Sir Augustus d’Este (1794-1848) described the circumstances preceding his development of neurological symptoms as follows:¹ “I travelled from Ramsgate to the Highlands of Scotland for the purpose of passing some days with a Relation for whom I had the affection of a Son. On my arrival I found him dead. Shortly after the funeral I was obliged to have my letters read to me, and their answers written for me, as my eyes were so attacked that when fixed upon minute objects indistinctness of vision was the consequence: Soon after I went to Ireland, and without any thing having been done to my eyes, they completely recovered their strength and distinctness of vision…" He then described a clinical course of relapsing-remitting neurologic symptoms merging into a progressive stage of unrelenting illness, most fitting with what we know today as multiple sclerosis (MS).¹ Why did Sir Augustus d'Este connect the event of the unexpected death to the onset of a lifelong neurologic disease?

Jean-Martin Charcot first described MS in a way close to what we know it as today. Charcot considered stress a factor in MS. He linked grief, vexation, and adverse changes in social circumstances to the onset of MS at that time.² I, as a practicing MS specialist, am surprised neither by Sir Augustus d'Este's diary nor by Charcot's earlier assessments of MS triggers.³ As I write this narrative, I think of the many times I heard from people diagnosed with MS. "It happened to me because of stress" is a statement not estranged from my daily clinical practice

MS as a multifactorial disease

It is tempting to make a case for emotional stress as a cause of MS, but one must remember that MS is a very complex disease with unclear etiologies. MS, a treatable but not yet curable disease, is the interplay between the genetics of the host and numerous environmental factors that exploit a susceptible immune system leading to unrelenting immune dysregulation.⁴ Recent studies have brought some pieces of this intricate puzzle together. The role of Epstein-Barr virus (EBV) in the pathogenesis of MS is being dissected.⁵ The possible synergy between vitamin D deficiency, EBV, and certain genetic variations is being studied.⁶ The roles of smoking, environmental toxins, obesity, diet, Western lifestyle, and the gut microbiome are some of the top areas of clinical, translational, and basic research.^7-11 But what about emotional stress? Where does it fit, if anywhere, in the current research paradigm?

Emotional stress and MS—Causality or not?

In the scientific method, several criteria must be proven for an element to be suspected in the etiology of a disease.¹² First, the suspect element must be present before the disease starts—i.e., a temporal association. Second, there must be a plausible biological explanation of how the suspect element acts in the disease's causation. Third, other variables that could confound the picture must be controlled for or dismissed. It is clear that no single factor is the cause of MS. By now, MS is agreed upon as a disease caused by multiple factors, some of which remain to be unraveled.⁹ The term "cause" has been utilized more recently by many authors when referring to EBV in relation to MS development, reasoning that in one study, in a small number of individuals with MS, EBV infection preceded the MS clinical diagnosis.¹³ Thus, the temporal association was provided. But does MS start at the onset of clinical symptoms?

For Sir Augustus d'Este, the disease may have started years before he visited the Highlands of Scotland, but only at that visit did MS become clinically apparent. So, the emotional trauma may have acted as a "trigger" for an MS flare-up rather than being a "cause" of MS. This might be a more plausible explanation of the association between emotional trauma and MS development. However, MS pathogenesis is complex, and one could argue that the disease starts many years before the first clinical symptoms that lead to diagnosis.

The MS prodrome has been demonstrated by several studies that suggest that MS may start many years before the clinical diagnosis.¹⁴ Radiologically isolated syndrome (RIS) further argues that MS may be clinically dormant for years, and clinical symptoms may not appear until later in the disease process.¹⁵ One may think that immune attacks on the optic nerves, spinal cord, or areas of the brainstem might be readily symptomatic compared to attacks on other structures of the central nervous system (e.g., periventricular or juxtacortical brain areas) that may be clinically silent. So, while for Sir Augustus d'Este it seemed that the disease started at the time of his visit to the Highlands of Scotland, it is equally plausible that it started years before the first clinical attack. Nevertheless, how could emotional stress play a role in the pathophysiology of MS?

Stress and the Immune System

At times of chronic stress, one may become more susceptible to infections. Reactivation of certain viruses can lead to oral ulcers, increased common cold symptoms, or other illnesses. For example, stress can reactivate herpes simplex type 1 and interestingly, EBV.^16,17 In MS, the immune system is dysregulated and has an autoimmune component. The effect of acute emotional stress differs from that of chronic stress.¹⁸ Several studies have examined the immune responses to both forms of stress.^19-21

Interestingly, acute stress activates cell-mediated immunity, increases immune cell trafficking to areas of injury, and, importantly, increases blood-brain barrier (BBB) permeability by activating resident mast cells in the brain and other areas, including the optic nerves.^22,23 Mast cell activation leads to BBB disruption, which is a key early step in the pathogenesis of MS. Thus, it is plausible that the proinflammatory changes associated with acute stress could be implicated in the pathogenesis of MS. This contrasts with chronic stress, which attenuates various immune responses, including suppressing cell-mediated immunity, but also dysregulate the immune system.

One could establish a biological plausibility for stress playing a role in the proinflammatory responses in MS. Whether it is causal or not, scientists can further explore the potential biologic explanations. While studying the association between acute stress and MS development or disease activity is difficult, several groups have examined the potential association. Many studies, however, have limitations due to the difficult nature of studying such an association, especially in quantifying or defining acute stress in general.

A limited number of studies on MS and stress: What do we know? And what are the challenges?

Rare studies have reported a potential association between MS development and stressful life events, while others reported no association.^24-26 Also, some studies observed an increase in MS relapses or the development of new magnetic resonance imaging (MRI) lesions following stressful life events or wartime, while others failed to show such an association.^26-30 There are few studies directly addressing the potential association between acute emotional stress and MS. The results of published studies are variable, and limitations are numerous. Limitations include the difficulty in measuring acute emotional stress, difficulty in its prediction, and ethical challenges of experimental design and recruiting participants. So, studies have focused on observational aspects, retrospective reviews, and surveys of memories prone to various biases. Rarely was the design of these clinical studies prospective. A few prospective studies reported an association between stressful life events and increased MS relapses and increased number of brain lesions.^27,31,32 Rare clinical trials have attempted to test stress reduction strategies and reported on the modest improvement of patient-reported outcomes and, in one study, a modest improvement in new MRI lesions.^33-35

Overall, several lines of evidence support a potential association between acute emotional stress and MS. Yet, the association is challenging to study, and future research might focus on stress-mitigation strategies and improving coping mechanisms in persons living with MS. It is important to note that it will be very difficult to design prospective studies to examine the potential association between acute emotional trauma and the development of de novo MS. Such studies will require a large number of participants (e.g., hundreds of thousands), long durations of follow-up (e.g., decades), and ways to classify repeated stressful events. An alternative approach is to ask persons newly diagnosed with MS at the time of initial diagnosis about any temporal association between their first symptom and stressful life events. However, this approach would provide some information on any association between the two, but not on causality of the disease itself.

Conclusion

The potential association between acute emotional stress and MS dates to the times of early descriptions of MS. Yet, research has been very limited and challenging. To date, the potential association remains elusive. Lines of evidence, while with limitations, have provided possible biologic explanations for the relationship between MS symptom onset and acute emotional stress. Although avoiding acute emotional stress is nearly impossible, incorporating global stress-coping strategies in early childhood education and secondary education might theoretically have potential beneficial effects on the subsequent risk of MS development or symptom flare-up, depending on a variety of factors.

But for now, when patients and colleagues ask me, “Can acute emotional stress be a ‘trigger’ for MS symptomology?,” my answer will remain, “Potentially, until proven otherwise.”

Sir Augustus d’Este (1794-1848) described the circumstances preceding his development of neurological symptoms as follows:¹ “I travelled from Ramsgate to the Highlands of Scotland for the purpose of passing some days with a Relation for whom I had the affection of a Son. On my arrival I found him dead. Shortly after the funeral I was obliged to have my letters read to me, and their answers written for me, as my eyes were so attacked that when fixed upon minute objects indistinctness of vision was the consequence: Soon after I went to Ireland, and without any thing having been done to my eyes, they completely recovered their strength and distinctness of vision…" He then described a clinical course of relapsing-remitting neurologic symptoms merging into a progressive stage of unrelenting illness, most fitting with what we know today as multiple sclerosis (MS).¹ Why did Sir Augustus d'Este connect the event of the unexpected death to the onset of a lifelong neurologic disease?

Jean-Martin Charcot first described MS in a way close to what we know it as today. Charcot considered stress a factor in MS. He linked grief, vexation, and adverse changes in social circumstances to the onset of MS at that time.² I, as a practicing MS specialist, am surprised neither by Sir Augustus d'Este's diary nor by Charcot's earlier assessments of MS triggers.³ As I write this narrative, I think of the many times I heard from people diagnosed with MS. "It happened to me because of stress" is a statement not estranged from my daily clinical practice

MS as a multifactorial disease

It is tempting to make a case for emotional stress as a cause of MS, but one must remember that MS is a very complex disease with unclear etiologies. MS, a treatable but not yet curable disease, is the interplay between the genetics of the host and numerous environmental factors that exploit a susceptible immune system leading to unrelenting immune dysregulation.⁴ Recent studies have brought some pieces of this intricate puzzle together. The role of Epstein-Barr virus (EBV) in the pathogenesis of MS is being dissected.⁵ The possible synergy between vitamin D deficiency, EBV, and certain genetic variations is being studied.⁶ The roles of smoking, environmental toxins, obesity, diet, Western lifestyle, and the gut microbiome are some of the top areas of clinical, translational, and basic research.^7-11 But what about emotional stress? Where does it fit, if anywhere, in the current research paradigm?

Emotional stress and MS—Causality or not?

In the scientific method, several criteria must be proven for an element to be suspected in the etiology of a disease.¹² First, the suspect element must be present before the disease starts—i.e., a temporal association. Second, there must be a plausible biological explanation of how the suspect element acts in the disease's causation. Third, other variables that could confound the picture must be controlled for or dismissed. It is clear that no single factor is the cause of MS. By now, MS is agreed upon as a disease caused by multiple factors, some of which remain to be unraveled.⁹ The term "cause" has been utilized more recently by many authors when referring to EBV in relation to MS development, reasoning that in one study, in a small number of individuals with MS, EBV infection preceded the MS clinical diagnosis.¹³ Thus, the temporal association was provided. But does MS start at the onset of clinical symptoms?

For Sir Augustus d'Este, the disease may have started years before he visited the Highlands of Scotland, but only at that visit did MS become clinically apparent. So, the emotional trauma may have acted as a "trigger" for an MS flare-up rather than being a "cause" of MS. This might be a more plausible explanation of the association between emotional trauma and MS development. However, MS pathogenesis is complex, and one could argue that the disease starts many years before the first clinical symptoms that lead to diagnosis.

The MS prodrome has been demonstrated by several studies that suggest that MS may start many years before the clinical diagnosis.¹⁴ Radiologically isolated syndrome (RIS) further argues that MS may be clinically dormant for years, and clinical symptoms may not appear until later in the disease process.¹⁵ One may think that immune attacks on the optic nerves, spinal cord, or areas of the brainstem might be readily symptomatic compared to attacks on other structures of the central nervous system (e.g., periventricular or juxtacortical brain areas) that may be clinically silent. So, while for Sir Augustus d'Este it seemed that the disease started at the time of his visit to the Highlands of Scotland, it is equally plausible that it started years before the first clinical attack. Nevertheless, how could emotional stress play a role in the pathophysiology of MS?

Stress and the Immune System

At times of chronic stress, one may become more susceptible to infections. Reactivation of certain viruses can lead to oral ulcers, increased common cold symptoms, or other illnesses. For example, stress can reactivate herpes simplex type 1 and interestingly, EBV.^16,17 In MS, the immune system is dysregulated and has an autoimmune component. The effect of acute emotional stress differs from that of chronic stress.¹⁸ Several studies have examined the immune responses to both forms of stress.^19-21

Interestingly, acute stress activates cell-mediated immunity, increases immune cell trafficking to areas of injury, and, importantly, increases blood-brain barrier (BBB) permeability by activating resident mast cells in the brain and other areas, including the optic nerves.^22,23 Mast cell activation leads to BBB disruption, which is a key early step in the pathogenesis of MS. Thus, it is plausible that the proinflammatory changes associated with acute stress could be implicated in the pathogenesis of MS. This contrasts with chronic stress, which attenuates various immune responses, including suppressing cell-mediated immunity, but also dysregulate the immune system.

One could establish a biological plausibility for stress playing a role in the proinflammatory responses in MS. Whether it is causal or not, scientists can further explore the potential biologic explanations. While studying the association between acute stress and MS development or disease activity is difficult, several groups have examined the potential association. Many studies, however, have limitations due to the difficult nature of studying such an association, especially in quantifying or defining acute stress in general.

A limited number of studies on MS and stress: What do we know? And what are the challenges?

Rare studies have reported a potential association between MS development and stressful life events, while others reported no association.^24-26 Also, some studies observed an increase in MS relapses or the development of new magnetic resonance imaging (MRI) lesions following stressful life events or wartime, while others failed to show such an association.^26-30 There are few studies directly addressing the potential association between acute emotional stress and MS. The results of published studies are variable, and limitations are numerous. Limitations include the difficulty in measuring acute emotional stress, difficulty in its prediction, and ethical challenges of experimental design and recruiting participants. So, studies have focused on observational aspects, retrospective reviews, and surveys of memories prone to various biases. Rarely was the design of these clinical studies prospective. A few prospective studies reported an association between stressful life events and increased MS relapses and increased number of brain lesions.^27,31,32 Rare clinical trials have attempted to test stress reduction strategies and reported on the modest improvement of patient-reported outcomes and, in one study, a modest improvement in new MRI lesions.^33-35

Overall, several lines of evidence support a potential association between acute emotional stress and MS. Yet, the association is challenging to study, and future research might focus on stress-mitigation strategies and improving coping mechanisms in persons living with MS. It is important to note that it will be very difficult to design prospective studies to examine the potential association between acute emotional trauma and the development of de novo MS. Such studies will require a large number of participants (e.g., hundreds of thousands), long durations of follow-up (e.g., decades), and ways to classify repeated stressful events. An alternative approach is to ask persons newly diagnosed with MS at the time of initial diagnosis about any temporal association between their first symptom and stressful life events. However, this approach would provide some information on any association between the two, but not on causality of the disease itself.

Conclusion

The potential association between acute emotional stress and MS dates to the times of early descriptions of MS. Yet, research has been very limited and challenging. To date, the potential association remains elusive. Lines of evidence, while with limitations, have provided possible biologic explanations for the relationship between MS symptom onset and acute emotional stress. Although avoiding acute emotional stress is nearly impossible, incorporating global stress-coping strategies in early childhood education and secondary education might theoretically have potential beneficial effects on the subsequent risk of MS development or symptom flare-up, depending on a variety of factors.

But for now, when patients and colleagues ask me, “Can acute emotional stress be a ‘trigger’ for MS symptomology?,” my answer will remain, “Potentially, until proven otherwise.”

Sir Augustus d’Este (1794-1848) described the circumstances preceding his development of neurological symptoms as follows:¹ “I travelled from Ramsgate to the Highlands of Scotland for the purpose of passing some days with a Relation for whom I had the affection of a Son. On my arrival I found him dead. Shortly after the funeral I was obliged to have my letters read to me, and their answers written for me, as my eyes were so attacked that when fixed upon minute objects indistinctness of vision was the consequence: Soon after I went to Ireland, and without any thing having been done to my eyes, they completely recovered their strength and distinctness of vision…" He then described a clinical course of relapsing-remitting neurologic symptoms merging into a progressive stage of unrelenting illness, most fitting with what we know today as multiple sclerosis (MS).¹ Why did Sir Augustus d'Este connect the event of the unexpected death to the onset of a lifelong neurologic disease?

Jean-Martin Charcot first described MS in a way close to what we know it as today. Charcot considered stress a factor in MS. He linked grief, vexation, and adverse changes in social circumstances to the onset of MS at that time.² I, as a practicing MS specialist, am surprised neither by Sir Augustus d'Este's diary nor by Charcot's earlier assessments of MS triggers.³ As I write this narrative, I think of the many times I heard from people diagnosed with MS. "It happened to me because of stress" is a statement not estranged from my daily clinical practice

MS as a multifactorial disease

It is tempting to make a case for emotional stress as a cause of MS, but one must remember that MS is a very complex disease with unclear etiologies. MS, a treatable but not yet curable disease, is the interplay between the genetics of the host and numerous environmental factors that exploit a susceptible immune system leading to unrelenting immune dysregulation.⁴ Recent studies have brought some pieces of this intricate puzzle together. The role of Epstein-Barr virus (EBV) in the pathogenesis of MS is being dissected.⁵ The possible synergy between vitamin D deficiency, EBV, and certain genetic variations is being studied.⁶ The roles of smoking, environmental toxins, obesity, diet, Western lifestyle, and the gut microbiome are some of the top areas of clinical, translational, and basic research.^7-11 But what about emotional stress? Where does it fit, if anywhere, in the current research paradigm?

Emotional stress and MS—Causality or not?

In the scientific method, several criteria must be proven for an element to be suspected in the etiology of a disease.¹² First, the suspect element must be present before the disease starts—i.e., a temporal association. Second, there must be a plausible biological explanation of how the suspect element acts in the disease's causation. Third, other variables that could confound the picture must be controlled for or dismissed. It is clear that no single factor is the cause of MS. By now, MS is agreed upon as a disease caused by multiple factors, some of which remain to be unraveled.⁹ The term "cause" has been utilized more recently by many authors when referring to EBV in relation to MS development, reasoning that in one study, in a small number of individuals with MS, EBV infection preceded the MS clinical diagnosis.¹³ Thus, the temporal association was provided. But does MS start at the onset of clinical symptoms?

For Sir Augustus d'Este, the disease may have started years before he visited the Highlands of Scotland, but only at that visit did MS become clinically apparent. So, the emotional trauma may have acted as a "trigger" for an MS flare-up rather than being a "cause" of MS. This might be a more plausible explanation of the association between emotional trauma and MS development. However, MS pathogenesis is complex, and one could argue that the disease starts many years before the first clinical symptoms that lead to diagnosis.

The MS prodrome has been demonstrated by several studies that suggest that MS may start many years before the clinical diagnosis.¹⁴ Radiologically isolated syndrome (RIS) further argues that MS may be clinically dormant for years, and clinical symptoms may not appear until later in the disease process.¹⁵ One may think that immune attacks on the optic nerves, spinal cord, or areas of the brainstem might be readily symptomatic compared to attacks on other structures of the central nervous system (e.g., periventricular or juxtacortical brain areas) that may be clinically silent. So, while for Sir Augustus d'Este it seemed that the disease started at the time of his visit to the Highlands of Scotland, it is equally plausible that it started years before the first clinical attack. Nevertheless, how could emotional stress play a role in the pathophysiology of MS?

Stress and the Immune System

At times of chronic stress, one may become more susceptible to infections. Reactivation of certain viruses can lead to oral ulcers, increased common cold symptoms, or other illnesses. For example, stress can reactivate herpes simplex type 1 and interestingly, EBV.^16,17 In MS, the immune system is dysregulated and has an autoimmune component. The effect of acute emotional stress differs from that of chronic stress.¹⁸ Several studies have examined the immune responses to both forms of stress.^19-21

Interestingly, acute stress activates cell-mediated immunity, increases immune cell trafficking to areas of injury, and, importantly, increases blood-brain barrier (BBB) permeability by activating resident mast cells in the brain and other areas, including the optic nerves.^22,23 Mast cell activation leads to BBB disruption, which is a key early step in the pathogenesis of MS. Thus, it is plausible that the proinflammatory changes associated with acute stress could be implicated in the pathogenesis of MS. This contrasts with chronic stress, which attenuates various immune responses, including suppressing cell-mediated immunity, but also dysregulate the immune system.

One could establish a biological plausibility for stress playing a role in the proinflammatory responses in MS. Whether it is causal or not, scientists can further explore the potential biologic explanations. While studying the association between acute stress and MS development or disease activity is difficult, several groups have examined the potential association. Many studies, however, have limitations due to the difficult nature of studying such an association, especially in quantifying or defining acute stress in general.

A limited number of studies on MS and stress: What do we know? And what are the challenges?

Rare studies have reported a potential association between MS development and stressful life events, while others reported no association.^24-26 Also, some studies observed an increase in MS relapses or the development of new magnetic resonance imaging (MRI) lesions following stressful life events or wartime, while others failed to show such an association.^26-30 There are few studies directly addressing the potential association between acute emotional stress and MS. The results of published studies are variable, and limitations are numerous. Limitations include the difficulty in measuring acute emotional stress, difficulty in its prediction, and ethical challenges of experimental design and recruiting participants. So, studies have focused on observational aspects, retrospective reviews, and surveys of memories prone to various biases. Rarely was the design of these clinical studies prospective. A few prospective studies reported an association between stressful life events and increased MS relapses and increased number of brain lesions.^27,31,32 Rare clinical trials have attempted to test stress reduction strategies and reported on the modest improvement of patient-reported outcomes and, in one study, a modest improvement in new MRI lesions.^33-35

Overall, several lines of evidence support a potential association between acute emotional stress and MS. Yet, the association is challenging to study, and future research might focus on stress-mitigation strategies and improving coping mechanisms in persons living with MS. It is important to note that it will be very difficult to design prospective studies to examine the potential association between acute emotional trauma and the development of de novo MS. Such studies will require a large number of participants (e.g., hundreds of thousands), long durations of follow-up (e.g., decades), and ways to classify repeated stressful events. An alternative approach is to ask persons newly diagnosed with MS at the time of initial diagnosis about any temporal association between their first symptom and stressful life events. However, this approach would provide some information on any association between the two, but not on causality of the disease itself.

Conclusion

The potential association between acute emotional stress and MS dates to the times of early descriptions of MS. Yet, research has been very limited and challenging. To date, the potential association remains elusive. Lines of evidence, while with limitations, have provided possible biologic explanations for the relationship between MS symptom onset and acute emotional stress. Although avoiding acute emotional stress is nearly impossible, incorporating global stress-coping strategies in early childhood education and secondary education might theoretically have potential beneficial effects on the subsequent risk of MS development or symptom flare-up, depending on a variety of factors.

But for now, when patients and colleagues ask me, “Can acute emotional stress be a ‘trigger’ for MS symptomology?,” my answer will remain, “Potentially, until proven otherwise.”

Key clinical point: Although a few biomarkers can assist in distinguishing psoriatic arthritis (PsA) from psoriasis or osteoarthritis, a precise diagnostic biomarker that can distinguish PsA from osteoarthritis and most other chronic inflammatory diseases has not yet been identified.

Major finding: Serum cartilage oligometrix metalloproteinase levels were significantly increased in patients with PsA compared with control individuals without chronic inflammatory diseases (standardized mean difference [SMD] 2.305; P = .003) and patients with osteoarthritis (SMD 0.783; P = .046). Serum matrix metalloproteinase-3 levels were significantly higher in patients with PsA vs psoriasis (SMD 0.419; P = .006) but could not distinguish patients with PsA from control individuals.

Study details: Findings are from a meta-analysis of 124 studies including patients with PsA.

Disclosures: This study did not report the source of funding. The authors declared no conflicts of interest.

Source: Wirth T et al. Biomarkers in psoriatic arthritis: A meta-analysis and systematic review. Front Immunol. 2022;13:1054539 (Nov 30). Doi: 10.3389/fimmu.2022.1054539

Key clinical point: Although a few biomarkers can assist in distinguishing psoriatic arthritis (PsA) from psoriasis or osteoarthritis, a precise diagnostic biomarker that can distinguish PsA from osteoarthritis and most other chronic inflammatory diseases has not yet been identified.

Major finding: Serum cartilage oligometrix metalloproteinase levels were significantly increased in patients with PsA compared with control individuals without chronic inflammatory diseases (standardized mean difference [SMD] 2.305; P = .003) and patients with osteoarthritis (SMD 0.783; P = .046). Serum matrix metalloproteinase-3 levels were significantly higher in patients with PsA vs psoriasis (SMD 0.419; P = .006) but could not distinguish patients with PsA from control individuals.

Study details: Findings are from a meta-analysis of 124 studies including patients with PsA.

Disclosures: This study did not report the source of funding. The authors declared no conflicts of interest.

Source: Wirth T et al. Biomarkers in psoriatic arthritis: A meta-analysis and systematic review. Front Immunol. 2022;13:1054539 (Nov 30). Doi: 10.3389/fimmu.2022.1054539

Key clinical point: Although a few biomarkers can assist in distinguishing psoriatic arthritis (PsA) from psoriasis or osteoarthritis, a precise diagnostic biomarker that can distinguish PsA from osteoarthritis and most other chronic inflammatory diseases has not yet been identified.

Major finding: Serum cartilage oligometrix metalloproteinase levels were significantly increased in patients with PsA compared with control individuals without chronic inflammatory diseases (standardized mean difference [SMD] 2.305; P = .003) and patients with osteoarthritis (SMD 0.783; P = .046). Serum matrix metalloproteinase-3 levels were significantly higher in patients with PsA vs psoriasis (SMD 0.419; P = .006) but could not distinguish patients with PsA from control individuals.

Study details: Findings are from a meta-analysis of 124 studies including patients with PsA.

Disclosures: This study did not report the source of funding. The authors declared no conflicts of interest.

Source: Wirth T et al. Biomarkers in psoriatic arthritis: A meta-analysis and systematic review. Front Immunol. 2022;13:1054539 (Nov 30). Doi: 10.3389/fimmu.2022.1054539

Key clinical point: Axial psoriatic arthritis (PsA) can be categorized as a distinct subtype of PsA because it exhibits clinical and radiological symptoms that are different from those of ankylosing spondylitis (AS) with psoriasis.

Major finding: Compared with patients with AS and psoriasis, patients with human leukocyte antigen (HLA)-B27-negative axial PsA had lesser inflammatory pain (P = .002), anterior uveitis (P = .014), and structural damage (P < .001) along with a higher prevalence of nail disease (P = .009) and were more likely to present with psoriasis before spondyloarthritis onset (P = .020). However, patients with HLA-B27-positive axial PsA vs AS and psoriasis reported lesser structural damage as revealed by Bath Ankylosing Spondylitis Radiology Index scores (P < .001).

Study details: This cross-sectional study included 109 patients with axial PsA and 127 patients with AS and current presentation or a history of skin psoriasis from the REGISPONSER registry.

Disclosures: The REGISPONSER registry is funded by the Spanish Society for Rheumatology. The authors declared no conflicts of interest.

Source: Michelena X et al. Characterising the axial phenotype of psoriatic arthritis: a study comparing axial psoriatic arthritis and ankylosing spondylitis with psoriasis from the REGISPONSER registry. RMD Open. 2022;8:e002513 (Dec 5). Doi: 10.1136/rmdopen-2022-002513

Key clinical point: Axial psoriatic arthritis (PsA) can be categorized as a distinct subtype of PsA because it exhibits clinical and radiological symptoms that are different from those of ankylosing spondylitis (AS) with psoriasis.

Major finding: Compared with patients with AS and psoriasis, patients with human leukocyte antigen (HLA)-B27-negative axial PsA had lesser inflammatory pain (P = .002), anterior uveitis (P = .014), and structural damage (P < .001) along with a higher prevalence of nail disease (P = .009) and were more likely to present with psoriasis before spondyloarthritis onset (P = .020). However, patients with HLA-B27-positive axial PsA vs AS and psoriasis reported lesser structural damage as revealed by Bath Ankylosing Spondylitis Radiology Index scores (P < .001).

Study details: This cross-sectional study included 109 patients with axial PsA and 127 patients with AS and current presentation or a history of skin psoriasis from the REGISPONSER registry.

Disclosures: The REGISPONSER registry is funded by the Spanish Society for Rheumatology. The authors declared no conflicts of interest.

Source: Michelena X et al. Characterising the axial phenotype of psoriatic arthritis: a study comparing axial psoriatic arthritis and ankylosing spondylitis with psoriasis from the REGISPONSER registry. RMD Open. 2022;8:e002513 (Dec 5). Doi: 10.1136/rmdopen-2022-002513

Key clinical point: Axial psoriatic arthritis (PsA) can be categorized as a distinct subtype of PsA because it exhibits clinical and radiological symptoms that are different from those of ankylosing spondylitis (AS) with psoriasis.

Major finding: Compared with patients with AS and psoriasis, patients with human leukocyte antigen (HLA)-B27-negative axial PsA had lesser inflammatory pain (P = .002), anterior uveitis (P = .014), and structural damage (P < .001) along with a higher prevalence of nail disease (P = .009) and were more likely to present with psoriasis before spondyloarthritis onset (P = .020). However, patients with HLA-B27-positive axial PsA vs AS and psoriasis reported lesser structural damage as revealed by Bath Ankylosing Spondylitis Radiology Index scores (P < .001).

Study details: This cross-sectional study included 109 patients with axial PsA and 127 patients with AS and current presentation or a history of skin psoriasis from the REGISPONSER registry.

Disclosures: The REGISPONSER registry is funded by the Spanish Society for Rheumatology. The authors declared no conflicts of interest.

Source: Michelena X et al. Characterising the axial phenotype of psoriatic arthritis: a study comparing axial psoriatic arthritis and ankylosing spondylitis with psoriasis from the REGISPONSER registry. RMD Open. 2022;8:e002513 (Dec 5). Doi: 10.1136/rmdopen-2022-002513

Key clinical point: Smoking and alcohol consumption were associated with a lower prevalence of arthritis and peripheral manifestations in patients with psoriatic arthritis (PsA).

Major finding: Smoking was associated with a lower prevalence of arthritis ever (odds ratio [OR] 0.63; 95% CI 0.41-0.95), and current alcohol consumption was associated with a lower prevalence of current arthritis or enthesitis (OR 0.61; 95% CI 0.47-0.79), current arthritis alone (OR 0.69; 95% CI 0.53-0.90), and current enthesitis alone (OR 0.49; 95% CI, 0.34-0.71).

Study details: Findings are from a multinational, cross-sectional study including patients with axial spondyloarthritis (n = 2717), peripheral spondyloarthritis (n = 432), and PsA (n = 1032).

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

Source: Ladehesa-Pineda ML et al. Smoking and alcohol consumption are associated with peripheral musculoskeletal involvement in patients with spondyloarthritis (including psoriatic arthritis). Results from the ASAS-PerSpA study. Semin Arthritis Rheum. 2022;58:152146 (Nov 30). Doi: 10.1016/j.semarthrit.2022.152146

Key clinical point: Smoking and alcohol consumption were associated with a lower prevalence of arthritis and peripheral manifestations in patients with psoriatic arthritis (PsA).

Major finding: Smoking was associated with a lower prevalence of arthritis ever (odds ratio [OR] 0.63; 95% CI 0.41-0.95), and current alcohol consumption was associated with a lower prevalence of current arthritis or enthesitis (OR 0.61; 95% CI 0.47-0.79), current arthritis alone (OR 0.69; 95% CI 0.53-0.90), and current enthesitis alone (OR 0.49; 95% CI, 0.34-0.71).

Study details: Findings are from a multinational, cross-sectional study including patients with axial spondyloarthritis (n = 2717), peripheral spondyloarthritis (n = 432), and PsA (n = 1032).

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

Source: Ladehesa-Pineda ML et al. Smoking and alcohol consumption are associated with peripheral musculoskeletal involvement in patients with spondyloarthritis (including psoriatic arthritis). Results from the ASAS-PerSpA study. Semin Arthritis Rheum. 2022;58:152146 (Nov 30). Doi: 10.1016/j.semarthrit.2022.152146

Key clinical point: Smoking and alcohol consumption were associated with a lower prevalence of arthritis and peripheral manifestations in patients with psoriatic arthritis (PsA).

Major finding: Smoking was associated with a lower prevalence of arthritis ever (odds ratio [OR] 0.63; 95% CI 0.41-0.95), and current alcohol consumption was associated with a lower prevalence of current arthritis or enthesitis (OR 0.61; 95% CI 0.47-0.79), current arthritis alone (OR 0.69; 95% CI 0.53-0.90), and current enthesitis alone (OR 0.49; 95% CI, 0.34-0.71).

Study details: Findings are from a multinational, cross-sectional study including patients with axial spondyloarthritis (n = 2717), peripheral spondyloarthritis (n = 432), and PsA (n = 1032).

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

Source: Ladehesa-Pineda ML et al. Smoking and alcohol consumption are associated with peripheral musculoskeletal involvement in patients with spondyloarthritis (including psoriatic arthritis). Results from the ASAS-PerSpA study. Semin Arthritis Rheum. 2022;58:152146 (Nov 30). Doi: 10.1016/j.semarthrit.2022.152146

Key clinical point: Cognitive abilities were altered in patients with psoriatic arthritis (PsA) compared with non-rheumatology reference individuals, with significant impairment in selective attention.

Major finding: Patients with PsA reported significant deficits in selective attention (mean difference [MD] −4.5), no effect on working memory (P = .662) and improvement in episodic short-term memory (MD 3.0; both P < .001) compared with matched reference subjects.

Study details: Findings are from a cross-sectional, exploratory study including 101 patients with axial spondyloarthritis, 117 patients with PsA, and matched non-rheumatology reference subjects without any diseases relevant to cognitive performance.

Disclosures: This study was funded by the RHADAR GbR, Germany. Some authors, including the lead author, declared receiving grants, consulting fees, speaker’s fees, travel support, honoraria, or advisory board support from several sources.

Source: Kleinert S et al. Impairment in cognitive function in patients with axial spondyloarthritis and psoriatic arthritis. Rheumatol Int. 2022 (Nov 28). Doi: 10.1007/s00296-022-05248-4

Key clinical point: Cognitive abilities were altered in patients with psoriatic arthritis (PsA) compared with non-rheumatology reference individuals, with significant impairment in selective attention.

Major finding: Patients with PsA reported significant deficits in selective attention (mean difference [MD] −4.5), no effect on working memory (P = .662) and improvement in episodic short-term memory (MD 3.0; both P < .001) compared with matched reference subjects.

Study details: Findings are from a cross-sectional, exploratory study including 101 patients with axial spondyloarthritis, 117 patients with PsA, and matched non-rheumatology reference subjects without any diseases relevant to cognitive performance.

Disclosures: This study was funded by the RHADAR GbR, Germany. Some authors, including the lead author, declared receiving grants, consulting fees, speaker’s fees, travel support, honoraria, or advisory board support from several sources.

Source: Kleinert S et al. Impairment in cognitive function in patients with axial spondyloarthritis and psoriatic arthritis. Rheumatol Int. 2022 (Nov 28). Doi: 10.1007/s00296-022-05248-4

Key clinical point: Cognitive abilities were altered in patients with psoriatic arthritis (PsA) compared with non-rheumatology reference individuals, with significant impairment in selective attention.

Major finding: Patients with PsA reported significant deficits in selective attention (mean difference [MD] −4.5), no effect on working memory (P = .662) and improvement in episodic short-term memory (MD 3.0; both P < .001) compared with matched reference subjects.

Study details: Findings are from a cross-sectional, exploratory study including 101 patients with axial spondyloarthritis, 117 patients with PsA, and matched non-rheumatology reference subjects without any diseases relevant to cognitive performance.

Disclosures: This study was funded by the RHADAR GbR, Germany. Some authors, including the lead author, declared receiving grants, consulting fees, speaker’s fees, travel support, honoraria, or advisory board support from several sources.

Source: Kleinert S et al. Impairment in cognitive function in patients with axial spondyloarthritis and psoriatic arthritis. Rheumatol Int. 2022 (Nov 28). Doi: 10.1007/s00296-022-05248-4

Key clinical point: Increasing disease activity and joint damage were significant risk factors for requiring musculoskeletal (MSK) surgery in patients with psoriatic arthritis (PsA).

Major finding: A greater number of damaged joints (hazard ratio [HR] 1.032; P < .001), presence of nail lesions (HR 2.079; P < .006), higher health assessment questionnaire scores (HR 2.012; P < .001), an elevated erythrocyte sedimentation rate (HR 2.365; P = .017), a greater number of actively inflamed joints (HR 1.037; P = .007), and human leukocyte antigen-B*27 positivity (HR 2.217; P = .048) were associated with an increased risk for surgery.

Study details: Findings are from a longitudinal, observational cohort study including 1574 patients with PsA, of which 11.8% underwent ≥1 MSK surgery attributable to PsA.

Disclosures: This study was supported by the Krembil Foundation, Toronto. The authors declared no conflicts of interest.

Source: Kwok TSH et al. Musculoskeletal surgery in psoriatic arthritis: Prevalence and risk factors. J Rheumatol. 2022 (Nov 15). Doi: 10.3899/jrheum.220908

Key clinical point: Increasing disease activity and joint damage were significant risk factors for requiring musculoskeletal (MSK) surgery in patients with psoriatic arthritis (PsA).

Major finding: A greater number of damaged joints (hazard ratio [HR] 1.032; P < .001), presence of nail lesions (HR 2.079; P < .006), higher health assessment questionnaire scores (HR 2.012; P < .001), an elevated erythrocyte sedimentation rate (HR 2.365; P = .017), a greater number of actively inflamed joints (HR 1.037; P = .007), and human leukocyte antigen-B*27 positivity (HR 2.217; P = .048) were associated with an increased risk for surgery.

Study details: Findings are from a longitudinal, observational cohort study including 1574 patients with PsA, of which 11.8% underwent ≥1 MSK surgery attributable to PsA.

Disclosures: This study was supported by the Krembil Foundation, Toronto. The authors declared no conflicts of interest.

Source: Kwok TSH et al. Musculoskeletal surgery in psoriatic arthritis: Prevalence and risk factors. J Rheumatol. 2022 (Nov 15). Doi: 10.3899/jrheum.220908

Key clinical point: Increasing disease activity and joint damage were significant risk factors for requiring musculoskeletal (MSK) surgery in patients with psoriatic arthritis (PsA).

Major finding: A greater number of damaged joints (hazard ratio [HR] 1.032; P < .001), presence of nail lesions (HR 2.079; P < .006), higher health assessment questionnaire scores (HR 2.012; P < .001), an elevated erythrocyte sedimentation rate (HR 2.365; P = .017), a greater number of actively inflamed joints (HR 1.037; P = .007), and human leukocyte antigen-B*27 positivity (HR 2.217; P = .048) were associated with an increased risk for surgery.

Study details: Findings are from a longitudinal, observational cohort study including 1574 patients with PsA, of which 11.8% underwent ≥1 MSK surgery attributable to PsA.

Disclosures: This study was supported by the Krembil Foundation, Toronto. The authors declared no conflicts of interest.

Source: Kwok TSH et al. Musculoskeletal surgery in psoriatic arthritis: Prevalence and risk factors. J Rheumatol. 2022 (Nov 15). Doi: 10.3899/jrheum.220908

Key clinical point: Psoriatic arthritis (PsA) was positively associated with Crohn’s disease and genetically predicted Crohn’s disease was associated with an increased risk for PsA, indicating a bidirectional causal relationship between the 2 diseases.

Major finding: PsA was associated with a 31.9% increased risk for Crohn’s disease (odds ratio [OR] 1.319; P < .001) and genetically predicted Crohn’s disease was linked to a 44.8% higher risk for PsA (OR 1.448; P = .001).

Study details: Findings are from a bidirectional 2-sample mendelian randomization study including 4510 patients with psoriasis, 1637 patients with PsA, and 212,242 control individuals along with 657 patients with Crohn’s disease, 2251 patients with ulcerative colitis, and 210,300 control individuals.

Disclosures: This study did not report the source of funding. The authors declared no conflicts of interest.

Source: Sun Y et al. The causal relationship between psoriasis, psoriatic arthritis, and inflammatory bowel diseases. Sci Rep. 2022;12:20526 (Nov 28). Doi: 10.1038/s41598-022-24872-5

Key clinical point: Psoriatic arthritis (PsA) was positively associated with Crohn’s disease and genetically predicted Crohn’s disease was associated with an increased risk for PsA, indicating a bidirectional causal relationship between the 2 diseases.

Major finding: PsA was associated with a 31.9% increased risk for Crohn’s disease (odds ratio [OR] 1.319; P < .001) and genetically predicted Crohn’s disease was linked to a 44.8% higher risk for PsA (OR 1.448; P = .001).

Study details: Findings are from a bidirectional 2-sample mendelian randomization study including 4510 patients with psoriasis, 1637 patients with PsA, and 212,242 control individuals along with 657 patients with Crohn’s disease, 2251 patients with ulcerative colitis, and 210,300 control individuals.

Disclosures: This study did not report the source of funding. The authors declared no conflicts of interest.

Source: Sun Y et al. The causal relationship between psoriasis, psoriatic arthritis, and inflammatory bowel diseases. Sci Rep. 2022;12:20526 (Nov 28). Doi: 10.1038/s41598-022-24872-5

Key clinical point: Psoriatic arthritis (PsA) was positively associated with Crohn’s disease and genetically predicted Crohn’s disease was associated with an increased risk for PsA, indicating a bidirectional causal relationship between the 2 diseases.

Major finding: PsA was associated with a 31.9% increased risk for Crohn’s disease (odds ratio [OR] 1.319; P < .001) and genetically predicted Crohn’s disease was linked to a 44.8% higher risk for PsA (OR 1.448; P = .001).

Study details: Findings are from a bidirectional 2-sample mendelian randomization study including 4510 patients with psoriasis, 1637 patients with PsA, and 212,242 control individuals along with 657 patients with Crohn’s disease, 2251 patients with ulcerative colitis, and 210,300 control individuals.

Disclosures: This study did not report the source of funding. The authors declared no conflicts of interest.

Source: Sun Y et al. The causal relationship between psoriasis, psoriatic arthritis, and inflammatory bowel diseases. Sci Rep. 2022;12:20526 (Nov 28). Doi: 10.1038/s41598-022-24872-5

Key clinical point: Nailfold capillary abnormalities were more prevalent in patients with psoriatic arthritis (PsA) than in patients with psoriasis vulgaris (PsV) and predicted the development of PsA in patients with psoriasis.

Major finding: Nailfold bleeding (NFB; 84.5% vs 34.7%) and enlarged capillaries (100.0% vs 25.4%; both P < .0001) were more prevalent in patients with PsA vs PsV, with both NFB (hazard ratio [HR] 2.75; P = .004) and enlarged capillaries (HR 4.49; P < .0001) predicting the development of PsA in patients with PsV.

Study details: Findings are from a prospective cohort study including 236 patients with PsV and 213 patients with PsA.

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

Source: Fukasawa T et al. Utility of nailfold capillary assessment for predicting psoriatic arthritis based on a prospective observational cohort study. Rheumatology (Oxford). 2022 (Nov 28). Doi: 10.1093/rheumatology/keac664

Key clinical point: Nailfold capillary abnormalities were more prevalent in patients with psoriatic arthritis (PsA) than in patients with psoriasis vulgaris (PsV) and predicted the development of PsA in patients with psoriasis.

Major finding: Nailfold bleeding (NFB; 84.5% vs 34.7%) and enlarged capillaries (100.0% vs 25.4%; both P < .0001) were more prevalent in patients with PsA vs PsV, with both NFB (hazard ratio [HR] 2.75; P = .004) and enlarged capillaries (HR 4.49; P < .0001) predicting the development of PsA in patients with PsV.

Study details: Findings are from a prospective cohort study including 236 patients with PsV and 213 patients with PsA.

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

Source: Fukasawa T et al. Utility of nailfold capillary assessment for predicting psoriatic arthritis based on a prospective observational cohort study. Rheumatology (Oxford). 2022 (Nov 28). Doi: 10.1093/rheumatology/keac664

Key clinical point: Nailfold capillary abnormalities were more prevalent in patients with psoriatic arthritis (PsA) than in patients with psoriasis vulgaris (PsV) and predicted the development of PsA in patients with psoriasis.

Major finding: Nailfold bleeding (NFB; 84.5% vs 34.7%) and enlarged capillaries (100.0% vs 25.4%; both P < .0001) were more prevalent in patients with PsA vs PsV, with both NFB (hazard ratio [HR] 2.75; P = .004) and enlarged capillaries (HR 4.49; P < .0001) predicting the development of PsA in patients with PsV.

Study details: Findings are from a prospective cohort study including 236 patients with PsV and 213 patients with PsA.

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

Source: Fukasawa T et al. Utility of nailfold capillary assessment for predicting psoriatic arthritis based on a prospective observational cohort study. Rheumatology (Oxford). 2022 (Nov 28). Doi: 10.1093/rheumatology/keac664

Key clinical point: Bimekizumab improved the signs and symptoms of psoriatic arthritis (PsA) in patients with previous inadequate response to or intolerance of tumor necrosis factor-alpha (TNFα) inhibitors without causing any unprecedented adverse events (AE).

Major finding: At week 16, a significantly higher proportion of patients receiving bimekizumab vs placebo achieved ≥50% improvement in American College of Rheumatology response (43% vs 7%; odds ratio 11.1; P < .0001), with treatment-emergent AE being reported by 40% of patients receiving bimekizumab and 33% of patients receiving placebo.

Study details: Findings are from the multicenter, phase 3 BE COMPLETE study including 400 patients with active PsA and previous inadequate response to or intolerance of TNFα inhibitors who were randomly assigned to receive 160 mg subcutaneous bimekizumab every 4 weeks or placebo.

Disclosures: This study was funded by UCB Pharma. Five authors declared being employees and shareholders of UCB Pharma, and the other authors reported ties with several sources, including UCB Pharma.

Source: Merola JF et al. Bimekizumab in patients with active psoriatic arthritis and previous inadequate response or intolerance to tumour necrosis factor-α inhibitors: A randomised, double-blind, placebo-controlled, phase 3 trial (BE COMPLETE). Lancet. 2022 (Dec 6). Doi: 10.1016/S0140-6736(22)02303-0

Key clinical point: Bimekizumab improved the signs and symptoms of psoriatic arthritis (PsA) in patients with previous inadequate response to or intolerance of tumor necrosis factor-alpha (TNFα) inhibitors without causing any unprecedented adverse events (AE).

Major finding: At week 16, a significantly higher proportion of patients receiving bimekizumab vs placebo achieved ≥50% improvement in American College of Rheumatology response (43% vs 7%; odds ratio 11.1; P < .0001), with treatment-emergent AE being reported by 40% of patients receiving bimekizumab and 33% of patients receiving placebo.

Study details: Findings are from the multicenter, phase 3 BE COMPLETE study including 400 patients with active PsA and previous inadequate response to or intolerance of TNFα inhibitors who were randomly assigned to receive 160 mg subcutaneous bimekizumab every 4 weeks or placebo.

Disclosures: This study was funded by UCB Pharma. Five authors declared being employees and shareholders of UCB Pharma, and the other authors reported ties with several sources, including UCB Pharma.

Source: Merola JF et al. Bimekizumab in patients with active psoriatic arthritis and previous inadequate response or intolerance to tumour necrosis factor-α inhibitors: A randomised, double-blind, placebo-controlled, phase 3 trial (BE COMPLETE). Lancet. 2022 (Dec 6). Doi: 10.1016/S0140-6736(22)02303-0

Key clinical point: Bimekizumab improved the signs and symptoms of psoriatic arthritis (PsA) in patients with previous inadequate response to or intolerance of tumor necrosis factor-alpha (TNFα) inhibitors without causing any unprecedented adverse events (AE).

Major finding: At week 16, a significantly higher proportion of patients receiving bimekizumab vs placebo achieved ≥50% improvement in American College of Rheumatology response (43% vs 7%; odds ratio 11.1; P < .0001), with treatment-emergent AE being reported by 40% of patients receiving bimekizumab and 33% of patients receiving placebo.

Study details: Findings are from the multicenter, phase 3 BE COMPLETE study including 400 patients with active PsA and previous inadequate response to or intolerance of TNFα inhibitors who were randomly assigned to receive 160 mg subcutaneous bimekizumab every 4 weeks or placebo.

Disclosures: This study was funded by UCB Pharma. Five authors declared being employees and shareholders of UCB Pharma, and the other authors reported ties with several sources, including UCB Pharma.

Source: Merola JF et al. Bimekizumab in patients with active psoriatic arthritis and previous inadequate response or intolerance to tumour necrosis factor-α inhibitors: A randomised, double-blind, placebo-controlled, phase 3 trial (BE COMPLETE). Lancet. 2022 (Dec 6). Doi: 10.1016/S0140-6736(22)02303-0

Key clinical point: A booster dose of BNT162b2 messenger ribonucleic acid (mRNA) SARS-CoV-2 vaccine (BioNTech-Pfizer) restored the anti-SARS-CoV-2 immunoglobulin G (IgG) levels in patients with psoriatic arthritis (PsA) who were receiving tumor necrosis factor (TNF) inhibitors.

Major finding: Although the mean anti-SARS-CoV-2 IgG levels were significantly lower in patients with PsA vs matched control individuals (2009.22 vs 6206.59 AU/mL; P = .0006) 4 months after two doses of vaccination, the mean IgG levels were similar between both groups after the booster dose (P = .20).

Study details: Findings are from a prospective study including 40 patients with PsA on TNF inhibitors and 40 matched control individuals who received two shots of the BNT162b2 mRNA vaccine.

Disclosures: This study did not report the source of funding. The authors declared no conflicts of interest.

Source: Venerito V et al. Anti-SARS-CoV-2 antibody decay after vaccination and immunogenicity of the booster dose of the BNT162b2 mRNA vaccine in patients with psoriatic arthritis on TNF inhibitors. Clin Exp Rheumatol. 2022 (Nov 24). Doi: 10.55563/clinexprheumatol/hptln9

Key clinical point: A booster dose of BNT162b2 messenger ribonucleic acid (mRNA) SARS-CoV-2 vaccine (BioNTech-Pfizer) restored the anti-SARS-CoV-2 immunoglobulin G (IgG) levels in patients with psoriatic arthritis (PsA) who were receiving tumor necrosis factor (TNF) inhibitors.

Major finding: Although the mean anti-SARS-CoV-2 IgG levels were significantly lower in patients with PsA vs matched control individuals (2009.22 vs 6206.59 AU/mL; P = .0006) 4 months after two doses of vaccination, the mean IgG levels were similar between both groups after the booster dose (P = .20).

Study details: Findings are from a prospective study including 40 patients with PsA on TNF inhibitors and 40 matched control individuals who received two shots of the BNT162b2 mRNA vaccine.

Disclosures: This study did not report the source of funding. The authors declared no conflicts of interest.

Source: Venerito V et al. Anti-SARS-CoV-2 antibody decay after vaccination and immunogenicity of the booster dose of the BNT162b2 mRNA vaccine in patients with psoriatic arthritis on TNF inhibitors. Clin Exp Rheumatol. 2022 (Nov 24). Doi: 10.55563/clinexprheumatol/hptln9

Key clinical point: A booster dose of BNT162b2 messenger ribonucleic acid (mRNA) SARS-CoV-2 vaccine (BioNTech-Pfizer) restored the anti-SARS-CoV-2 immunoglobulin G (IgG) levels in patients with psoriatic arthritis (PsA) who were receiving tumor necrosis factor (TNF) inhibitors.

Major finding: Although the mean anti-SARS-CoV-2 IgG levels were significantly lower in patients with PsA vs matched control individuals (2009.22 vs 6206.59 AU/mL; P = .0006) 4 months after two doses of vaccination, the mean IgG levels were similar between both groups after the booster dose (P = .20).

Study details: Findings are from a prospective study including 40 patients with PsA on TNF inhibitors and 40 matched control individuals who received two shots of the BNT162b2 mRNA vaccine.

Disclosures: This study did not report the source of funding. The authors declared no conflicts of interest.

Source: Venerito V et al. Anti-SARS-CoV-2 antibody decay after vaccination and immunogenicity of the booster dose of the BNT162b2 mRNA vaccine in patients with psoriatic arthritis on TNF inhibitors. Clin Exp Rheumatol. 2022 (Nov 24). Doi: 10.55563/clinexprheumatol/hptln9