhagic findings consistent with cephalohematoma. Management of cephalohematoma mainly is observational, as the mass slowly regresses and the accumulated blood gradually is reabsorbed.

Fungal scalp infections (tinea capitis) are common in the pediatric population. The peak incidence of this infection has been reported in children aged 3 to 7 years, with Trichophyton tonsurans and Microsporum canis as the usual causative organisms.¹¹ Clinical features of tinea capitis include scaly patches with hair loss, hair loss with black pigmented dots at the follicular openings, diffuse scalp scaling with subtle hair loss, and cervical lymphadenopathy.¹² Although less common, tinea capitis can progress to a more severe form known as a kerion, which is characterized by a tender plaque with pustules and crusting. A kerion can result in permanent scarring and alopecia if left untreated.¹² In our patient, a nodule with scaling and faint erythema was observed, but no black pigmented dots at the follicular orifices were present. Therefore, a potassium hydroxide wet mount preparation used to diagnose tinea capitis was unnecessary. Systemic oral antifungal therapy such as fluconazole or terbinafine is the standard treatment for tinea capitis.

The Diagnosis: Subcutaneous Fat Necrosis

Histopathology revealed lobular panniculitis with lymphohistiocytic inflammation, lipid crystals, and calcifications in our patient (Figure). Subcutaneous fat necrosis (SCFN) was diagnosed based on these characteristic histopathologic findings. No further treatment was pursued.

Subcutaneous fat necrosis is a rare, self-limiting panniculitis that typically resolves within several weeks to months without scarring. It manifests as red or violaceous subcutaneous nodules or plaques most commonly on the buttocks, trunk, proximal arms and legs, and cheeks.¹ Histopathology reveals lobular panniculitis with dense granulomatous infiltrates of histiocytes, eosinophils, and multinucleated giant cells with needle-shaped crystals. Focal areas of fat necrosis with calcification also can be seen.²

The epidemiology of SCFN is unknown. Most cases occur in healthy full-term to postterm neonates who experience hypoxia, other prenatal stressors, or therapeutic hypothermia for the treatment of hypoxic-ischemic encephalopathy.³ Although the etiology is unclear, certain inciting factors such as local tissue hypoxia, cold exposure, meconium aspiration, maternal diabetes, preeclampsia, and mechanical pressure have been proposed. Our patient underwent hypothermic cooling protocol, and it has been suggested that the increased saturated to unsaturated fat concentration in the skin of newborns increases the melting point, thus predisposing them to fat crystalization.⁴ Cases of SCFN involving the scalp are rare; therefore, any newborns receiving hypothermic therapy for hypoxic-ischemic encephalopathy should have a thorough skin examination with possible biopsy of lesions that are characteristic of SCFN, such as red or violaceous subcutaneous nodules or plaques, for specific disease identification.

The main complication of SCFN is hypercalcemia, which occurs in approximately 50% of cases. Other serum abnormalities include hyperglycemia, hypertriglyceridemia, and thrombocytopenia, though these findings are not as well associated.⁴ Patients with associated hypercalcemia may be asymptomatic, as in our patient, but other presentations include irritability, weakness, anorexia, vomiting, renal failure, failure to thrive, and encephalopathy. Nephrocalcinosis is a common complication of severe hypercalcemia; however, there is little evidence of associated major renal dysfunction.⁵ The exact mechanism of hypercalcemia is poorly understood. A widely accepted theory postulates that a granulomatous inflammatory infiltrate upregulates 1-α-hydroxylase activity, which enzymatically converts 25-hydroxyvitamin D to its active form, 1,25-dihydroxycholecalciferol, which increases bone resorption and calcium absorption through the gastrointestinal tract and renal systems. Treatments for hypercalcemia include hyperhydration, calcium-wasting diuretics, and low calcium intake.⁶ Furthermore, calcium levels should be obtained at the time of diagnosis and 30, 45, and 60 days after the lesions resolve.⁴

Subcutaneous fat necrosis needs to be differentiated from the more severe panniculitis, sclerema neonatorum (SN), which typically affects critically ill, preterm, and small-for-gestational-age newborns. It is associated with a high mortality rate and is characterized by skin and subadjacent tissue structures. The process typically begins in the thighs, buttocks, or trunk and spreads diffusely, sparing the fat-free palms, soles, and genitalia.⁷ Although our patient was born preterm, the physical characteristics of the nodule and the lack of severe illness placed SN lower on our differential. Histopathologic differences between SCFN and SN involve the extent of tissue fibrosis and presence of inflammatory cells. Sclerema neonatorum typically manifests with thickened connective tissue with a sparse inflammatory infiltrate, including lymphocytes, histiocytes, and multinucleated giant cells.⁷ Conversely, SCFN manifests with fat necrosis with an extensive inflammatory infiltrate. It is important to be able to distinguish between these 2 conditions, as both have vastly different prognoses.

Cold panniculitis, sometimes called “popsicle panniculitis,” is a phenomenon in which cold contact with the skin causes eruption of firm, erythematous, indurated plaques at the site of exposure. This self-limiting condition typically appears hours to days after cold exposure and spontaneously resolves in a few weeks.⁸ Therapeutic hypothermic protocol treatment involves using cooling devices to lower the body temperature for a short duration. The temperature typically is lowered to approximately 32 °C to 36 °C. These temperatures are not low enough to induce cold panniculitis, which is more commonly seen in facial ice applications when managing supraventricular tachycardia in neonates.

Cephalohematoma is a birthing injury that causes blood accumulation within the subperiosteal space. During parturition, the compressive and sheering forces on the calvarium rupture the vessels passing through the periosteum, causing blood to pool slowly into the subperiostium; thus, a cephalohematoma usually manifests later at 1 to 3 days of life as localized head swelling.⁹ The bleeding typically does not cross suture lines and is primarily found in the occipital or parietal regions. The incidence has been reported to be 0.4% to 2.5% of all live births.¹⁰ Although the location of the nodule in our patient was in the occipital region, imaging and biopsy results did not show hemorrhagic findings consistent with cephalohematoma. Management of cephalohematoma mainly is observational, as the mass slowly regresses and the accumulated blood gradually is reabsorbed.

Fungal scalp infections (tinea capitis) are common in the pediatric population. The peak incidence of this infection has been reported in children aged 3 to 7 years, with Trichophyton tonsurans and Microsporum canis as the usual causative organisms.¹¹ Clinical features of tinea capitis include scaly patches with hair loss, hair loss with black pigmented dots at the follicular openings, diffuse scalp scaling with subtle hair loss, and cervical lymphadenopathy.¹² Although less common, tinea capitis can progress to a more severe form known as a kerion, which is characterized by a tender plaque with pustules and crusting. A kerion can result in permanent scarring and alopecia if left untreated.¹² In our patient, a nodule with scaling and faint erythema was observed, but no black pigmented dots at the follicular orifices were present. Therefore, a potassium hydroxide wet mount preparation used to diagnose tinea capitis was unnecessary. Systemic oral antifungal therapy such as fluconazole or terbinafine is the standard treatment for tinea capitis.

The Diagnosis: Subcutaneous Fat Necrosis

Histopathology revealed lobular panniculitis with lymphohistiocytic inflammation, lipid crystals, and calcifications in our patient (Figure). Subcutaneous fat necrosis (SCFN) was diagnosed based on these characteristic histopathologic findings. No further treatment was pursued.

Subcutaneous fat necrosis is a rare, self-limiting panniculitis that typically resolves within several weeks to months without scarring. It manifests as red or violaceous subcutaneous nodules or plaques most commonly on the buttocks, trunk, proximal arms and legs, and cheeks.¹ Histopathology reveals lobular panniculitis with dense granulomatous infiltrates of histiocytes, eosinophils, and multinucleated giant cells with needle-shaped crystals. Focal areas of fat necrosis with calcification also can be seen.²

The epidemiology of SCFN is unknown. Most cases occur in healthy full-term to postterm neonates who experience hypoxia, other prenatal stressors, or therapeutic hypothermia for the treatment of hypoxic-ischemic encephalopathy.³ Although the etiology is unclear, certain inciting factors such as local tissue hypoxia, cold exposure, meconium aspiration, maternal diabetes, preeclampsia, and mechanical pressure have been proposed. Our patient underwent hypothermic cooling protocol, and it has been suggested that the increased saturated to unsaturated fat concentration in the skin of newborns increases the melting point, thus predisposing them to fat crystalization.⁴ Cases of SCFN involving the scalp are rare; therefore, any newborns receiving hypothermic therapy for hypoxic-ischemic encephalopathy should have a thorough skin examination with possible biopsy of lesions that are characteristic of SCFN, such as red or violaceous subcutaneous nodules or plaques, for specific disease identification.

The main complication of SCFN is hypercalcemia, which occurs in approximately 50% of cases. Other serum abnormalities include hyperglycemia, hypertriglyceridemia, and thrombocytopenia, though these findings are not as well associated.⁴ Patients with associated hypercalcemia may be asymptomatic, as in our patient, but other presentations include irritability, weakness, anorexia, vomiting, renal failure, failure to thrive, and encephalopathy. Nephrocalcinosis is a common complication of severe hypercalcemia; however, there is little evidence of associated major renal dysfunction.⁵ The exact mechanism of hypercalcemia is poorly understood. A widely accepted theory postulates that a granulomatous inflammatory infiltrate upregulates 1-α-hydroxylase activity, which enzymatically converts 25-hydroxyvitamin D to its active form, 1,25-dihydroxycholecalciferol, which increases bone resorption and calcium absorption through the gastrointestinal tract and renal systems. Treatments for hypercalcemia include hyperhydration, calcium-wasting diuretics, and low calcium intake.⁶ Furthermore, calcium levels should be obtained at the time of diagnosis and 30, 45, and 60 days after the lesions resolve.⁴

Subcutaneous fat necrosis needs to be differentiated from the more severe panniculitis, sclerema neonatorum (SN), which typically affects critically ill, preterm, and small-for-gestational-age newborns. It is associated with a high mortality rate and is characterized by skin and subadjacent tissue structures. The process typically begins in the thighs, buttocks, or trunk and spreads diffusely, sparing the fat-free palms, soles, and genitalia.⁷ Although our patient was born preterm, the physical characteristics of the nodule and the lack of severe illness placed SN lower on our differential. Histopathologic differences between SCFN and SN involve the extent of tissue fibrosis and presence of inflammatory cells. Sclerema neonatorum typically manifests with thickened connective tissue with a sparse inflammatory infiltrate, including lymphocytes, histiocytes, and multinucleated giant cells.⁷ Conversely, SCFN manifests with fat necrosis with an extensive inflammatory infiltrate. It is important to be able to distinguish between these 2 conditions, as both have vastly different prognoses.

Cold panniculitis, sometimes called “popsicle panniculitis,” is a phenomenon in which cold contact with the skin causes eruption of firm, erythematous, indurated plaques at the site of exposure. This self-limiting condition typically appears hours to days after cold exposure and spontaneously resolves in a few weeks.⁸ Therapeutic hypothermic protocol treatment involves using cooling devices to lower the body temperature for a short duration. The temperature typically is lowered to approximately 32 °C to 36 °C. These temperatures are not low enough to induce cold panniculitis, which is more commonly seen in facial ice applications when managing supraventricular tachycardia in neonates.

Cephalohematoma is a birthing injury that causes blood accumulation within the subperiosteal space. During parturition, the compressive and sheering forces on the calvarium rupture the vessels passing through the periosteum, causing blood to pool slowly into the subperiostium; thus, a cephalohematoma usually manifests later at 1 to 3 days of life as localized head swelling.⁹ The bleeding typically does not cross suture lines and is primarily found in the occipital or parietal regions. The incidence has been reported to be 0.4% to 2.5% of all live births.¹⁰ Although the location of the nodule in our patient was in the occipital region, imaging and biopsy results did not show hemorrhagic findings consistent with cephalohematoma. Management of cephalohematoma mainly is observational, as the mass slowly regresses and the accumulated blood gradually is reabsorbed.

Fungal scalp infections (tinea capitis) are common in the pediatric population. The peak incidence of this infection has been reported in children aged 3 to 7 years, with Trichophyton tonsurans and Microsporum canis as the usual causative organisms.¹¹ Clinical features of tinea capitis include scaly patches with hair loss, hair loss with black pigmented dots at the follicular openings, diffuse scalp scaling with subtle hair loss, and cervical lymphadenopathy.¹² Although less common, tinea capitis can progress to a more severe form known as a kerion, which is characterized by a tender plaque with pustules and crusting. A kerion can result in permanent scarring and alopecia if left untreated.¹² In our patient, a nodule with scaling and faint erythema was observed, but no black pigmented dots at the follicular orifices were present. Therefore, a potassium hydroxide wet mount preparation used to diagnose tinea capitis was unnecessary. Systemic oral antifungal therapy such as fluconazole or terbinafine is the standard treatment for tinea capitis.

Key clinical point: Anti-calcitonin gene-related peptide monoclonal antibodies (anti-CGRP mAb) showed superior efficacy to botulinum toxin A (BoNT-A) in reducing the migraine burden in patients with chronic migraine (CM).

Major finding: Anti-CGRP mAbs vs BoNT-A led to significant reductions in mean Headache Impact Test-6 and Allodynia Symptoms Checklist-12 scores at 6 months (mean change −11.1 vs −3.2 points, P < .0001; and −5.2 vs −0.5 points, P = .0056, respectively) and 12 months (mean change −11.4 vs −3.6 points, P = .0042; and −6.0 vs −0.9 points, P = .0011, respectively).

Study details: This exploratory analysis of the real-world effectiveness of anti-CGRP mAb vs BoNT-A included 126 patients with CM who were treated with anti-CGRP mAb (n = 36) or BoNT-A (n = 90).

Disclosures: The study was supported by the Italian Ministry of Health. Some authors declared receiving funding, travel grants, honoraria, or personal fees for participation in advisory boards, speaker panels, and clinical investigation studies from various sources.

Source: Montisano DA, Giossi R, Canella M, et al. Reducing the impact of headache and allodynia score in chronic migraine: An exploratory analysis from the Real-world Effectiveness of Anti-CGRP Monoclonal Antibodies Compared to Onabotulinum Toxin A (RAMO) Study. Toxins. 2024;16(4):178. doi: 10.3390/toxins16040178 Source

Key clinical point: Anti-calcitonin gene-related peptide monoclonal antibodies (anti-CGRP mAb) showed superior efficacy to botulinum toxin A (BoNT-A) in reducing the migraine burden in patients with chronic migraine (CM).

Major finding: Anti-CGRP mAbs vs BoNT-A led to significant reductions in mean Headache Impact Test-6 and Allodynia Symptoms Checklist-12 scores at 6 months (mean change −11.1 vs −3.2 points, P < .0001; and −5.2 vs −0.5 points, P = .0056, respectively) and 12 months (mean change −11.4 vs −3.6 points, P = .0042; and −6.0 vs −0.9 points, P = .0011, respectively).

Study details: This exploratory analysis of the real-world effectiveness of anti-CGRP mAb vs BoNT-A included 126 patients with CM who were treated with anti-CGRP mAb (n = 36) or BoNT-A (n = 90).

Disclosures: The study was supported by the Italian Ministry of Health. Some authors declared receiving funding, travel grants, honoraria, or personal fees for participation in advisory boards, speaker panels, and clinical investigation studies from various sources.

Source: Montisano DA, Giossi R, Canella M, et al. Reducing the impact of headache and allodynia score in chronic migraine: An exploratory analysis from the Real-world Effectiveness of Anti-CGRP Monoclonal Antibodies Compared to Onabotulinum Toxin A (RAMO) Study. Toxins. 2024;16(4):178. doi: 10.3390/toxins16040178 Source

Key clinical point: Anti-calcitonin gene-related peptide monoclonal antibodies (anti-CGRP mAb) showed superior efficacy to botulinum toxin A (BoNT-A) in reducing the migraine burden in patients with chronic migraine (CM).

Major finding: Anti-CGRP mAbs vs BoNT-A led to significant reductions in mean Headache Impact Test-6 and Allodynia Symptoms Checklist-12 scores at 6 months (mean change −11.1 vs −3.2 points, P < .0001; and −5.2 vs −0.5 points, P = .0056, respectively) and 12 months (mean change −11.4 vs −3.6 points, P = .0042; and −6.0 vs −0.9 points, P = .0011, respectively).

Study details: This exploratory analysis of the real-world effectiveness of anti-CGRP mAb vs BoNT-A included 126 patients with CM who were treated with anti-CGRP mAb (n = 36) or BoNT-A (n = 90).

Disclosures: The study was supported by the Italian Ministry of Health. Some authors declared receiving funding, travel grants, honoraria, or personal fees for participation in advisory boards, speaker panels, and clinical investigation studies from various sources.

Source: Montisano DA, Giossi R, Canella M, et al. Reducing the impact of headache and allodynia score in chronic migraine: An exploratory analysis from the Real-world Effectiveness of Anti-CGRP Monoclonal Antibodies Compared to Onabotulinum Toxin A (RAMO) Study. Toxins. 2024;16(4):178. doi: 10.3390/toxins16040178 Source