Key clinical point: Patients diagnosed with psoriasis at an older vs younger age had a significantly shorter interval between psoriasis and psoriatic arthritis (PsA) diagnoses and also showed a higher likelihood of developing PsA within 6 months of having psoriasis.

Major finding: Patients with psoriasis onset at the age of 42.6 vs 18.9 years had a 62% shorter time interval between psoriasis and PsA diagnoses (exponentiated estimate 0.38; P < .001) and were ~4.6 times more likely to have a concurrent onset of PsA within 6 months of having psoriasis (odds ratio 4.56; P < .001).

Study details: This registry-based study included 384 patients diagnosed with PsA either after or concurrently with their psoriasis diagnosis.

Disclosures: This study was supported in part by a grant from the US National Institutes of Health. One author declared receiving payment or honoraria from and holding leadership or fiduciary roles with various sources.

Source: Cheemalavagu S, Jin Y, Husni ME. What clinical factors affect length of transition to psoriatic arthritis in patients with psoriasis? ACR Open Rheumatol. 2024 (June 28). Doi: 10.1002/acr2.11703 Source

Key clinical point: Patients diagnosed with psoriasis at an older vs younger age had a significantly shorter interval between psoriasis and psoriatic arthritis (PsA) diagnoses and also showed a higher likelihood of developing PsA within 6 months of having psoriasis.

Major finding: Patients with psoriasis onset at the age of 42.6 vs 18.9 years had a 62% shorter time interval between psoriasis and PsA diagnoses (exponentiated estimate 0.38; P < .001) and were ~4.6 times more likely to have a concurrent onset of PsA within 6 months of having psoriasis (odds ratio 4.56; P < .001).

Study details: This registry-based study included 384 patients diagnosed with PsA either after or concurrently with their psoriasis diagnosis.

Disclosures: This study was supported in part by a grant from the US National Institutes of Health. One author declared receiving payment or honoraria from and holding leadership or fiduciary roles with various sources.

Source: Cheemalavagu S, Jin Y, Husni ME. What clinical factors affect length of transition to psoriatic arthritis in patients with psoriasis? ACR Open Rheumatol. 2024 (June 28). Doi: 10.1002/acr2.11703 Source

Key clinical point: Patients diagnosed with psoriasis at an older vs younger age had a significantly shorter interval between psoriasis and psoriatic arthritis (PsA) diagnoses and also showed a higher likelihood of developing PsA within 6 months of having psoriasis.

Major finding: Patients with psoriasis onset at the age of 42.6 vs 18.9 years had a 62% shorter time interval between psoriasis and PsA diagnoses (exponentiated estimate 0.38; P < .001) and were ~4.6 times more likely to have a concurrent onset of PsA within 6 months of having psoriasis (odds ratio 4.56; P < .001).

Study details: This registry-based study included 384 patients diagnosed with PsA either after or concurrently with their psoriasis diagnosis.

Disclosures: This study was supported in part by a grant from the US National Institutes of Health. One author declared receiving payment or honoraria from and holding leadership or fiduciary roles with various sources.

Source: Cheemalavagu S, Jin Y, Husni ME. What clinical factors affect length of transition to psoriatic arthritis in patients with psoriasis? ACR Open Rheumatol. 2024 (June 28). Doi: 10.1002/acr2.11703 Source

Everyone takes a pharmacology class in medical school that includes a lecture on beta receptors. They’re in the heart (beta-1) and lungs (beta-2), and drug compounds agonize or antagonize one or both. The professor will caution against using antagonists (beta blockade) for patients with chronic obstructive pulmonary disease (COPD) lest they further impair the patient’s irreversibly narrowed airways. Obsequious students mature into obsequious doctors, intent on “doing no harm.” For better or worse, you withhold beta-blockers from your patient with COPD and comorbid cardiac disease.

Perhaps because the pulmonologist isn’t usually the one who decides whether a beta-blocker is prescribed, I’ve been napping on this topic since training. Early in fellowship, I read an ACP Journal Club article about a Cochrane systematic review (yes, I read a review of a review) that concluded that beta-blockers are fine in patients with COPD. The summary appealed to my bias towards evidence-based medicine (EBM) supplanting physiology, medical school, and everything else. I was more apt to believe my stodgy residency attendings than the stodgy pharmacology professor. Even though COPD and cardiovascular disease share multiple risk factors, I had never reinvestigated the relationship between beta-blockers and COPD.

Turns out that while I was sleeping, the debate continued. Go figure. Just last month a prospective, observational study published in JAMA Network Open found that beta-blockers did not increase the risk for cardiovascular or respiratory events among patients with COPD being discharged after hospitalization for acute myocardial infarction. Although this could be viewed as a triumph for EBM over physiology and a validation of my decade-plus of intellectual laziness, the results are actually pretty thin. These studies, in which patients with an indication for a therapy (a beta-blocker in this case) are analyzed by whether or not they received it, are problematic. The fanciest statistics — in this case, they used propensity scores — can’t control for residual confounding. What drove the physicians to prescribe in some cases but not others? We can only guess.

This might be okay if there hadn’t been a randomized controlled trial (RCT) published in 2019 in The New England Journal of Medicine that found that beta-blockers increase the risk for severe COPD exacerbations. In EBM, the RCT trumps all. Ironically, this trial was designed to test whether beta-blockers reduce severe COPD exacerbations. Yes, we’d come full circle. There was enough biologic plausibility to support a positive effect, or so thought the study authors and the Department of Defense (DOD) — for reasons I can’t possibly guess, the DOD funded this RCT. My pharmacology professor must be rolling over in his tenure.

The RCT did leave beta-blockers some wiggle room. The authors purposely excluded anyone with a cardiovascular indication for a beta-blocker. The intent was to ensure beneficial effects were isolated to respiratory and not cardiovascular outcomes. Of course, the reason I’m writing and you’re reading this is that COPD and cardiovascular disease co-occur at a high rate. The RCT notwithstanding, we prescribe beta-blockers to patients with COPD because they have a cardiac indication, not to reduce acute COPD exacerbations. So, it’s possible there’d be a net beta-blocker benefit in patients with COPD and comorbid heart disease.

That’s where the JAMA Network Open study comes in, but as discussed, methodologic weaknesses preclude its being the final word. That said, I think it’s unlikely we’ll see a COPD with comorbid cardiac disease RCT performed to assess whether beta-blockers provide a net benefit, unless maybe the DOD wants to fund another one of these. In the meantime, I’m calling clinical equipoise and punting. Fortunately for me, I don’t have to prescribe beta-blockers. I suppose I could consider stopping them in my patient with severe COPD, the one I can’t keep out of the hospital, but I’m not convinced that would make much difference.
 

Dr. Holley is professor of medicine at Uniformed Services University in Bethesda, Maryland, and a pulmonary/sleep and critical care medicine physician at MedStar Washington Hospital Center in Washington, DC. He reported conflicts of interest with Metapharm, CHEST College, and WebMD.

A version of this article first appeared on Medscape.com.

Everyone takes a pharmacology class in medical school that includes a lecture on beta receptors. They’re in the heart (beta-1) and lungs (beta-2), and drug compounds agonize or antagonize one or both. The professor will caution against using antagonists (beta blockade) for patients with chronic obstructive pulmonary disease (COPD) lest they further impair the patient’s irreversibly narrowed airways. Obsequious students mature into obsequious doctors, intent on “doing no harm.” For better or worse, you withhold beta-blockers from your patient with COPD and comorbid cardiac disease.

Perhaps because the pulmonologist isn’t usually the one who decides whether a beta-blocker is prescribed, I’ve been napping on this topic since training. Early in fellowship, I read an ACP Journal Club article about a Cochrane systematic review (yes, I read a review of a review) that concluded that beta-blockers are fine in patients with COPD. The summary appealed to my bias towards evidence-based medicine (EBM) supplanting physiology, medical school, and everything else. I was more apt to believe my stodgy residency attendings than the stodgy pharmacology professor. Even though COPD and cardiovascular disease share multiple risk factors, I had never reinvestigated the relationship between beta-blockers and COPD.

Turns out that while I was sleeping, the debate continued. Go figure. Just last month a prospective, observational study published in JAMA Network Open found that beta-blockers did not increase the risk for cardiovascular or respiratory events among patients with COPD being discharged after hospitalization for acute myocardial infarction. Although this could be viewed as a triumph for EBM over physiology and a validation of my decade-plus of intellectual laziness, the results are actually pretty thin. These studies, in which patients with an indication for a therapy (a beta-blocker in this case) are analyzed by whether or not they received it, are problematic. The fanciest statistics — in this case, they used propensity scores — can’t control for residual confounding. What drove the physicians to prescribe in some cases but not others? We can only guess.

This might be okay if there hadn’t been a randomized controlled trial (RCT) published in 2019 in The New England Journal of Medicine that found that beta-blockers increase the risk for severe COPD exacerbations. In EBM, the RCT trumps all. Ironically, this trial was designed to test whether beta-blockers reduce severe COPD exacerbations. Yes, we’d come full circle. There was enough biologic plausibility to support a positive effect, or so thought the study authors and the Department of Defense (DOD) — for reasons I can’t possibly guess, the DOD funded this RCT. My pharmacology professor must be rolling over in his tenure.

The RCT did leave beta-blockers some wiggle room. The authors purposely excluded anyone with a cardiovascular indication for a beta-blocker. The intent was to ensure beneficial effects were isolated to respiratory and not cardiovascular outcomes. Of course, the reason I’m writing and you’re reading this is that COPD and cardiovascular disease co-occur at a high rate. The RCT notwithstanding, we prescribe beta-blockers to patients with COPD because they have a cardiac indication, not to reduce acute COPD exacerbations. So, it’s possible there’d be a net beta-blocker benefit in patients with COPD and comorbid heart disease.

That’s where the JAMA Network Open study comes in, but as discussed, methodologic weaknesses preclude its being the final word. That said, I think it’s unlikely we’ll see a COPD with comorbid cardiac disease RCT performed to assess whether beta-blockers provide a net benefit, unless maybe the DOD wants to fund another one of these. In the meantime, I’m calling clinical equipoise and punting. Fortunately for me, I don’t have to prescribe beta-blockers. I suppose I could consider stopping them in my patient with severe COPD, the one I can’t keep out of the hospital, but I’m not convinced that would make much difference.
 

Dr. Holley is professor of medicine at Uniformed Services University in Bethesda, Maryland, and a pulmonary/sleep and critical care medicine physician at MedStar Washington Hospital Center in Washington, DC. He reported conflicts of interest with Metapharm, CHEST College, and WebMD.

A version of this article first appeared on Medscape.com.

Everyone takes a pharmacology class in medical school that includes a lecture on beta receptors. They’re in the heart (beta-1) and lungs (beta-2), and drug compounds agonize or antagonize one or both. The professor will caution against using antagonists (beta blockade) for patients with chronic obstructive pulmonary disease (COPD) lest they further impair the patient’s irreversibly narrowed airways. Obsequious students mature into obsequious doctors, intent on “doing no harm.” For better or worse, you withhold beta-blockers from your patient with COPD and comorbid cardiac disease.

Perhaps because the pulmonologist isn’t usually the one who decides whether a beta-blocker is prescribed, I’ve been napping on this topic since training. Early in fellowship, I read an ACP Journal Club article about a Cochrane systematic review (yes, I read a review of a review) that concluded that beta-blockers are fine in patients with COPD. The summary appealed to my bias towards evidence-based medicine (EBM) supplanting physiology, medical school, and everything else. I was more apt to believe my stodgy residency attendings than the stodgy pharmacology professor. Even though COPD and cardiovascular disease share multiple risk factors, I had never reinvestigated the relationship between beta-blockers and COPD.

Turns out that while I was sleeping, the debate continued. Go figure. Just last month a prospective, observational study published in JAMA Network Open found that beta-blockers did not increase the risk for cardiovascular or respiratory events among patients with COPD being discharged after hospitalization for acute myocardial infarction. Although this could be viewed as a triumph for EBM over physiology and a validation of my decade-plus of intellectual laziness, the results are actually pretty thin. These studies, in which patients with an indication for a therapy (a beta-blocker in this case) are analyzed by whether or not they received it, are problematic. The fanciest statistics — in this case, they used propensity scores — can’t control for residual confounding. What drove the physicians to prescribe in some cases but not others? We can only guess.

This might be okay if there hadn’t been a randomized controlled trial (RCT) published in 2019 in The New England Journal of Medicine that found that beta-blockers increase the risk for severe COPD exacerbations. In EBM, the RCT trumps all. Ironically, this trial was designed to test whether beta-blockers reduce severe COPD exacerbations. Yes, we’d come full circle. There was enough biologic plausibility to support a positive effect, or so thought the study authors and the Department of Defense (DOD) — for reasons I can’t possibly guess, the DOD funded this RCT. My pharmacology professor must be rolling over in his tenure.

The RCT did leave beta-blockers some wiggle room. The authors purposely excluded anyone with a cardiovascular indication for a beta-blocker. The intent was to ensure beneficial effects were isolated to respiratory and not cardiovascular outcomes. Of course, the reason I’m writing and you’re reading this is that COPD and cardiovascular disease co-occur at a high rate. The RCT notwithstanding, we prescribe beta-blockers to patients with COPD because they have a cardiac indication, not to reduce acute COPD exacerbations. So, it’s possible there’d be a net beta-blocker benefit in patients with COPD and comorbid heart disease.

That’s where the JAMA Network Open study comes in, but as discussed, methodologic weaknesses preclude its being the final word. That said, I think it’s unlikely we’ll see a COPD with comorbid cardiac disease RCT performed to assess whether beta-blockers provide a net benefit, unless maybe the DOD wants to fund another one of these. In the meantime, I’m calling clinical equipoise and punting. Fortunately for me, I don’t have to prescribe beta-blockers. I suppose I could consider stopping them in my patient with severe COPD, the one I can’t keep out of the hospital, but I’m not convinced that would make much difference.
 

Dr. Holley is professor of medicine at Uniformed Services University in Bethesda, Maryland, and a pulmonary/sleep and critical care medicine physician at MedStar Washington Hospital Center in Washington, DC. He reported conflicts of interest with Metapharm, CHEST College, and WebMD.

A version of this article first appeared on Medscape.com.

Key clinical point: Parental migraine was associated with an increased risk for major mental disorders in the offspring, including attention deficit/hyperactivity disorder (ADHD), bipolar disorder, and depressive disorder.

Major finding: Offspring of parents with vs without migraine had a significantly higher risk for ADHD (hazard ratio [HR] 1.37; 95% CI 1.25-1.50), bipolar disorder (HR 1.35; 95% CI 1.06-1.71), and depressive disorder (HR 1.33; 95% CI 1.21-1.47). Sub-analyses revealed that only maternal migraine was a significant risk factor for these disorders.

Study details: This study used data from the Taiwan National Health Insurance Research Database and included 22,747 offspring of parents with migraine and 227,470 matched offspring of parents without migraine.

Disclosures: This study was supported by grants from the Taipei Veterans General Hospital, Yen Tjing Ling Medical Foundation, and Ministry of Science and Technology, Taiwan. The authors declared no conflicts of interest.

Source: Li D-J, Tsai S-J, Chen T-J, et al. Risk of major mental disorders in the offspring of parents with migraine. Ann Gen Psychiatry. 2024;23:23 (Jun 22). Doi: 10.1186/s12991-024-00508-y Source

Key clinical point: Parental migraine was associated with an increased risk for major mental disorders in the offspring, including attention deficit/hyperactivity disorder (ADHD), bipolar disorder, and depressive disorder.

Major finding: Offspring of parents with vs without migraine had a significantly higher risk for ADHD (hazard ratio [HR] 1.37; 95% CI 1.25-1.50), bipolar disorder (HR 1.35; 95% CI 1.06-1.71), and depressive disorder (HR 1.33; 95% CI 1.21-1.47). Sub-analyses revealed that only maternal migraine was a significant risk factor for these disorders.

Study details: This study used data from the Taiwan National Health Insurance Research Database and included 22,747 offspring of parents with migraine and 227,470 matched offspring of parents without migraine.

Disclosures: This study was supported by grants from the Taipei Veterans General Hospital, Yen Tjing Ling Medical Foundation, and Ministry of Science and Technology, Taiwan. The authors declared no conflicts of interest.

Source: Li D-J, Tsai S-J, Chen T-J, et al. Risk of major mental disorders in the offspring of parents with migraine. Ann Gen Psychiatry. 2024;23:23 (Jun 22). Doi: 10.1186/s12991-024-00508-y Source

Key clinical point: Parental migraine was associated with an increased risk for major mental disorders in the offspring, including attention deficit/hyperactivity disorder (ADHD), bipolar disorder, and depressive disorder.

Major finding: Offspring of parents with vs without migraine had a significantly higher risk for ADHD (hazard ratio [HR] 1.37; 95% CI 1.25-1.50), bipolar disorder (HR 1.35; 95% CI 1.06-1.71), and depressive disorder (HR 1.33; 95% CI 1.21-1.47). Sub-analyses revealed that only maternal migraine was a significant risk factor for these disorders.

Study details: This study used data from the Taiwan National Health Insurance Research Database and included 22,747 offspring of parents with migraine and 227,470 matched offspring of parents without migraine.

Disclosures: This study was supported by grants from the Taipei Veterans General Hospital, Yen Tjing Ling Medical Foundation, and Ministry of Science and Technology, Taiwan. The authors declared no conflicts of interest.

Source: Li D-J, Tsai S-J, Chen T-J, et al. Risk of major mental disorders in the offspring of parents with migraine. Ann Gen Psychiatry. 2024;23:23 (Jun 22). Doi: 10.1186/s12991-024-00508-y Source

Key clinical point: Dietary vitamin C intake was negatively associated with the risk for severe headache or migraine.

Major finding: Each 1 mg/day increase in dietary vitamin C intake was significantly associated with a 6% lower risk for severe headache or migraine (adjusted odd ratio [aOR] 0.94; P = .0007). This inverse association between dietary vitamin C intake and severe headache or migraine risk was significant in women (aOR 0.90; 95% CI 0.87-0.85) but not in men.

Study details: This cross-sectional study included 13,445 participants from the National Health and Nutrition Examination Survey, of whom 2745 (20.42%) had severe headache or migraine.

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

Source: Zheng Y, Jin J, Wei C, Huang C. Association of dietary vitamin C consumption with severe headache or migraine among adults: A cross-sectional study of NHANES 1999–2004. Front Nutr. 2024;11:fnut.2024.1412031 (Jun 18). Doi: 10.3389/fnut.2024.1412031 Source

Key clinical point: Dietary vitamin C intake was negatively associated with the risk for severe headache or migraine.

Major finding: Each 1 mg/day increase in dietary vitamin C intake was significantly associated with a 6% lower risk for severe headache or migraine (adjusted odd ratio [aOR] 0.94; P = .0007). This inverse association between dietary vitamin C intake and severe headache or migraine risk was significant in women (aOR 0.90; 95% CI 0.87-0.85) but not in men.

Study details: This cross-sectional study included 13,445 participants from the National Health and Nutrition Examination Survey, of whom 2745 (20.42%) had severe headache or migraine.

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

Source: Zheng Y, Jin J, Wei C, Huang C. Association of dietary vitamin C consumption with severe headache or migraine among adults: A cross-sectional study of NHANES 1999–2004. Front Nutr. 2024;11:fnut.2024.1412031 (Jun 18). Doi: 10.3389/fnut.2024.1412031 Source

Key clinical point: Dietary vitamin C intake was negatively associated with the risk for severe headache or migraine.

Major finding: Each 1 mg/day increase in dietary vitamin C intake was significantly associated with a 6% lower risk for severe headache or migraine (adjusted odd ratio [aOR] 0.94; P = .0007). This inverse association between dietary vitamin C intake and severe headache or migraine risk was significant in women (aOR 0.90; 95% CI 0.87-0.85) but not in men.

Study details: This cross-sectional study included 13,445 participants from the National Health and Nutrition Examination Survey, of whom 2745 (20.42%) had severe headache or migraine.

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

Source: Zheng Y, Jin J, Wei C, Huang C. Association of dietary vitamin C consumption with severe headache or migraine among adults: A cross-sectional study of NHANES 1999–2004. Front Nutr. 2024;11:fnut.2024.1412031 (Jun 18). Doi: 10.3389/fnut.2024.1412031 Source

Key clinical point: Prophylactic migraine therapy with calcitonin gene-related peptide (CGRP) antibodies showed sustained benefits in patients with migraine and medication overuse headache (MOH) or medication overuse (MO) for up to a year.

Major findings: All patients, including those with episodic migraine (EM) with MO, EM without MO, chronic migraine (CM) with MOH, or CM without MOH, had significant reductions in monthly headache days, monthly migraine days, and acute medication days at the last observation timepoint within the first year of CGRP therapy from baseline (all P < .0001). Relapse rates were lower (15.4%) in patients with CM with MOH after successful initiation of CGRP treatment.

Study details: This retrospective real-world analysis included 112 patients with EM (35 with MO and 77 without MO) and 179 patients with CM (109 with MOH and 70 without MOH).

Disclosures: This study was funded by Projekt DEAL. Some authors declared receiving travel fees, honoraria, or scientific support from or serving as consultants or advisors for various sources.

Source: Scheffler A, Basten J, Menzel L, et al. Persistent effectiveness of CGRP antibody therapy in migraine and comorbid medication overuse or medication overuse headache - a retrospective real-world analysis. J Headache Pain. 2024;25:109 (Jul 4). Doi: 10.1186/s10194-024-01813-3 Source

Key clinical point: Prophylactic migraine therapy with calcitonin gene-related peptide (CGRP) antibodies showed sustained benefits in patients with migraine and medication overuse headache (MOH) or medication overuse (MO) for up to a year.

Major findings: All patients, including those with episodic migraine (EM) with MO, EM without MO, chronic migraine (CM) with MOH, or CM without MOH, had significant reductions in monthly headache days, monthly migraine days, and acute medication days at the last observation timepoint within the first year of CGRP therapy from baseline (all P < .0001). Relapse rates were lower (15.4%) in patients with CM with MOH after successful initiation of CGRP treatment.

Study details: This retrospective real-world analysis included 112 patients with EM (35 with MO and 77 without MO) and 179 patients with CM (109 with MOH and 70 without MOH).

Disclosures: This study was funded by Projekt DEAL. Some authors declared receiving travel fees, honoraria, or scientific support from or serving as consultants or advisors for various sources.

Source: Scheffler A, Basten J, Menzel L, et al. Persistent effectiveness of CGRP antibody therapy in migraine and comorbid medication overuse or medication overuse headache - a retrospective real-world analysis. J Headache Pain. 2024;25:109 (Jul 4). Doi: 10.1186/s10194-024-01813-3 Source

Key clinical point: Prophylactic migraine therapy with calcitonin gene-related peptide (CGRP) antibodies showed sustained benefits in patients with migraine and medication overuse headache (MOH) or medication overuse (MO) for up to a year.

Major findings: All patients, including those with episodic migraine (EM) with MO, EM without MO, chronic migraine (CM) with MOH, or CM without MOH, had significant reductions in monthly headache days, monthly migraine days, and acute medication days at the last observation timepoint within the first year of CGRP therapy from baseline (all P < .0001). Relapse rates were lower (15.4%) in patients with CM with MOH after successful initiation of CGRP treatment.

Study details: This retrospective real-world analysis included 112 patients with EM (35 with MO and 77 without MO) and 179 patients with CM (109 with MOH and 70 without MOH).

Disclosures: This study was funded by Projekt DEAL. Some authors declared receiving travel fees, honoraria, or scientific support from or serving as consultants or advisors for various sources.

Source: Scheffler A, Basten J, Menzel L, et al. Persistent effectiveness of CGRP antibody therapy in migraine and comorbid medication overuse or medication overuse headache - a retrospective real-world analysis. J Headache Pain. 2024;25:109 (Jul 4). Doi: 10.1186/s10194-024-01813-3 Source

Key clinical point: Patients with migraine who experienced neck pain with headache (NPWH) had a higher prevalence of disability, depression, anxiety, and allodynia, as well as a lower quality of life, greater work productivity losses, and poorer acute treatment optimization than those without NPWH.

Major findings: Patients with vs without NPWH showed a higher prevalence of moderate to severe disability (47.7% vs 28.9%), depression (40.2% vs 28.2%), anxiety (41.2% vs 29.2%), allodynia (54.0% vs 36.6%), and poor acute treatment optimization (61.1% vs 53.3%; P < .001 for all). They also had lower quality of life scores (60.0 vs 68.6) and higher work productivity loss scores (50.0 vs 30.0; P < .001 for both).

Study details: This analysis of the Chronic Migraine Epidemiology and Outcomes – International study included 14, 492 patients with migraine, of whom 9896 (68.3%) had NPWH.

Disclosures: This study was funded by Allergan (now AbbVie). One author declared being an employee or a stockholder of AbbVie. Several authors declared having ties with various sources, including AbbVie.

Source: Matharu M, Katsarava Z, Buse DC, et al. Characterizing neck pain during headache among people with migraine: Multicountry results from the Chronic Migraine Epidemiology and Outcomes – International (CaMEO-I) cross-sectional study. Headache. 2024;64:750-763 (Jun 22). Doi: 10.1111/head.14753 Source

Key clinical point: Patients with migraine who experienced neck pain with headache (NPWH) had a higher prevalence of disability, depression, anxiety, and allodynia, as well as a lower quality of life, greater work productivity losses, and poorer acute treatment optimization than those without NPWH.

Major findings: Patients with vs without NPWH showed a higher prevalence of moderate to severe disability (47.7% vs 28.9%), depression (40.2% vs 28.2%), anxiety (41.2% vs 29.2%), allodynia (54.0% vs 36.6%), and poor acute treatment optimization (61.1% vs 53.3%; P < .001 for all). They also had lower quality of life scores (60.0 vs 68.6) and higher work productivity loss scores (50.0 vs 30.0; P < .001 for both).

Study details: This analysis of the Chronic Migraine Epidemiology and Outcomes – International study included 14, 492 patients with migraine, of whom 9896 (68.3%) had NPWH.

Disclosures: This study was funded by Allergan (now AbbVie). One author declared being an employee or a stockholder of AbbVie. Several authors declared having ties with various sources, including AbbVie.

Source: Matharu M, Katsarava Z, Buse DC, et al. Characterizing neck pain during headache among people with migraine: Multicountry results from the Chronic Migraine Epidemiology and Outcomes – International (CaMEO-I) cross-sectional study. Headache. 2024;64:750-763 (Jun 22). Doi: 10.1111/head.14753 Source

Key clinical point: Patients with migraine who experienced neck pain with headache (NPWH) had a higher prevalence of disability, depression, anxiety, and allodynia, as well as a lower quality of life, greater work productivity losses, and poorer acute treatment optimization than those without NPWH.

Major findings: Patients with vs without NPWH showed a higher prevalence of moderate to severe disability (47.7% vs 28.9%), depression (40.2% vs 28.2%), anxiety (41.2% vs 29.2%), allodynia (54.0% vs 36.6%), and poor acute treatment optimization (61.1% vs 53.3%; P < .001 for all). They also had lower quality of life scores (60.0 vs 68.6) and higher work productivity loss scores (50.0 vs 30.0; P < .001 for both).

Study details: This analysis of the Chronic Migraine Epidemiology and Outcomes – International study included 14, 492 patients with migraine, of whom 9896 (68.3%) had NPWH.

Disclosures: This study was funded by Allergan (now AbbVie). One author declared being an employee or a stockholder of AbbVie. Several authors declared having ties with various sources, including AbbVie.

Source: Matharu M, Katsarava Z, Buse DC, et al. Characterizing neck pain during headache among people with migraine: Multicountry results from the Chronic Migraine Epidemiology and Outcomes – International (CaMEO-I) cross-sectional study. Headache. 2024;64:750-763 (Jun 22). Doi: 10.1111/head.14753 Source

Key clinical point: Patients with inflammatory bowel disease (IBD) and chronic migraine (CM) had higher serum levels of alpha-calcitonin gene-related peptide (CGRP) than patients with only IBD.

Major findings: The alpha-CGRP levels were significantly higher in patients with IBD (56.9 vs 37.2 pg/mL; P = .003) or CM (53.0 vs 37.2 pg/mL; P = .019) than healthy control participants without a history of IBD and CM. The levels of this peptide in the serum were further increased in patients with IBD and concomitant migraine compared with those with only IBD (70.9 vs 53.7 pg/mL; P = .046).

Study details: This cross-sectional study compared the serum CGRP levels in 96 patients with IBD, 50 patients with CM, and 50 healthy control participants without a history of IBD and CM.

Disclosures: This study was funded by Instituto de Salud Carlos III, Spain. The authors declared no conflicts of interest.

Source: Pascual-Mato M, Gárate G, González-Quintanilla V, et al. Differences in circulating alpha-calcitonin gene-related peptide levels in inflammatory bowel disease and its relation to migraine comorbidity: A cross-sectional study. Headache. 2024;64:849-858 (Jun 24). Doi: 10.1111/head.14768 Source

Key clinical point: Patients with inflammatory bowel disease (IBD) and chronic migraine (CM) had higher serum levels of alpha-calcitonin gene-related peptide (CGRP) than patients with only IBD.

Major findings: The alpha-CGRP levels were significantly higher in patients with IBD (56.9 vs 37.2 pg/mL; P = .003) or CM (53.0 vs 37.2 pg/mL; P = .019) than healthy control participants without a history of IBD and CM. The levels of this peptide in the serum were further increased in patients with IBD and concomitant migraine compared with those with only IBD (70.9 vs 53.7 pg/mL; P = .046).

Study details: This cross-sectional study compared the serum CGRP levels in 96 patients with IBD, 50 patients with CM, and 50 healthy control participants without a history of IBD and CM.

Disclosures: This study was funded by Instituto de Salud Carlos III, Spain. The authors declared no conflicts of interest.

Source: Pascual-Mato M, Gárate G, González-Quintanilla V, et al. Differences in circulating alpha-calcitonin gene-related peptide levels in inflammatory bowel disease and its relation to migraine comorbidity: A cross-sectional study. Headache. 2024;64:849-858 (Jun 24). Doi: 10.1111/head.14768 Source

Key clinical point: Patients with inflammatory bowel disease (IBD) and chronic migraine (CM) had higher serum levels of alpha-calcitonin gene-related peptide (CGRP) than patients with only IBD.

Major findings: The alpha-CGRP levels were significantly higher in patients with IBD (56.9 vs 37.2 pg/mL; P = .003) or CM (53.0 vs 37.2 pg/mL; P = .019) than healthy control participants without a history of IBD and CM. The levels of this peptide in the serum were further increased in patients with IBD and concomitant migraine compared with those with only IBD (70.9 vs 53.7 pg/mL; P = .046).

Study details: This cross-sectional study compared the serum CGRP levels in 96 patients with IBD, 50 patients with CM, and 50 healthy control participants without a history of IBD and CM.

Disclosures: This study was funded by Instituto de Salud Carlos III, Spain. The authors declared no conflicts of interest.

Source: Pascual-Mato M, Gárate G, González-Quintanilla V, et al. Differences in circulating alpha-calcitonin gene-related peptide levels in inflammatory bowel disease and its relation to migraine comorbidity: A cross-sectional study. Headache. 2024;64:849-858 (Jun 24). Doi: 10.1111/head.14768 Source

Key clinical point: Long-term eptinezumab treatment showed benefits in patients with chronic migraine (CM) who had concomitant medication-overuse headache (MOH).

Major findings: After eptinezumab treatment, the average number of headache days per 3 months reduced from 15.8 days (mean 47.5 headache days/month) at baseline to 3.8 days (mean 11.3 headache days/month) at 104 weeks, along with reductions observed in the Migraine Disability Assessment (mean change −51.9 points) and 6-item Headache Impact Test (mean change −9.7 points) scores. More than half (57.1%) the patients showed an improvement in their patient-identified most bothersome symptom at as early as 4 weeks.

Study details: This post hoc analysis of the PREVAIL study included 49 patients with CM and concomitant MOH.

Disclosures: This publication was supported by H. Lundbeck A/S, Copenhagen, Denmark. Two authors declared being employees of H. Lundbeck A/S. The other authors declared having ties with various sources, including H. Lundbeck A/S.

Source: Blumenfeld A, Kudrow D, McAllister P, et al. Long-term effectiveness of eptinezumab in the treatment of patients with chronic migraine and medication-overuse headache. Headache. 2024;64:738-749 (Jun 24). Doi: 10.1111/head.14767 Source

Key clinical point: Long-term eptinezumab treatment showed benefits in patients with chronic migraine (CM) who had concomitant medication-overuse headache (MOH).

Major findings: After eptinezumab treatment, the average number of headache days per 3 months reduced from 15.8 days (mean 47.5 headache days/month) at baseline to 3.8 days (mean 11.3 headache days/month) at 104 weeks, along with reductions observed in the Migraine Disability Assessment (mean change −51.9 points) and 6-item Headache Impact Test (mean change −9.7 points) scores. More than half (57.1%) the patients showed an improvement in their patient-identified most bothersome symptom at as early as 4 weeks.

Study details: This post hoc analysis of the PREVAIL study included 49 patients with CM and concomitant MOH.

Disclosures: This publication was supported by H. Lundbeck A/S, Copenhagen, Denmark. Two authors declared being employees of H. Lundbeck A/S. The other authors declared having ties with various sources, including H. Lundbeck A/S.

Source: Blumenfeld A, Kudrow D, McAllister P, et al. Long-term effectiveness of eptinezumab in the treatment of patients with chronic migraine and medication-overuse headache. Headache. 2024;64:738-749 (Jun 24). Doi: 10.1111/head.14767 Source

Key clinical point: Long-term eptinezumab treatment showed benefits in patients with chronic migraine (CM) who had concomitant medication-overuse headache (MOH).

Major findings: After eptinezumab treatment, the average number of headache days per 3 months reduced from 15.8 days (mean 47.5 headache days/month) at baseline to 3.8 days (mean 11.3 headache days/month) at 104 weeks, along with reductions observed in the Migraine Disability Assessment (mean change −51.9 points) and 6-item Headache Impact Test (mean change −9.7 points) scores. More than half (57.1%) the patients showed an improvement in their patient-identified most bothersome symptom at as early as 4 weeks.

Study details: This post hoc analysis of the PREVAIL study included 49 patients with CM and concomitant MOH.

Disclosures: This publication was supported by H. Lundbeck A/S, Copenhagen, Denmark. Two authors declared being employees of H. Lundbeck A/S. The other authors declared having ties with various sources, including H. Lundbeck A/S.

Source: Blumenfeld A, Kudrow D, McAllister P, et al. Long-term effectiveness of eptinezumab in the treatment of patients with chronic migraine and medication-overuse headache. Headache. 2024;64:738-749 (Jun 24). Doi: 10.1111/head.14767 Source

Key clinical point: Calcitonin gene-related peptide (CGRP)–induced migraine attacks did not affect therapeutic response to erenumab in patients with migraine.

Major finding: Overall, a similar proportion of patients who experienced vs did not experience CGRP-induced migraine attacks had a ≥50% reduction in monthly migraine days during weeks 13-24 following erenumab treatment (61% vs 52%; odds ratio [OR] 1.42; P = .498). No significant differences were seen between the two patient groups that achieved a ≥50% reduction in monthly migraine or headache days of moderate to severe intensity (OR 1.25; P = .625).

Study details: This interim analysis of the REFORM study included 124 patients with migraine who received CGRP infusion on a single experimental day and subsequently a 24-week treatment with erenumab.

Disclosures: This study was funded by Novartis Pharma and the Lundbeck Foundation. Two authors declared being employees of or holding shares in Novartis Pharma AG. Several authors declared receiving personal fees from various sources, including Novartis, outside of the submitted work. One author is an associate editor for Cephalalgia.

Source: Al-Khazali HM, Ashina H, Christensen RH, et al. Hypersensitivity to CGRP as a predictive biomarker of migraine prevention with erenumab. Cephalalgia. 2024;44(6):3331024241258734 (Jun 11). Doi: 10.1177/03331024241258734 Source

Key clinical point: Calcitonin gene-related peptide (CGRP)–induced migraine attacks did not affect therapeutic response to erenumab in patients with migraine.

Major finding: Overall, a similar proportion of patients who experienced vs did not experience CGRP-induced migraine attacks had a ≥50% reduction in monthly migraine days during weeks 13-24 following erenumab treatment (61% vs 52%; odds ratio [OR] 1.42; P = .498). No significant differences were seen between the two patient groups that achieved a ≥50% reduction in monthly migraine or headache days of moderate to severe intensity (OR 1.25; P = .625).

Study details: This interim analysis of the REFORM study included 124 patients with migraine who received CGRP infusion on a single experimental day and subsequently a 24-week treatment with erenumab.

Disclosures: This study was funded by Novartis Pharma and the Lundbeck Foundation. Two authors declared being employees of or holding shares in Novartis Pharma AG. Several authors declared receiving personal fees from various sources, including Novartis, outside of the submitted work. One author is an associate editor for Cephalalgia.

Source: Al-Khazali HM, Ashina H, Christensen RH, et al. Hypersensitivity to CGRP as a predictive biomarker of migraine prevention with erenumab. Cephalalgia. 2024;44(6):3331024241258734 (Jun 11). Doi: 10.1177/03331024241258734 Source

Key clinical point: Calcitonin gene-related peptide (CGRP)–induced migraine attacks did not affect therapeutic response to erenumab in patients with migraine.

Major finding: Overall, a similar proportion of patients who experienced vs did not experience CGRP-induced migraine attacks had a ≥50% reduction in monthly migraine days during weeks 13-24 following erenumab treatment (61% vs 52%; odds ratio [OR] 1.42; P = .498). No significant differences were seen between the two patient groups that achieved a ≥50% reduction in monthly migraine or headache days of moderate to severe intensity (OR 1.25; P = .625).

Study details: This interim analysis of the REFORM study included 124 patients with migraine who received CGRP infusion on a single experimental day and subsequently a 24-week treatment with erenumab.

Disclosures: This study was funded by Novartis Pharma and the Lundbeck Foundation. Two authors declared being employees of or holding shares in Novartis Pharma AG. Several authors declared receiving personal fees from various sources, including Novartis, outside of the submitted work. One author is an associate editor for Cephalalgia.

Source: Al-Khazali HM, Ashina H, Christensen RH, et al. Hypersensitivity to CGRP as a predictive biomarker of migraine prevention with erenumab. Cephalalgia. 2024;44(6):3331024241258734 (Jun 11). Doi: 10.1177/03331024241258734 Source

Key clinical point: In patients with episodic migraine (EM) or chronic migraine (CM), erenumab treatment interruption was associated with increased monthly migraine days (MMD) and worsening of migraine disability; these effects ameliorated on treatment restart.

Major finding: After erenumab treatment interruption for 3 months, the number of monthly migraine days (MMD) increased from 6.1 to 10.9 days for patients with EM and from 11.4 to 16.8 days for patients with CM; the modified Migraine Disability Assessment scores (mMIDAS) also worsened during this period. Both MMD and mMIDAS scores improved upon restarting treatment.

Study details: This interim analysis of the 24-month, multicentric, non-interventional observational study included 172 patients with CM or EM who received erenumab and underwent treatment interruptions on average 11.2 months after initiation, with interruptions lasting for a mean duration of 4 months.

Disclosures: This study was funded by Novartis Pharma Schweiz AG. Four authors declared being full-time employees of Novartis Pharma Schweiz AG, and others declared having ties with various sources, including Novartis.

Source: Gantenbein AR, Bonvin C, Kamm CP, et al. Implications of therapy interruption on monthly migraine days and modified migraine disability assessment in patients treated with erenumab for chronic and episodic migraine: SQUARE study interim results. J Neurol. 2024 (Jun 13). Doi: 10.1007/s00415-024-12470-6 Source

Key clinical point: In patients with episodic migraine (EM) or chronic migraine (CM), erenumab treatment interruption was associated with increased monthly migraine days (MMD) and worsening of migraine disability; these effects ameliorated on treatment restart.

Major finding: After erenumab treatment interruption for 3 months, the number of monthly migraine days (MMD) increased from 6.1 to 10.9 days for patients with EM and from 11.4 to 16.8 days for patients with CM; the modified Migraine Disability Assessment scores (mMIDAS) also worsened during this period. Both MMD and mMIDAS scores improved upon restarting treatment.

Study details: This interim analysis of the 24-month, multicentric, non-interventional observational study included 172 patients with CM or EM who received erenumab and underwent treatment interruptions on average 11.2 months after initiation, with interruptions lasting for a mean duration of 4 months.

Disclosures: This study was funded by Novartis Pharma Schweiz AG. Four authors declared being full-time employees of Novartis Pharma Schweiz AG, and others declared having ties with various sources, including Novartis.

Source: Gantenbein AR, Bonvin C, Kamm CP, et al. Implications of therapy interruption on monthly migraine days and modified migraine disability assessment in patients treated with erenumab for chronic and episodic migraine: SQUARE study interim results. J Neurol. 2024 (Jun 13). Doi: 10.1007/s00415-024-12470-6 Source

Key clinical point: In patients with episodic migraine (EM) or chronic migraine (CM), erenumab treatment interruption was associated with increased monthly migraine days (MMD) and worsening of migraine disability; these effects ameliorated on treatment restart.

Major finding: After erenumab treatment interruption for 3 months, the number of monthly migraine days (MMD) increased from 6.1 to 10.9 days for patients with EM and from 11.4 to 16.8 days for patients with CM; the modified Migraine Disability Assessment scores (mMIDAS) also worsened during this period. Both MMD and mMIDAS scores improved upon restarting treatment.

Study details: This interim analysis of the 24-month, multicentric, non-interventional observational study included 172 patients with CM or EM who received erenumab and underwent treatment interruptions on average 11.2 months after initiation, with interruptions lasting for a mean duration of 4 months.

Disclosures: This study was funded by Novartis Pharma Schweiz AG. Four authors declared being full-time employees of Novartis Pharma Schweiz AG, and others declared having ties with various sources, including Novartis.

Source: Gantenbein AR, Bonvin C, Kamm CP, et al. Implications of therapy interruption on monthly migraine days and modified migraine disability assessment in patients treated with erenumab for chronic and episodic migraine: SQUARE study interim results. J Neurol. 2024 (Jun 13). Doi: 10.1007/s00415-024-12470-6 Source