Rheumatology News

This transcript has been edited for clarity. 

Matthew F. Watto, MD: Welcome back to The Curbsiders. I’m Dr Matthew Frank Watto, here with my great friend and America’s primary care physician, Dr Paul Nelson Williams. Paul, how are you feeling about sports injuries? 

Paul N. Williams, MD: I’m feeling great, Matt.

Watto: You had a sports injury of the hip. Maybe that’s an overshare, Paul, but we talked about it on a podcast with Dr Carlin Senter (part 1 and part 2).

Williams: I think I’ve shared more than my hip injury, for sure. 

Watto: Whenever a patient presented with hip pain, I used to pray it was trochanteric bursitis, which now I know is not really the right thing to think about. Intra-articular hip pain presents as anterior hip pain, usually in the crease of the hip. Depending on the patient’s age and history, the differential for that type of pain includes iliopsoas tendonitis, FAI syndrome, a labral tear, a bone stress injury of the femoral neck, or osteoarthritis. 

So, what exactly is FAI and how might we diagnose it? 

Williams: FAI is what the cool kids call femoral acetabular impingement, and it’s exactly what it sounds like.

 

Something is pinching or impinging upon the joint itself and preventing full range of motion. This is a ball-and-socket joint, so it should have tremendous range of motion, able to move in all planes. If it’s impinged, then pain will occur with certain movements. There’s a cam type, which is characterized by enlargement of the femoral head neck junction, or a pincer type, which has more to do with overhang of the acetabulum, and it can also be mixed. In any case, impingement upon the patient’s full range of motion results in pain. 

You evaluate this with a couple of tests — the FABER and the FADIR. 

The FABER is flexion, abduction, and external rotation, and the FADIR is flexion, adduction, and internal rotation. If you elicit anterior pain with either of those tests, it’s probably one of the intra-articular pathologies, although it is hard to know for sure which one it is because these tests are fairly sensitive but not very specific. 

Watto: You can get x-rays to help with the diagnosis. You would order two views of the hip: an AP of the pelvis, which is just a straight-on shot to look for arthritis or fracture. Is there a healthy joint line there? The second is the Dunn view, in which the hip is flexed 90 degrees and abducted about 20 degrees. You are looking for fracture or impingement. You can diagnose FAI based on that view, and you might be able to diagnose a hip stress injury or osteoarthritis.

Unfortunately, you’re not going to see a labral tear, but Dr Senter said that both FAI and labral tears are treated the same way, with physical therapy. Patients with FAI who aren’t getting better might end up going for surgery, so at some point I would refer them to orthopedic surgery. But I feel much more comfortable now diagnosing these conditions with these tests.

Let’s talk a little bit about trochanteric pain syndrome. I used to think it was all bursitis. Why is that not correct? 

Williams: It’s nice of you to feign ignorance for the purpose of education. It used to be thought of as bursitis, but these days we know it is probably more likely a tendinopathy. 

 

Trochanteric pain syndrome was formerly known as trochanteric bursitis, but the bursa is not typically involved. Trochanteric pain syndrome is a tendinopathy of the surrounding structures: the gluteus medius, the iliotibial band, and the tensor fascia latae. The way these structures relate looks a bit like the face of a clock, as you can see on the infographic. In general, you manage this condition the same way you do with bursitis — physical therapy. You can also give corticosteroid injections. Physical therapy is probably more durable in terms of pain relief and functionality, but in the short term, corticosteroids might provide some degree of analgesia as well. 

Watto: The last thing we wanted to mention is bone stress injury, which can occur in high-mileage runners (20 miles or more per week). Patients with bone stress injury need to rest, usually non‒weight bearing, for a period of time. 

 

Treatment of a bone stress fracture depends on which side it’s on (top or bottom). If it’s on the top of the femoral neck (the tension side), it has to be fixed. If it’s on the compression side (the bottom side of the femoral neck), it might be able to be managed conservatively, but many patients are going to need surgery. This is a big deal. But it’s a spectrum; in some cases the bone is merely irritated and unhappy, without a break in the cortex. Those patients might not need surgery. 

In patients with a fracture of the femoral neck — especially younger, healthier patients — you should think about getting a bone density test and screening for relative energy deficiency in sport. This used to be called the female athlete triad, which includes disrupted menstrual cycles, being underweight, and fracture. We should be screening patients, asking them in a nonjudgmental way about their relationship with food, to make sure they are getting an appropriate number of calories.

They are actually in an energy deficit. They’re not eating enough to maintain a healthy body with so much activity. 

Williams: If you’re interested in this topic, you should refer to the full podcast with Dr Senter which is chock-full of helpful information.

Dr Watto, Clinical Assistant Professor, Department of Medicine, Perelman School of Medicine at University of Pennsylvania; Internist, Department of Medicine, Hospital Medicine Section, Pennsylvania Hospital, Philadelphia, Pennsylvania, has disclosed no relevant financial relationships. Dr Williams, Associate Professor of Clinical Medicine, Department of General Internal Medicine, Lewis Katz School of Medicine; Staff Physician, Department of General Internal Medicine, Temple Internal Medicine Associates, Philadelphia, Pennsylvania, disclosed ties with The Curbsiders.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity. 

Matthew F. Watto, MD: Welcome back to The Curbsiders. I’m Dr Matthew Frank Watto, here with my great friend and America’s primary care physician, Dr Paul Nelson Williams. Paul, how are you feeling about sports injuries? 

Paul N. Williams, MD: I’m feeling great, Matt.

Watto: You had a sports injury of the hip. Maybe that’s an overshare, Paul, but we talked about it on a podcast with Dr Carlin Senter (part 1 and part 2).

Williams: I think I’ve shared more than my hip injury, for sure. 

Watto: Whenever a patient presented with hip pain, I used to pray it was trochanteric bursitis, which now I know is not really the right thing to think about. Intra-articular hip pain presents as anterior hip pain, usually in the crease of the hip. Depending on the patient’s age and history, the differential for that type of pain includes iliopsoas tendonitis, FAI syndrome, a labral tear, a bone stress injury of the femoral neck, or osteoarthritis. 

So, what exactly is FAI and how might we diagnose it? 

Williams: FAI is what the cool kids call femoral acetabular impingement, and it’s exactly what it sounds like.

 

Something is pinching or impinging upon the joint itself and preventing full range of motion. This is a ball-and-socket joint, so it should have tremendous range of motion, able to move in all planes. If it’s impinged, then pain will occur with certain movements. There’s a cam type, which is characterized by enlargement of the femoral head neck junction, or a pincer type, which has more to do with overhang of the acetabulum, and it can also be mixed. In any case, impingement upon the patient’s full range of motion results in pain. 

You evaluate this with a couple of tests — the FABER and the FADIR. 

The FABER is flexion, abduction, and external rotation, and the FADIR is flexion, adduction, and internal rotation. If you elicit anterior pain with either of those tests, it’s probably one of the intra-articular pathologies, although it is hard to know for sure which one it is because these tests are fairly sensitive but not very specific. 

Watto: You can get x-rays to help with the diagnosis. You would order two views of the hip: an AP of the pelvis, which is just a straight-on shot to look for arthritis or fracture. Is there a healthy joint line there? The second is the Dunn view, in which the hip is flexed 90 degrees and abducted about 20 degrees. You are looking for fracture or impingement. You can diagnose FAI based on that view, and you might be able to diagnose a hip stress injury or osteoarthritis.

Unfortunately, you’re not going to see a labral tear, but Dr Senter said that both FAI and labral tears are treated the same way, with physical therapy. Patients with FAI who aren’t getting better might end up going for surgery, so at some point I would refer them to orthopedic surgery. But I feel much more comfortable now diagnosing these conditions with these tests.

Let’s talk a little bit about trochanteric pain syndrome. I used to think it was all bursitis. Why is that not correct? 

Williams: It’s nice of you to feign ignorance for the purpose of education. It used to be thought of as bursitis, but these days we know it is probably more likely a tendinopathy. 

 

Trochanteric pain syndrome was formerly known as trochanteric bursitis, but the bursa is not typically involved. Trochanteric pain syndrome is a tendinopathy of the surrounding structures: the gluteus medius, the iliotibial band, and the tensor fascia latae. The way these structures relate looks a bit like the face of a clock, as you can see on the infographic. In general, you manage this condition the same way you do with bursitis — physical therapy. You can also give corticosteroid injections. Physical therapy is probably more durable in terms of pain relief and functionality, but in the short term, corticosteroids might provide some degree of analgesia as well. 

Watto: The last thing we wanted to mention is bone stress injury, which can occur in high-mileage runners (20 miles or more per week). Patients with bone stress injury need to rest, usually non‒weight bearing, for a period of time. 

 

Treatment of a bone stress fracture depends on which side it’s on (top or bottom). If it’s on the top of the femoral neck (the tension side), it has to be fixed. If it’s on the compression side (the bottom side of the femoral neck), it might be able to be managed conservatively, but many patients are going to need surgery. This is a big deal. But it’s a spectrum; in some cases the bone is merely irritated and unhappy, without a break in the cortex. Those patients might not need surgery. 

In patients with a fracture of the femoral neck — especially younger, healthier patients — you should think about getting a bone density test and screening for relative energy deficiency in sport. This used to be called the female athlete triad, which includes disrupted menstrual cycles, being underweight, and fracture. We should be screening patients, asking them in a nonjudgmental way about their relationship with food, to make sure they are getting an appropriate number of calories.

They are actually in an energy deficit. They’re not eating enough to maintain a healthy body with so much activity. 

Williams: If you’re interested in this topic, you should refer to the full podcast with Dr Senter which is chock-full of helpful information.

Dr Watto, Clinical Assistant Professor, Department of Medicine, Perelman School of Medicine at University of Pennsylvania; Internist, Department of Medicine, Hospital Medicine Section, Pennsylvania Hospital, Philadelphia, Pennsylvania, has disclosed no relevant financial relationships. Dr Williams, Associate Professor of Clinical Medicine, Department of General Internal Medicine, Lewis Katz School of Medicine; Staff Physician, Department of General Internal Medicine, Temple Internal Medicine Associates, Philadelphia, Pennsylvania, disclosed ties with The Curbsiders.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity. 

Matthew F. Watto, MD: Welcome back to The Curbsiders. I’m Dr Matthew Frank Watto, here with my great friend and America’s primary care physician, Dr Paul Nelson Williams. Paul, how are you feeling about sports injuries? 

Paul N. Williams, MD: I’m feeling great, Matt.

Watto: You had a sports injury of the hip. Maybe that’s an overshare, Paul, but we talked about it on a podcast with Dr Carlin Senter (part 1 and part 2).

Williams: I think I’ve shared more than my hip injury, for sure. 

Watto: Whenever a patient presented with hip pain, I used to pray it was trochanteric bursitis, which now I know is not really the right thing to think about. Intra-articular hip pain presents as anterior hip pain, usually in the crease of the hip. Depending on the patient’s age and history, the differential for that type of pain includes iliopsoas tendonitis, FAI syndrome, a labral tear, a bone stress injury of the femoral neck, or osteoarthritis. 

So, what exactly is FAI and how might we diagnose it? 

Williams: FAI is what the cool kids call femoral acetabular impingement, and it’s exactly what it sounds like.

 

Something is pinching or impinging upon the joint itself and preventing full range of motion. This is a ball-and-socket joint, so it should have tremendous range of motion, able to move in all planes. If it’s impinged, then pain will occur with certain movements. There’s a cam type, which is characterized by enlargement of the femoral head neck junction, or a pincer type, which has more to do with overhang of the acetabulum, and it can also be mixed. In any case, impingement upon the patient’s full range of motion results in pain. 

You evaluate this with a couple of tests — the FABER and the FADIR. 

The FABER is flexion, abduction, and external rotation, and the FADIR is flexion, adduction, and internal rotation. If you elicit anterior pain with either of those tests, it’s probably one of the intra-articular pathologies, although it is hard to know for sure which one it is because these tests are fairly sensitive but not very specific. 

Watto: You can get x-rays to help with the diagnosis. You would order two views of the hip: an AP of the pelvis, which is just a straight-on shot to look for arthritis or fracture. Is there a healthy joint line there? The second is the Dunn view, in which the hip is flexed 90 degrees and abducted about 20 degrees. You are looking for fracture or impingement. You can diagnose FAI based on that view, and you might be able to diagnose a hip stress injury or osteoarthritis.

Unfortunately, you’re not going to see a labral tear, but Dr Senter said that both FAI and labral tears are treated the same way, with physical therapy. Patients with FAI who aren’t getting better might end up going for surgery, so at some point I would refer them to orthopedic surgery. But I feel much more comfortable now diagnosing these conditions with these tests.

Let’s talk a little bit about trochanteric pain syndrome. I used to think it was all bursitis. Why is that not correct? 

Williams: It’s nice of you to feign ignorance for the purpose of education. It used to be thought of as bursitis, but these days we know it is probably more likely a tendinopathy. 

 

Trochanteric pain syndrome was formerly known as trochanteric bursitis, but the bursa is not typically involved. Trochanteric pain syndrome is a tendinopathy of the surrounding structures: the gluteus medius, the iliotibial band, and the tensor fascia latae. The way these structures relate looks a bit like the face of a clock, as you can see on the infographic. In general, you manage this condition the same way you do with bursitis — physical therapy. You can also give corticosteroid injections. Physical therapy is probably more durable in terms of pain relief and functionality, but in the short term, corticosteroids might provide some degree of analgesia as well. 

Watto: The last thing we wanted to mention is bone stress injury, which can occur in high-mileage runners (20 miles or more per week). Patients with bone stress injury need to rest, usually non‒weight bearing, for a period of time. 

 

Treatment of a bone stress fracture depends on which side it’s on (top or bottom). If it’s on the top of the femoral neck (the tension side), it has to be fixed. If it’s on the compression side (the bottom side of the femoral neck), it might be able to be managed conservatively, but many patients are going to need surgery. This is a big deal. But it’s a spectrum; in some cases the bone is merely irritated and unhappy, without a break in the cortex. Those patients might not need surgery. 

In patients with a fracture of the femoral neck — especially younger, healthier patients — you should think about getting a bone density test and screening for relative energy deficiency in sport. This used to be called the female athlete triad, which includes disrupted menstrual cycles, being underweight, and fracture. We should be screening patients, asking them in a nonjudgmental way about their relationship with food, to make sure they are getting an appropriate number of calories.

They are actually in an energy deficit. They’re not eating enough to maintain a healthy body with so much activity. 

Williams: If you’re interested in this topic, you should refer to the full podcast with Dr Senter which is chock-full of helpful information.

Dr Watto, Clinical Assistant Professor, Department of Medicine, Perelman School of Medicine at University of Pennsylvania; Internist, Department of Medicine, Hospital Medicine Section, Pennsylvania Hospital, Philadelphia, Pennsylvania, has disclosed no relevant financial relationships. Dr Williams, Associate Professor of Clinical Medicine, Department of General Internal Medicine, Lewis Katz School of Medicine; Staff Physician, Department of General Internal Medicine, Temple Internal Medicine Associates, Philadelphia, Pennsylvania, disclosed ties with The Curbsiders.

A version of this article appeared on Medscape.com.

NEW YORK — Over the past year, new evidence has emerged in support of the idea that psoriatic arthritis (PsA) is neither exclusively immune mediated nor a classic autoimmune disease, but that both mechanisms may be essential in disease pathogenesis, and that innate immune cells may possess adaptive properties that may lead to worsening of inflammation of the skin and joints.

Recent findings help dermatologists and rheumatologists to better understand the pathogenesis of PsA and may lead to more targeted and personalized therapies, Christopher Ritchlin, MD, MPH, who’s led research into the pathogenesis of inflammatory diseases, reported at the NYU Langone Advanced Seminar in Psoriasis and Psoriatic Arthritis.

Psoriasis and PsA, along with ankylosing spondylitis and Crohn’s disease, have been thought to be either immune mediated or a classic autoimmune disorder, Ritchlin, a rheumatologist and internist and director of the Clinical Immunology Research Unit at the University of Rochester in New York, said in an interview. “But emerging data reveal that these disorders might be triggered and sustained by both autoimmune and immune-mediated events,” he said.

 

Autoimmunity vs Immune Mediated

Autoimmune diseases are characterized by a specific autoantigen and antibody, such as the anti–cyclic citrullinated peptide antibody seen in rheumatoid arthritis, Ritchlin said. He cited a 2023 literature review from Italy that identified five autoantibodies and polymorphisms in PsA.

“In an immune-mediated disease, we demonstrate profound dysregulation of immune cells that promote inflammation, but we have not identified a specific autoantigen,” he said. “There’s an inflammatory response, which can be very severe, but we don’t know if it’s responding to an autoantigen or it’s just dysregulation of the T cells or the B cells or both.”

In a humanized mouse model developed by Maria Garcia-Hernandez, PhD, in Ritchlin’s lab, researchers found that both immunoglobulins and immune cells are required to recapitulate the skin and joint phenotypes. Ritchlin said that further analyses identified a putative autoantigen, which current experiments now underway are looking to confirm and should help discern distinctions in pathogenesis between a response to an autoantigen or cell dysregulation.

“There may be more than one type of immune inflammatory reaction that’s ongoing in individual tissue, and it may be different from one tissue to another,” Ritchlin said in an interview.

The immune-mediated and autoimmune properties of PsA are important to investigate, Jose U. Scher, MD, director of the Arthritis Clinic and Psoriatic Arthritis Center at NYU Langone Health in New York City, said in an interview.

“Classically considered an autoimmune disease, [PsA] may be better classified as an immune-mediated inflammatory disease,” Scher said. He noted one feature that makes PsA differ from classic autoimmunity is that it does not affect women predominantly.

“The fundamental question is whether there are elements of classic autoimmunity such as B cells that should be integrated into the research for future identification of novel therapeutics,” Scher said.

 

The ‘Additional Mechanism’

The additional mechanism Ritchlin referred to is “this idea of trained immunity,” he said, “where innate immune cells — fibroblasts, monocytes, keratinocytes — that are not considered to have [the] adaptive memory characteristic of T cells and B cells but act in an environment of inflammation and can actually develop sustained altered phenotypes in response to inflammation.”

A 2024 report from Europe outlined four characteristics of trained immunity, Ritchlin said, including that it is “antigen agnostic” and results from long-term reprogramming of cells through epigenetic and metabolic mechanisms. The effects of trained immunity are shorter in duration than that of classical adaptive immunity, he said.

These reprogrammed innate immune cells “retain a form of ‘memory’ after an initial stimulus, which can lead to enhanced or altered responses upon subsequent challenges,” Scher said.

In the context of PsA, Scher said, monocytes that express heightened inflammatory responses driven by metabolic and epigenetic reprogramming can become “trained” by triggers such as infections, cytokines (such as interleukin [IL]–1 beta and IL-17), or damage-associated molecular patterns that have been epigenetically modified to respond at higher rates in a future encounter with exacerbated production of proinflammatory cytokines, persistent inflammation, and flares.

Ritchlin explained how this emerging understanding of the mechanisms driving psoriasis and PsA is driving research into treatments.

“If you know that monocytes are undergoing change — these are innate cells, they’re not antigen driven — but that change is based on some type of pathway that makes the cell more inflammatory, then you can think about trying to block that pathway,” he said.

The goal would be to normalize the cellular environment that’s otherwise becoming activated to create the signs and symptoms of psoriasis and PsA, he said.

The other potential therapeutic target would be T cells, Ritchlin said. “There now are T cells that have been identified that have very specific alpha-beta receptors that are expanded in the peripheral blood, uveal fluid, and joints of HLAB27-positive patients with ankylosing spondylitis and anterior uveitis, which is thought to be immune mediated, not autoimmune.” 

Those HLAB27-positive patients “have expansion of a certain subtype of T cells, they have a specific receptor, and specific autoantigens have been identified pointing to a potential autoimmune response,” Ritchlin added.

An antibody that binds and removes specific T-cell receptor subsets may be an effective strategy without being immunosuppressive, Ritchlin said. “That’s real exciting, and we’re all hoping that is going to be a therapeutic approach that could be successful.”

Ritchlin disclosed financial relationships with AbbVie, Amgen, Bristol-Myers Squibb, Janssen, Novartis, Pfizer, and UCB. Scher had no relevant financial relationships.

A version of this article appeared on Medscape.com.

NEW YORK — Over the past year, new evidence has emerged in support of the idea that psoriatic arthritis (PsA) is neither exclusively immune mediated nor a classic autoimmune disease, but that both mechanisms may be essential in disease pathogenesis, and that innate immune cells may possess adaptive properties that may lead to worsening of inflammation of the skin and joints.

Recent findings help dermatologists and rheumatologists to better understand the pathogenesis of PsA and may lead to more targeted and personalized therapies, Christopher Ritchlin, MD, MPH, who’s led research into the pathogenesis of inflammatory diseases, reported at the NYU Langone Advanced Seminar in Psoriasis and Psoriatic Arthritis.

Psoriasis and PsA, along with ankylosing spondylitis and Crohn’s disease, have been thought to be either immune mediated or a classic autoimmune disorder, Ritchlin, a rheumatologist and internist and director of the Clinical Immunology Research Unit at the University of Rochester in New York, said in an interview. “But emerging data reveal that these disorders might be triggered and sustained by both autoimmune and immune-mediated events,” he said.

 

Autoimmunity vs Immune Mediated

Autoimmune diseases are characterized by a specific autoantigen and antibody, such as the anti–cyclic citrullinated peptide antibody seen in rheumatoid arthritis, Ritchlin said. He cited a 2023 literature review from Italy that identified five autoantibodies and polymorphisms in PsA.

“In an immune-mediated disease, we demonstrate profound dysregulation of immune cells that promote inflammation, but we have not identified a specific autoantigen,” he said. “There’s an inflammatory response, which can be very severe, but we don’t know if it’s responding to an autoantigen or it’s just dysregulation of the T cells or the B cells or both.”

In a humanized mouse model developed by Maria Garcia-Hernandez, PhD, in Ritchlin’s lab, researchers found that both immunoglobulins and immune cells are required to recapitulate the skin and joint phenotypes. Ritchlin said that further analyses identified a putative autoantigen, which current experiments now underway are looking to confirm and should help discern distinctions in pathogenesis between a response to an autoantigen or cell dysregulation.

“There may be more than one type of immune inflammatory reaction that’s ongoing in individual tissue, and it may be different from one tissue to another,” Ritchlin said in an interview.

The immune-mediated and autoimmune properties of PsA are important to investigate, Jose U. Scher, MD, director of the Arthritis Clinic and Psoriatic Arthritis Center at NYU Langone Health in New York City, said in an interview.

“Classically considered an autoimmune disease, [PsA] may be better classified as an immune-mediated inflammatory disease,” Scher said. He noted one feature that makes PsA differ from classic autoimmunity is that it does not affect women predominantly.

“The fundamental question is whether there are elements of classic autoimmunity such as B cells that should be integrated into the research for future identification of novel therapeutics,” Scher said.

 

The ‘Additional Mechanism’

The additional mechanism Ritchlin referred to is “this idea of trained immunity,” he said, “where innate immune cells — fibroblasts, monocytes, keratinocytes — that are not considered to have [the] adaptive memory characteristic of T cells and B cells but act in an environment of inflammation and can actually develop sustained altered phenotypes in response to inflammation.”

A 2024 report from Europe outlined four characteristics of trained immunity, Ritchlin said, including that it is “antigen agnostic” and results from long-term reprogramming of cells through epigenetic and metabolic mechanisms. The effects of trained immunity are shorter in duration than that of classical adaptive immunity, he said.

These reprogrammed innate immune cells “retain a form of ‘memory’ after an initial stimulus, which can lead to enhanced or altered responses upon subsequent challenges,” Scher said.

In the context of PsA, Scher said, monocytes that express heightened inflammatory responses driven by metabolic and epigenetic reprogramming can become “trained” by triggers such as infections, cytokines (such as interleukin [IL]–1 beta and IL-17), or damage-associated molecular patterns that have been epigenetically modified to respond at higher rates in a future encounter with exacerbated production of proinflammatory cytokines, persistent inflammation, and flares.

Ritchlin explained how this emerging understanding of the mechanisms driving psoriasis and PsA is driving research into treatments.

“If you know that monocytes are undergoing change — these are innate cells, they’re not antigen driven — but that change is based on some type of pathway that makes the cell more inflammatory, then you can think about trying to block that pathway,” he said.

The goal would be to normalize the cellular environment that’s otherwise becoming activated to create the signs and symptoms of psoriasis and PsA, he said.

The other potential therapeutic target would be T cells, Ritchlin said. “There now are T cells that have been identified that have very specific alpha-beta receptors that are expanded in the peripheral blood, uveal fluid, and joints of HLAB27-positive patients with ankylosing spondylitis and anterior uveitis, which is thought to be immune mediated, not autoimmune.” 

Those HLAB27-positive patients “have expansion of a certain subtype of T cells, they have a specific receptor, and specific autoantigens have been identified pointing to a potential autoimmune response,” Ritchlin added.

An antibody that binds and removes specific T-cell receptor subsets may be an effective strategy without being immunosuppressive, Ritchlin said. “That’s real exciting, and we’re all hoping that is going to be a therapeutic approach that could be successful.”

Ritchlin disclosed financial relationships with AbbVie, Amgen, Bristol-Myers Squibb, Janssen, Novartis, Pfizer, and UCB. Scher had no relevant financial relationships.

A version of this article appeared on Medscape.com.

NEW YORK — Over the past year, new evidence has emerged in support of the idea that psoriatic arthritis (PsA) is neither exclusively immune mediated nor a classic autoimmune disease, but that both mechanisms may be essential in disease pathogenesis, and that innate immune cells may possess adaptive properties that may lead to worsening of inflammation of the skin and joints.

Recent findings help dermatologists and rheumatologists to better understand the pathogenesis of PsA and may lead to more targeted and personalized therapies, Christopher Ritchlin, MD, MPH, who’s led research into the pathogenesis of inflammatory diseases, reported at the NYU Langone Advanced Seminar in Psoriasis and Psoriatic Arthritis.

Psoriasis and PsA, along with ankylosing spondylitis and Crohn’s disease, have been thought to be either immune mediated or a classic autoimmune disorder, Ritchlin, a rheumatologist and internist and director of the Clinical Immunology Research Unit at the University of Rochester in New York, said in an interview. “But emerging data reveal that these disorders might be triggered and sustained by both autoimmune and immune-mediated events,” he said.

 

Autoimmunity vs Immune Mediated

Autoimmune diseases are characterized by a specific autoantigen and antibody, such as the anti–cyclic citrullinated peptide antibody seen in rheumatoid arthritis, Ritchlin said. He cited a 2023 literature review from Italy that identified five autoantibodies and polymorphisms in PsA.

“In an immune-mediated disease, we demonstrate profound dysregulation of immune cells that promote inflammation, but we have not identified a specific autoantigen,” he said. “There’s an inflammatory response, which can be very severe, but we don’t know if it’s responding to an autoantigen or it’s just dysregulation of the T cells or the B cells or both.”

In a humanized mouse model developed by Maria Garcia-Hernandez, PhD, in Ritchlin’s lab, researchers found that both immunoglobulins and immune cells are required to recapitulate the skin and joint phenotypes. Ritchlin said that further analyses identified a putative autoantigen, which current experiments now underway are looking to confirm and should help discern distinctions in pathogenesis between a response to an autoantigen or cell dysregulation.

“There may be more than one type of immune inflammatory reaction that’s ongoing in individual tissue, and it may be different from one tissue to another,” Ritchlin said in an interview.

The immune-mediated and autoimmune properties of PsA are important to investigate, Jose U. Scher, MD, director of the Arthritis Clinic and Psoriatic Arthritis Center at NYU Langone Health in New York City, said in an interview.

“Classically considered an autoimmune disease, [PsA] may be better classified as an immune-mediated inflammatory disease,” Scher said. He noted one feature that makes PsA differ from classic autoimmunity is that it does not affect women predominantly.

“The fundamental question is whether there are elements of classic autoimmunity such as B cells that should be integrated into the research for future identification of novel therapeutics,” Scher said.

 

The ‘Additional Mechanism’

The additional mechanism Ritchlin referred to is “this idea of trained immunity,” he said, “where innate immune cells — fibroblasts, monocytes, keratinocytes — that are not considered to have [the] adaptive memory characteristic of T cells and B cells but act in an environment of inflammation and can actually develop sustained altered phenotypes in response to inflammation.”

A 2024 report from Europe outlined four characteristics of trained immunity, Ritchlin said, including that it is “antigen agnostic” and results from long-term reprogramming of cells through epigenetic and metabolic mechanisms. The effects of trained immunity are shorter in duration than that of classical adaptive immunity, he said.

These reprogrammed innate immune cells “retain a form of ‘memory’ after an initial stimulus, which can lead to enhanced or altered responses upon subsequent challenges,” Scher said.

In the context of PsA, Scher said, monocytes that express heightened inflammatory responses driven by metabolic and epigenetic reprogramming can become “trained” by triggers such as infections, cytokines (such as interleukin [IL]–1 beta and IL-17), or damage-associated molecular patterns that have been epigenetically modified to respond at higher rates in a future encounter with exacerbated production of proinflammatory cytokines, persistent inflammation, and flares.

Ritchlin explained how this emerging understanding of the mechanisms driving psoriasis and PsA is driving research into treatments.

“If you know that monocytes are undergoing change — these are innate cells, they’re not antigen driven — but that change is based on some type of pathway that makes the cell more inflammatory, then you can think about trying to block that pathway,” he said.

The goal would be to normalize the cellular environment that’s otherwise becoming activated to create the signs and symptoms of psoriasis and PsA, he said.

The other potential therapeutic target would be T cells, Ritchlin said. “There now are T cells that have been identified that have very specific alpha-beta receptors that are expanded in the peripheral blood, uveal fluid, and joints of HLAB27-positive patients with ankylosing spondylitis and anterior uveitis, which is thought to be immune mediated, not autoimmune.” 

Those HLAB27-positive patients “have expansion of a certain subtype of T cells, they have a specific receptor, and specific autoantigens have been identified pointing to a potential autoimmune response,” Ritchlin added.

An antibody that binds and removes specific T-cell receptor subsets may be an effective strategy without being immunosuppressive, Ritchlin said. “That’s real exciting, and we’re all hoping that is going to be a therapeutic approach that could be successful.”

Ritchlin disclosed financial relationships with AbbVie, Amgen, Bristol-Myers Squibb, Janssen, Novartis, Pfizer, and UCB. Scher had no relevant financial relationships.

A version of this article appeared on Medscape.com.

TOPLINE:

Sjögren disease (SjD) presents three distinct phenotypes ― B-cell active with low symptom burden, high systemic activity with high symptom burden, and low systemic activity with high symptom burden; each phenotype has unique cytokine profiles and interferon (IFN) signatures, with elevated cytokine levels for T and B lymphocyte activation in the first two groups and a prominent IFN signature in the B-cell active group.

METHODOLOGY:

• Researchers conducted this study to assess whether three distinct phenotypes of patients with SjD were associated with distinct pathophysiological pathways and IFN signatures.
• They included 395 patients (median age, 53 years; 94% women) from the Assessment of Systemic Signs and Evolution in Sjögren’s Syndrome (ASSESS) cohort who met the 2002 American-European Consensus Group criteria for SjD.
• A panel of biomarkers including IFN alpha-2, IFN gamma, CXCL10, CXCL13, B-cell activating factor, interleukin (IL) 7, FLT3, CCL19, and tumor necrosis factor receptor II (TNF-RII) was compared between the three phenotypes.
• The IFN signature was assessed using whole blood transcriptomic analysis.
• Analysis compared systemic and symptomatic evolution and assessed the risk for new immunosuppressant prescription and lymphoma development across three clusters on the basis of the IFN signature.

TAKEAWAY:

• Higher levels of CXCL13, IL-7, and TNF-RII cytokines were found in both the B-cell active and high systemic activity groups than in the low systemic activity group (P < .05 for all).
• The low systemic activity cluster with reduced cytokine levels showed less disease progression, with no instances of lymphoma reported in this group.
• A high IFN signature was found in a higher percentage of patients in the B-cell active group (57%) than in the high systemic activity (48%) and low systemic activity (38%) groups.
• In the B-cell active cluster, this high IFN signature was associated with an increased risk for new immunosuppressant prescription, indicating greater disease progression (hazard ratio, 9.38; P = .0032); also, all cases of lymphoma within this group were found in individuals exhibiting a high IFN signature.

IN PRACTICE:

“Our study demonstrated that our stratification, defined by symptoms, systemic clinical signs, and routine biological data, is based on different pathophysiological pathways, particularly B and T lymphocyte activation and the interferon alpha pathway. The latter could help predict the evolution of the BALS cluster, a biological but minimally symptomatic cluster, to consider closer monitoring and/or early treatments to prevent complications,” the authors wrote.

SOURCE:

The study was led by Yann Nguyen, MD, PhD, Department of Rheumatology, Hôpital Bicêtre, Assistance Publique — Hôpitaux de Paris, Université Paris-Saclay, Paris, France, and was published online on December 25, 2024, in Arthritis & Rheumatology.

LIMITATIONS:

The study evaluated only a few cytokines at the time of inclusion in the ASSESS cohort, which may not have captured the full range of biologic markers relevant to SjD. The evolution of systemic activity defined using the European Alliance of Associations for Rheumatology Sjogren’s Syndrome Disease Activity Index showed no difference according to the IFN signature in the B-cell active with low symptom burden cluster, possibly due to treatments received between annual evaluations.

DISCLOSURES:

The ASSESS cohort is supported by research grants from the French Society of Rheumatology. Some authors reported receiving grants, payments, honoraria, consulting fees, and support for attending meetings and having contracts or other ties with pharmaceutical companies.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

Sjögren disease (SjD) presents three distinct phenotypes ― B-cell active with low symptom burden, high systemic activity with high symptom burden, and low systemic activity with high symptom burden; each phenotype has unique cytokine profiles and interferon (IFN) signatures, with elevated cytokine levels for T and B lymphocyte activation in the first two groups and a prominent IFN signature in the B-cell active group.

METHODOLOGY:

• Researchers conducted this study to assess whether three distinct phenotypes of patients with SjD were associated with distinct pathophysiological pathways and IFN signatures.
• They included 395 patients (median age, 53 years; 94% women) from the Assessment of Systemic Signs and Evolution in Sjögren’s Syndrome (ASSESS) cohort who met the 2002 American-European Consensus Group criteria for SjD.
• A panel of biomarkers including IFN alpha-2, IFN gamma, CXCL10, CXCL13, B-cell activating factor, interleukin (IL) 7, FLT3, CCL19, and tumor necrosis factor receptor II (TNF-RII) was compared between the three phenotypes.
• The IFN signature was assessed using whole blood transcriptomic analysis.
• Analysis compared systemic and symptomatic evolution and assessed the risk for new immunosuppressant prescription and lymphoma development across three clusters on the basis of the IFN signature.

TAKEAWAY:

• Higher levels of CXCL13, IL-7, and TNF-RII cytokines were found in both the B-cell active and high systemic activity groups than in the low systemic activity group (P < .05 for all).
• The low systemic activity cluster with reduced cytokine levels showed less disease progression, with no instances of lymphoma reported in this group.
• A high IFN signature was found in a higher percentage of patients in the B-cell active group (57%) than in the high systemic activity (48%) and low systemic activity (38%) groups.
• In the B-cell active cluster, this high IFN signature was associated with an increased risk for new immunosuppressant prescription, indicating greater disease progression (hazard ratio, 9.38; P = .0032); also, all cases of lymphoma within this group were found in individuals exhibiting a high IFN signature.

IN PRACTICE:

“Our study demonstrated that our stratification, defined by symptoms, systemic clinical signs, and routine biological data, is based on different pathophysiological pathways, particularly B and T lymphocyte activation and the interferon alpha pathway. The latter could help predict the evolution of the BALS cluster, a biological but minimally symptomatic cluster, to consider closer monitoring and/or early treatments to prevent complications,” the authors wrote.

SOURCE:

The study was led by Yann Nguyen, MD, PhD, Department of Rheumatology, Hôpital Bicêtre, Assistance Publique — Hôpitaux de Paris, Université Paris-Saclay, Paris, France, and was published online on December 25, 2024, in Arthritis & Rheumatology.

LIMITATIONS:

The study evaluated only a few cytokines at the time of inclusion in the ASSESS cohort, which may not have captured the full range of biologic markers relevant to SjD. The evolution of systemic activity defined using the European Alliance of Associations for Rheumatology Sjogren’s Syndrome Disease Activity Index showed no difference according to the IFN signature in the B-cell active with low symptom burden cluster, possibly due to treatments received between annual evaluations.

DISCLOSURES:

The ASSESS cohort is supported by research grants from the French Society of Rheumatology. Some authors reported receiving grants, payments, honoraria, consulting fees, and support for attending meetings and having contracts or other ties with pharmaceutical companies.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

Sjögren disease (SjD) presents three distinct phenotypes ― B-cell active with low symptom burden, high systemic activity with high symptom burden, and low systemic activity with high symptom burden; each phenotype has unique cytokine profiles and interferon (IFN) signatures, with elevated cytokine levels for T and B lymphocyte activation in the first two groups and a prominent IFN signature in the B-cell active group.

METHODOLOGY:

• Researchers conducted this study to assess whether three distinct phenotypes of patients with SjD were associated with distinct pathophysiological pathways and IFN signatures.
• They included 395 patients (median age, 53 years; 94% women) from the Assessment of Systemic Signs and Evolution in Sjögren’s Syndrome (ASSESS) cohort who met the 2002 American-European Consensus Group criteria for SjD.
• A panel of biomarkers including IFN alpha-2, IFN gamma, CXCL10, CXCL13, B-cell activating factor, interleukin (IL) 7, FLT3, CCL19, and tumor necrosis factor receptor II (TNF-RII) was compared between the three phenotypes.
• The IFN signature was assessed using whole blood transcriptomic analysis.
• Analysis compared systemic and symptomatic evolution and assessed the risk for new immunosuppressant prescription and lymphoma development across three clusters on the basis of the IFN signature.

TAKEAWAY:

• Higher levels of CXCL13, IL-7, and TNF-RII cytokines were found in both the B-cell active and high systemic activity groups than in the low systemic activity group (P < .05 for all).
• The low systemic activity cluster with reduced cytokine levels showed less disease progression, with no instances of lymphoma reported in this group.
• A high IFN signature was found in a higher percentage of patients in the B-cell active group (57%) than in the high systemic activity (48%) and low systemic activity (38%) groups.
• In the B-cell active cluster, this high IFN signature was associated with an increased risk for new immunosuppressant prescription, indicating greater disease progression (hazard ratio, 9.38; P = .0032); also, all cases of lymphoma within this group were found in individuals exhibiting a high IFN signature.

IN PRACTICE:

“Our study demonstrated that our stratification, defined by symptoms, systemic clinical signs, and routine biological data, is based on different pathophysiological pathways, particularly B and T lymphocyte activation and the interferon alpha pathway. The latter could help predict the evolution of the BALS cluster, a biological but minimally symptomatic cluster, to consider closer monitoring and/or early treatments to prevent complications,” the authors wrote.

SOURCE:

The study was led by Yann Nguyen, MD, PhD, Department of Rheumatology, Hôpital Bicêtre, Assistance Publique — Hôpitaux de Paris, Université Paris-Saclay, Paris, France, and was published online on December 25, 2024, in Arthritis & Rheumatology.

LIMITATIONS:

The study evaluated only a few cytokines at the time of inclusion in the ASSESS cohort, which may not have captured the full range of biologic markers relevant to SjD. The evolution of systemic activity defined using the European Alliance of Associations for Rheumatology Sjogren’s Syndrome Disease Activity Index showed no difference according to the IFN signature in the B-cell active with low symptom burden cluster, possibly due to treatments received between annual evaluations.

DISCLOSURES:

The ASSESS cohort is supported by research grants from the French Society of Rheumatology. Some authors reported receiving grants, payments, honoraria, consulting fees, and support for attending meetings and having contracts or other ties with pharmaceutical companies.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

Could an artificial intelligence (AI)–driven tool that mines medical records for suspected cases of osteoporosis be so successful that it becomes a potential liability? Yes, according to Christopher White, PhD, executive director of Maridulu Budyari Gumal, the Sydney Partnership for Health, Education, Research, and Enterprise, a research translation center in Liverpool, Australia.

In a thought-provoking presentation at the Endocrine Society’s AI in Healthcare Virtual Summit, White described the results after his fracture liaison team at Prince of Wales Hospital in Randwick, Australia, tried to plug the “osteoporosis treatment gap” by mining medical records to identify patients with the disorder.

 

‘Be Careful What You Wish For’

White and colleagues developed a robust standalone database over 20 years that informed fracture risk among patients with osteoporosis in Sydney. The database included all relevant clinical information, as well as bone density measurements, on about 30,000 patients and could be interrogated for randomized controlled trial recruitment.

However, a “crisis” occurred around 2011, when the team received a recruitment request for the first head-to-head comparison of alendronate with romosozumab. “We had numerous postmenopausal women in the age range with the required bone density, but we hadn’t captured the severity of their vertebral fracture or how many they actually had,” White told the this news organization. For recruitment into the study, participants must have had at least two moderate or severe vertebral fractures or a proximal vertebral fracture that was sustained between 3 and 24 months before recruitment.

White turned to his hospital’s mainframe, which had coding data and time intervals for patients who were admitted with vertebral or hip fractures. He calculated how many patients who met the study criteria had been discharged and how many of those he thought he’d be able to capture through the mainframe. He was confident he would have enough, but he was wrong. He underrecruited and could not participate in the trial.

Determined not to wind up in a similar situation in the future, he investigated and found that other centers were struggling with similar problems. This led to a collaboration with four investigators who were using AI and Advanced Encryption Standard (AES) coding to identify patients at risk for osteoporotic fractures. White, meanwhile, had developed a natural language processing tool called XRAIT that also identified patients at fracture risk. A study comparing the two electronic search programs, which screen medical records for fractures, found that both reliably identified patients who had had a fracture. White and his colleagues concluded that hybrid tools combining XRAIT and AES would likely improve the identification of patients with osteoporosis who would require follow-up or might participate in future trials.

Those patients were not being identified sooner for multiple reasons, White explained. Sometimes, the radiologist would report osteoporosis, but it wouldn’t get coded. Or, in the emergency department, a patient with a fracture would be treated and then sent home, and the possibility of osteoporosis wasn’t reported.

“As we went deeper and deeper with our tools into the medical record, we found more and more patients who hadn’t been coded or reported but who actually had osteoporosis,” White said. “It was incredibly prevalent.”

But the number of patients identified was more than the hospital could comfortably handle.

Ironically, he added, “To my relief and probably not to the benefit of the patients, there was a system upgrade of the radiology reporting system, which was incompatible with the natural language processing technology that I had installed. The AI was turned off at that point, but I had a look over the edge and into the mine pit.”

“The lesson learned,” White told this news organization, is “If you mine the medical record for unidentified patients before you know what to do with the output, you create a medico-legal minefield. You need to be careful what you wish for with technology, because it may actually come true.”

 

Grappling With the Treatment Gap

An (over)abundance of patients is likely contributing to the “osteoporosis treatment gap” that Australia’s fracture liaison services, which handle many of these patients, are grappling with. One recent meta-analysis showed that not all eligible patients are treated and that not all patients who are treated actually start treatment. Another study showed that only a minority of patients — anywhere between 20% and 40% — who start are still persisting at about 3 years, White said.

Various types of fracture liaison services exist, he noted. The model that has been shown to best promote adherence is the one requiring clinicians to “identify, educate [usually, the primary care physician], evaluate, start treatment, continue treatment, and follow-up at 12 months for to confirm that there is adherence.”

What’s happening now, he said, is that the technology is identifying a high number of vertebral crush fractures, and there’s no education or evaluation. “The radiologist just refers the patient to a primary care physician and hopes for the best. AI isn’t contributing to solving the treatment gap problem; it’s amplifying it. It’s ahead of the ability of organizations to accommodate the findings.”

Solutions, he said, would require support at the top of health systems and organizations, and funding to proceed; data surveys concentrating on vertical integration of the medical record to follow patients wherever they are — eg, hospital, primary care — in their health journeys; a workflow with synchronous diagnosis and treatment planning, delivery, monitoring, and payment; and clinical and community champions advocating and “leading the charge in health tech.”

Furthermore, he advised, organizations need to be “very, very careful with safety and security — that is, managing the digital risks.”

“Oscar Wilde said there are two tragedies in life: One is not getting what one wants, and the other is getting it,” White concluded. “In my career, we’ve moved on from not knowing how to treat osteoporosis to knowing how to treat it. And that is both an asset and a liability.”

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

Could an artificial intelligence (AI)–driven tool that mines medical records for suspected cases of osteoporosis be so successful that it becomes a potential liability? Yes, according to Christopher White, PhD, executive director of Maridulu Budyari Gumal, the Sydney Partnership for Health, Education, Research, and Enterprise, a research translation center in Liverpool, Australia.

In a thought-provoking presentation at the Endocrine Society’s AI in Healthcare Virtual Summit, White described the results after his fracture liaison team at Prince of Wales Hospital in Randwick, Australia, tried to plug the “osteoporosis treatment gap” by mining medical records to identify patients with the disorder.

 

‘Be Careful What You Wish For’

White and colleagues developed a robust standalone database over 20 years that informed fracture risk among patients with osteoporosis in Sydney. The database included all relevant clinical information, as well as bone density measurements, on about 30,000 patients and could be interrogated for randomized controlled trial recruitment.

However, a “crisis” occurred around 2011, when the team received a recruitment request for the first head-to-head comparison of alendronate with romosozumab. “We had numerous postmenopausal women in the age range with the required bone density, but we hadn’t captured the severity of their vertebral fracture or how many they actually had,” White told the this news organization. For recruitment into the study, participants must have had at least two moderate or severe vertebral fractures or a proximal vertebral fracture that was sustained between 3 and 24 months before recruitment.

White turned to his hospital’s mainframe, which had coding data and time intervals for patients who were admitted with vertebral or hip fractures. He calculated how many patients who met the study criteria had been discharged and how many of those he thought he’d be able to capture through the mainframe. He was confident he would have enough, but he was wrong. He underrecruited and could not participate in the trial.

Determined not to wind up in a similar situation in the future, he investigated and found that other centers were struggling with similar problems. This led to a collaboration with four investigators who were using AI and Advanced Encryption Standard (AES) coding to identify patients at risk for osteoporotic fractures. White, meanwhile, had developed a natural language processing tool called XRAIT that also identified patients at fracture risk. A study comparing the two electronic search programs, which screen medical records for fractures, found that both reliably identified patients who had had a fracture. White and his colleagues concluded that hybrid tools combining XRAIT and AES would likely improve the identification of patients with osteoporosis who would require follow-up or might participate in future trials.

Those patients were not being identified sooner for multiple reasons, White explained. Sometimes, the radiologist would report osteoporosis, but it wouldn’t get coded. Or, in the emergency department, a patient with a fracture would be treated and then sent home, and the possibility of osteoporosis wasn’t reported.

“As we went deeper and deeper with our tools into the medical record, we found more and more patients who hadn’t been coded or reported but who actually had osteoporosis,” White said. “It was incredibly prevalent.”

But the number of patients identified was more than the hospital could comfortably handle.

Ironically, he added, “To my relief and probably not to the benefit of the patients, there was a system upgrade of the radiology reporting system, which was incompatible with the natural language processing technology that I had installed. The AI was turned off at that point, but I had a look over the edge and into the mine pit.”

“The lesson learned,” White told this news organization, is “If you mine the medical record for unidentified patients before you know what to do with the output, you create a medico-legal minefield. You need to be careful what you wish for with technology, because it may actually come true.”

 

Grappling With the Treatment Gap

An (over)abundance of patients is likely contributing to the “osteoporosis treatment gap” that Australia’s fracture liaison services, which handle many of these patients, are grappling with. One recent meta-analysis showed that not all eligible patients are treated and that not all patients who are treated actually start treatment. Another study showed that only a minority of patients — anywhere between 20% and 40% — who start are still persisting at about 3 years, White said.

Various types of fracture liaison services exist, he noted. The model that has been shown to best promote adherence is the one requiring clinicians to “identify, educate [usually, the primary care physician], evaluate, start treatment, continue treatment, and follow-up at 12 months for to confirm that there is adherence.”

What’s happening now, he said, is that the technology is identifying a high number of vertebral crush fractures, and there’s no education or evaluation. “The radiologist just refers the patient to a primary care physician and hopes for the best. AI isn’t contributing to solving the treatment gap problem; it’s amplifying it. It’s ahead of the ability of organizations to accommodate the findings.”

Solutions, he said, would require support at the top of health systems and organizations, and funding to proceed; data surveys concentrating on vertical integration of the medical record to follow patients wherever they are — eg, hospital, primary care — in their health journeys; a workflow with synchronous diagnosis and treatment planning, delivery, monitoring, and payment; and clinical and community champions advocating and “leading the charge in health tech.”

Furthermore, he advised, organizations need to be “very, very careful with safety and security — that is, managing the digital risks.”

“Oscar Wilde said there are two tragedies in life: One is not getting what one wants, and the other is getting it,” White concluded. “In my career, we’ve moved on from not knowing how to treat osteoporosis to knowing how to treat it. And that is both an asset and a liability.”

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

Could an artificial intelligence (AI)–driven tool that mines medical records for suspected cases of osteoporosis be so successful that it becomes a potential liability? Yes, according to Christopher White, PhD, executive director of Maridulu Budyari Gumal, the Sydney Partnership for Health, Education, Research, and Enterprise, a research translation center in Liverpool, Australia.

In a thought-provoking presentation at the Endocrine Society’s AI in Healthcare Virtual Summit, White described the results after his fracture liaison team at Prince of Wales Hospital in Randwick, Australia, tried to plug the “osteoporosis treatment gap” by mining medical records to identify patients with the disorder.

 

‘Be Careful What You Wish For’

White and colleagues developed a robust standalone database over 20 years that informed fracture risk among patients with osteoporosis in Sydney. The database included all relevant clinical information, as well as bone density measurements, on about 30,000 patients and could be interrogated for randomized controlled trial recruitment.

However, a “crisis” occurred around 2011, when the team received a recruitment request for the first head-to-head comparison of alendronate with romosozumab. “We had numerous postmenopausal women in the age range with the required bone density, but we hadn’t captured the severity of their vertebral fracture or how many they actually had,” White told the this news organization. For recruitment into the study, participants must have had at least two moderate or severe vertebral fractures or a proximal vertebral fracture that was sustained between 3 and 24 months before recruitment.

White turned to his hospital’s mainframe, which had coding data and time intervals for patients who were admitted with vertebral or hip fractures. He calculated how many patients who met the study criteria had been discharged and how many of those he thought he’d be able to capture through the mainframe. He was confident he would have enough, but he was wrong. He underrecruited and could not participate in the trial.

Determined not to wind up in a similar situation in the future, he investigated and found that other centers were struggling with similar problems. This led to a collaboration with four investigators who were using AI and Advanced Encryption Standard (AES) coding to identify patients at risk for osteoporotic fractures. White, meanwhile, had developed a natural language processing tool called XRAIT that also identified patients at fracture risk. A study comparing the two electronic search programs, which screen medical records for fractures, found that both reliably identified patients who had had a fracture. White and his colleagues concluded that hybrid tools combining XRAIT and AES would likely improve the identification of patients with osteoporosis who would require follow-up or might participate in future trials.

Those patients were not being identified sooner for multiple reasons, White explained. Sometimes, the radiologist would report osteoporosis, but it wouldn’t get coded. Or, in the emergency department, a patient with a fracture would be treated and then sent home, and the possibility of osteoporosis wasn’t reported.

“As we went deeper and deeper with our tools into the medical record, we found more and more patients who hadn’t been coded or reported but who actually had osteoporosis,” White said. “It was incredibly prevalent.”

But the number of patients identified was more than the hospital could comfortably handle.

Ironically, he added, “To my relief and probably not to the benefit of the patients, there was a system upgrade of the radiology reporting system, which was incompatible with the natural language processing technology that I had installed. The AI was turned off at that point, but I had a look over the edge and into the mine pit.”

“The lesson learned,” White told this news organization, is “If you mine the medical record for unidentified patients before you know what to do with the output, you create a medico-legal minefield. You need to be careful what you wish for with technology, because it may actually come true.”

 

Grappling With the Treatment Gap

An (over)abundance of patients is likely contributing to the “osteoporosis treatment gap” that Australia’s fracture liaison services, which handle many of these patients, are grappling with. One recent meta-analysis showed that not all eligible patients are treated and that not all patients who are treated actually start treatment. Another study showed that only a minority of patients — anywhere between 20% and 40% — who start are still persisting at about 3 years, White said.

Various types of fracture liaison services exist, he noted. The model that has been shown to best promote adherence is the one requiring clinicians to “identify, educate [usually, the primary care physician], evaluate, start treatment, continue treatment, and follow-up at 12 months for to confirm that there is adherence.”

What’s happening now, he said, is that the technology is identifying a high number of vertebral crush fractures, and there’s no education or evaluation. “The radiologist just refers the patient to a primary care physician and hopes for the best. AI isn’t contributing to solving the treatment gap problem; it’s amplifying it. It’s ahead of the ability of organizations to accommodate the findings.”

Solutions, he said, would require support at the top of health systems and organizations, and funding to proceed; data surveys concentrating on vertical integration of the medical record to follow patients wherever they are — eg, hospital, primary care — in their health journeys; a workflow with synchronous diagnosis and treatment planning, delivery, monitoring, and payment; and clinical and community champions advocating and “leading the charge in health tech.”

Furthermore, he advised, organizations need to be “very, very careful with safety and security — that is, managing the digital risks.”

“Oscar Wilde said there are two tragedies in life: One is not getting what one wants, and the other is getting it,” White concluded. “In my career, we’ve moved on from not knowing how to treat osteoporosis to knowing how to treat it. And that is both an asset and a liability.”

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

The woman, in severe pain from hip and knee osteoarthritis, was confined to a wheelchair and had been told that would likely be for life. To qualify for hip replacement surgery, she needed to lose 100 pounds, a seemingly impossible goal. But she wanted to try.

“We tried a couple of medicines — oral medicines off-label — topiramate, phentermine,” said Leslie Golden, MD, MPH, DABM, a family medicine physician and obesity medicine specialist in Watertown, Wisconsin, 42 miles northeast of Madison.

They weren’t enough. But then Golden turned to glucagon-like peptide 1 (GLP-1) receptor agonists, and they delivered.

“She did lose a significant amount of weight and was able to get the hip replacement,” said Golden.

It took a couple of years. However, seeing her walk into her office, rather than wheel in, “is still one of the joys of my practice,” Golden said. “She’s so grateful. She felt everyone else had written her off.”

As she told Golden: “If I fell and broke my leg today, they would take me to surgery without concern.”

Because her hip replacement was viewed as a nonemergency procedure, the accepted threshold for elective safe surgery was a body mass index (BMI) < 40. That BMI cutoff can vary from provider to provider and medical facility to medical facility but is often required for other surgeries as well, including kidney and lung transplants, gender-affirming surgery, bariatric surgery, hernia surgery, and in vitro fertilization procedures.

Golden is at the forefront of a growing trend — obesity medicine physicians collaborating with surgeons to prescribe the more effective GLP-1s and get surgery candidates to the starting line. She worked with Rajit Chakravarty, MD, an adult reconstructive surgeon who practices in Watertown and nearby Madison, to oversee the weight loss.

 

High BMIs & Surgery Issues

High BMIs have long been linked with postsurgery complications, poor wound healing, and other issues, although some research now is questioning some of those associations. Even so, surgeons have long stressed weight loss for their patients with obesity before orthopedic and other procedures.

These days, surgeons are more likely to need to have that talk. In the last decade, the age-adjusted prevalence of severe obesity — a BMI of ≥ 40 — has increased from 7.7% to 9.7% of US adults. The number of joint replacements is also rising — more than 700,000 total knee arthroplasty (TKA) and more than 450,000 total hip arthroplasty (THA), according to the American Academy of Orthopaedic Surgeons. As the population ages, those numbers are expected to increase.

 

Making the GLP-1 Choice

GLP-1s aren’t the only choice, of course. But they’re often more effective, as Golden found, than other medications. And when his patients with obesity are offered bariatric surgery or GLP-1s, “people definitely want to avoid the bariatric surgery,” Chakravarty said.

With the Food and Drug Administration (FDA) approval of semaglutide (Wegovy) in June 2021 for chronic weight management and then tirzepatide (Zepbound) in November 2023, interest has boomed, he said, among his surgery candidates with a high BMI.

The FDA approved Wegovy based on clinical trials, including one in which participants lost an average of 12.4% of initial body weight compared with those on placebo. It approved Zepbound based on clinical trials, including one in which those on Zepbound lost an average of 18% of their body weight, compared with those on placebo.

The wheelchair-bound woman, now 65, began with a BMI of 63, Golden said. She negotiated a cutoff of 45 with the surgeon and got the go-ahead. Currently, her BMI is 36 as she stayed on the medications.

Beyond the benefit of GLP-1s helping patients meet the BMI cutoff, some research finds fewer postoperative infections and readmissions with their use. This study found the medications did lower both, and another found reduced readmissions and complications.

 

Growing Partnerships, Increasing Success

Helping patients lose weight isn’t just about lowering the BMI, Chakravarty pointed out. The aim is to improve nutritional health — to teach patients how to eat healthfully for their needs, in turn improving other health barometers. Referring them to an obesity medicine physician helps to meet those goals.

When Daniel Wiznia, MD, a Yale Medicine orthopedic surgeon and codirector of the Avascular Necrosis Program, has a patient who must delay a TKA or THA until they meet a BMI cutoff, he refers that patient to the Yale Medicine Center for Weight Management, New Haven, Connecticut, to learn about weight loss, including the options of anti-obesity medications or bariatric surgery.

Taking the GLP-1s can be a game changer, according to Wiznia and John Morton, MD, MPH, FACS, FASMBS, Yale’s medical director of Bariatric Surgery and professor and vice chair of surgery, who is a physician-director of the center. The program includes other options, such as bariatric surgery, and emphasizes diet and other lifestyle measures. GLP-1s give about a 15% weight loss, Morton said, compared with bariatric surgery providing up to 30%.

Sarah Stombaugh, MD, a family medicine and obesity medicine physician in Charlottesville, Virginia, often gets referrals from two orthopedic surgeons in her community. One recent patient in her early 60s had a BMI of 43.2, too high to qualify for the TKA she needed. On GLP-1s, the initial goal was to decrease a weight of 244 to 225, bringing the BMI to 39.9. The woman did that, then kept losing before her surgery was scheduled, getting to a weight of 210 or a BMI of 37 and staying there for 3 months before the surgery.

She had the TKA, and 5 months out, she is doing well, Stombaugh said. “We do medical weight loss primarily with the GLP-1s because they’re simply the best, the most effective,” Stombaugh said. She does occasionally use oral medications such as naltrexone/bupropion (Contrave).

Stombaugh sees the collaborating trend as still evolving. When she attends obesity medicine conferences, not all her colleagues report they are partnering with surgeons. But she predicts the practice will increase, saying the popularization of what she terms the more effective GLP-1 medications Wegovy and Zepbound is driving it. Partnering with the surgeon requires a conversation at the beginning, when the referral is made, about goals. After that, she sees her patient monthly and sends progress notes to the surgeon.

Golden collaborates with three orthopedic groups in her area, primarily for knee and hip surgeries, but has also helped patients meet the BMI cutoff before spine-related surgeries. She is helping a lung transplant patient now. She has seen several patients who must meet BMI requirements before starting in vitro fertilization, due to the need for conscious sedation for egg retrieval. She has had a few patients who had to meet a BMI cutoff for nonemergency hernia repair.

 

Insurance Issues

Insurance remains an issue for the pricey medications. “Only about a third of patients are routinely covered with insurance,” Morton said.

However, it’s improving, he said. Golden also finds about a third of private payers cover the medication but tries to use manufacturers’ coupons to help defray the costs (from about $1000 or $1400 to about $500 a month). She has sometimes gotten enough samples to get patients to their BMI goal

Morton consulted for Novo Nordisk, Eli Lilly, Olympus, Teleflex, and Johnson & Johnson.

A version of this article appeared on Medscape.com.

The woman, in severe pain from hip and knee osteoarthritis, was confined to a wheelchair and had been told that would likely be for life. To qualify for hip replacement surgery, she needed to lose 100 pounds, a seemingly impossible goal. But she wanted to try.

“We tried a couple of medicines — oral medicines off-label — topiramate, phentermine,” said Leslie Golden, MD, MPH, DABM, a family medicine physician and obesity medicine specialist in Watertown, Wisconsin, 42 miles northeast of Madison.

They weren’t enough. But then Golden turned to glucagon-like peptide 1 (GLP-1) receptor agonists, and they delivered.

“She did lose a significant amount of weight and was able to get the hip replacement,” said Golden.

It took a couple of years. However, seeing her walk into her office, rather than wheel in, “is still one of the joys of my practice,” Golden said. “She’s so grateful. She felt everyone else had written her off.”

As she told Golden: “If I fell and broke my leg today, they would take me to surgery without concern.”

Because her hip replacement was viewed as a nonemergency procedure, the accepted threshold for elective safe surgery was a body mass index (BMI) < 40. That BMI cutoff can vary from provider to provider and medical facility to medical facility but is often required for other surgeries as well, including kidney and lung transplants, gender-affirming surgery, bariatric surgery, hernia surgery, and in vitro fertilization procedures.

Golden is at the forefront of a growing trend — obesity medicine physicians collaborating with surgeons to prescribe the more effective GLP-1s and get surgery candidates to the starting line. She worked with Rajit Chakravarty, MD, an adult reconstructive surgeon who practices in Watertown and nearby Madison, to oversee the weight loss.

 

High BMIs & Surgery Issues

High BMIs have long been linked with postsurgery complications, poor wound healing, and other issues, although some research now is questioning some of those associations. Even so, surgeons have long stressed weight loss for their patients with obesity before orthopedic and other procedures.

These days, surgeons are more likely to need to have that talk. In the last decade, the age-adjusted prevalence of severe obesity — a BMI of ≥ 40 — has increased from 7.7% to 9.7% of US adults. The number of joint replacements is also rising — more than 700,000 total knee arthroplasty (TKA) and more than 450,000 total hip arthroplasty (THA), according to the American Academy of Orthopaedic Surgeons. As the population ages, those numbers are expected to increase.

 

Making the GLP-1 Choice

GLP-1s aren’t the only choice, of course. But they’re often more effective, as Golden found, than other medications. And when his patients with obesity are offered bariatric surgery or GLP-1s, “people definitely want to avoid the bariatric surgery,” Chakravarty said.

With the Food and Drug Administration (FDA) approval of semaglutide (Wegovy) in June 2021 for chronic weight management and then tirzepatide (Zepbound) in November 2023, interest has boomed, he said, among his surgery candidates with a high BMI.

The FDA approved Wegovy based on clinical trials, including one in which participants lost an average of 12.4% of initial body weight compared with those on placebo. It approved Zepbound based on clinical trials, including one in which those on Zepbound lost an average of 18% of their body weight, compared with those on placebo.

The wheelchair-bound woman, now 65, began with a BMI of 63, Golden said. She negotiated a cutoff of 45 with the surgeon and got the go-ahead. Currently, her BMI is 36 as she stayed on the medications.

Beyond the benefit of GLP-1s helping patients meet the BMI cutoff, some research finds fewer postoperative infections and readmissions with their use. This study found the medications did lower both, and another found reduced readmissions and complications.

 

Growing Partnerships, Increasing Success

Helping patients lose weight isn’t just about lowering the BMI, Chakravarty pointed out. The aim is to improve nutritional health — to teach patients how to eat healthfully for their needs, in turn improving other health barometers. Referring them to an obesity medicine physician helps to meet those goals.

When Daniel Wiznia, MD, a Yale Medicine orthopedic surgeon and codirector of the Avascular Necrosis Program, has a patient who must delay a TKA or THA until they meet a BMI cutoff, he refers that patient to the Yale Medicine Center for Weight Management, New Haven, Connecticut, to learn about weight loss, including the options of anti-obesity medications or bariatric surgery.

Taking the GLP-1s can be a game changer, according to Wiznia and John Morton, MD, MPH, FACS, FASMBS, Yale’s medical director of Bariatric Surgery and professor and vice chair of surgery, who is a physician-director of the center. The program includes other options, such as bariatric surgery, and emphasizes diet and other lifestyle measures. GLP-1s give about a 15% weight loss, Morton said, compared with bariatric surgery providing up to 30%.

Sarah Stombaugh, MD, a family medicine and obesity medicine physician in Charlottesville, Virginia, often gets referrals from two orthopedic surgeons in her community. One recent patient in her early 60s had a BMI of 43.2, too high to qualify for the TKA she needed. On GLP-1s, the initial goal was to decrease a weight of 244 to 225, bringing the BMI to 39.9. The woman did that, then kept losing before her surgery was scheduled, getting to a weight of 210 or a BMI of 37 and staying there for 3 months before the surgery.

She had the TKA, and 5 months out, she is doing well, Stombaugh said. “We do medical weight loss primarily with the GLP-1s because they’re simply the best, the most effective,” Stombaugh said. She does occasionally use oral medications such as naltrexone/bupropion (Contrave).

Stombaugh sees the collaborating trend as still evolving. When she attends obesity medicine conferences, not all her colleagues report they are partnering with surgeons. But she predicts the practice will increase, saying the popularization of what she terms the more effective GLP-1 medications Wegovy and Zepbound is driving it. Partnering with the surgeon requires a conversation at the beginning, when the referral is made, about goals. After that, she sees her patient monthly and sends progress notes to the surgeon.

Golden collaborates with three orthopedic groups in her area, primarily for knee and hip surgeries, but has also helped patients meet the BMI cutoff before spine-related surgeries. She is helping a lung transplant patient now. She has seen several patients who must meet BMI requirements before starting in vitro fertilization, due to the need for conscious sedation for egg retrieval. She has had a few patients who had to meet a BMI cutoff for nonemergency hernia repair.

 

Insurance Issues

Insurance remains an issue for the pricey medications. “Only about a third of patients are routinely covered with insurance,” Morton said.

However, it’s improving, he said. Golden also finds about a third of private payers cover the medication but tries to use manufacturers’ coupons to help defray the costs (from about $1000 or $1400 to about $500 a month). She has sometimes gotten enough samples to get patients to their BMI goal

Morton consulted for Novo Nordisk, Eli Lilly, Olympus, Teleflex, and Johnson & Johnson.

A version of this article appeared on Medscape.com.

The woman, in severe pain from hip and knee osteoarthritis, was confined to a wheelchair and had been told that would likely be for life. To qualify for hip replacement surgery, she needed to lose 100 pounds, a seemingly impossible goal. But she wanted to try.

“We tried a couple of medicines — oral medicines off-label — topiramate, phentermine,” said Leslie Golden, MD, MPH, DABM, a family medicine physician and obesity medicine specialist in Watertown, Wisconsin, 42 miles northeast of Madison.

They weren’t enough. But then Golden turned to glucagon-like peptide 1 (GLP-1) receptor agonists, and they delivered.

“She did lose a significant amount of weight and was able to get the hip replacement,” said Golden.

It took a couple of years. However, seeing her walk into her office, rather than wheel in, “is still one of the joys of my practice,” Golden said. “She’s so grateful. She felt everyone else had written her off.”

As she told Golden: “If I fell and broke my leg today, they would take me to surgery without concern.”

Because her hip replacement was viewed as a nonemergency procedure, the accepted threshold for elective safe surgery was a body mass index (BMI) < 40. That BMI cutoff can vary from provider to provider and medical facility to medical facility but is often required for other surgeries as well, including kidney and lung transplants, gender-affirming surgery, bariatric surgery, hernia surgery, and in vitro fertilization procedures.

Golden is at the forefront of a growing trend — obesity medicine physicians collaborating with surgeons to prescribe the more effective GLP-1s and get surgery candidates to the starting line. She worked with Rajit Chakravarty, MD, an adult reconstructive surgeon who practices in Watertown and nearby Madison, to oversee the weight loss.

 

High BMIs & Surgery Issues

High BMIs have long been linked with postsurgery complications, poor wound healing, and other issues, although some research now is questioning some of those associations. Even so, surgeons have long stressed weight loss for their patients with obesity before orthopedic and other procedures.

These days, surgeons are more likely to need to have that talk. In the last decade, the age-adjusted prevalence of severe obesity — a BMI of ≥ 40 — has increased from 7.7% to 9.7% of US adults. The number of joint replacements is also rising — more than 700,000 total knee arthroplasty (TKA) and more than 450,000 total hip arthroplasty (THA), according to the American Academy of Orthopaedic Surgeons. As the population ages, those numbers are expected to increase.

 

Making the GLP-1 Choice

GLP-1s aren’t the only choice, of course. But they’re often more effective, as Golden found, than other medications. And when his patients with obesity are offered bariatric surgery or GLP-1s, “people definitely want to avoid the bariatric surgery,” Chakravarty said.

With the Food and Drug Administration (FDA) approval of semaglutide (Wegovy) in June 2021 for chronic weight management and then tirzepatide (Zepbound) in November 2023, interest has boomed, he said, among his surgery candidates with a high BMI.

The FDA approved Wegovy based on clinical trials, including one in which participants lost an average of 12.4% of initial body weight compared with those on placebo. It approved Zepbound based on clinical trials, including one in which those on Zepbound lost an average of 18% of their body weight, compared with those on placebo.

The wheelchair-bound woman, now 65, began with a BMI of 63, Golden said. She negotiated a cutoff of 45 with the surgeon and got the go-ahead. Currently, her BMI is 36 as she stayed on the medications.

Beyond the benefit of GLP-1s helping patients meet the BMI cutoff, some research finds fewer postoperative infections and readmissions with their use. This study found the medications did lower both, and another found reduced readmissions and complications.

 

Growing Partnerships, Increasing Success

Helping patients lose weight isn’t just about lowering the BMI, Chakravarty pointed out. The aim is to improve nutritional health — to teach patients how to eat healthfully for their needs, in turn improving other health barometers. Referring them to an obesity medicine physician helps to meet those goals.

When Daniel Wiznia, MD, a Yale Medicine orthopedic surgeon and codirector of the Avascular Necrosis Program, has a patient who must delay a TKA or THA until they meet a BMI cutoff, he refers that patient to the Yale Medicine Center for Weight Management, New Haven, Connecticut, to learn about weight loss, including the options of anti-obesity medications or bariatric surgery.

Taking the GLP-1s can be a game changer, according to Wiznia and John Morton, MD, MPH, FACS, FASMBS, Yale’s medical director of Bariatric Surgery and professor and vice chair of surgery, who is a physician-director of the center. The program includes other options, such as bariatric surgery, and emphasizes diet and other lifestyle measures. GLP-1s give about a 15% weight loss, Morton said, compared with bariatric surgery providing up to 30%.

Sarah Stombaugh, MD, a family medicine and obesity medicine physician in Charlottesville, Virginia, often gets referrals from two orthopedic surgeons in her community. One recent patient in her early 60s had a BMI of 43.2, too high to qualify for the TKA she needed. On GLP-1s, the initial goal was to decrease a weight of 244 to 225, bringing the BMI to 39.9. The woman did that, then kept losing before her surgery was scheduled, getting to a weight of 210 or a BMI of 37 and staying there for 3 months before the surgery.

She had the TKA, and 5 months out, she is doing well, Stombaugh said. “We do medical weight loss primarily with the GLP-1s because they’re simply the best, the most effective,” Stombaugh said. She does occasionally use oral medications such as naltrexone/bupropion (Contrave).

Stombaugh sees the collaborating trend as still evolving. When she attends obesity medicine conferences, not all her colleagues report they are partnering with surgeons. But she predicts the practice will increase, saying the popularization of what she terms the more effective GLP-1 medications Wegovy and Zepbound is driving it. Partnering with the surgeon requires a conversation at the beginning, when the referral is made, about goals. After that, she sees her patient monthly and sends progress notes to the surgeon.

Golden collaborates with three orthopedic groups in her area, primarily for knee and hip surgeries, but has also helped patients meet the BMI cutoff before spine-related surgeries. She is helping a lung transplant patient now. She has seen several patients who must meet BMI requirements before starting in vitro fertilization, due to the need for conscious sedation for egg retrieval. She has had a few patients who had to meet a BMI cutoff for nonemergency hernia repair.

 

Insurance Issues

Insurance remains an issue for the pricey medications. “Only about a third of patients are routinely covered with insurance,” Morton said.

However, it’s improving, he said. Golden also finds about a third of private payers cover the medication but tries to use manufacturers’ coupons to help defray the costs (from about $1000 or $1400 to about $500 a month). She has sometimes gotten enough samples to get patients to their BMI goal

Morton consulted for Novo Nordisk, Eli Lilly, Olympus, Teleflex, and Johnson & Johnson.

A version of this article appeared on Medscape.com.

TOPLINE:

Patients with systemic lupus erythematosus (SLE) face more than double the risk for atherosclerotic plaque progression than healthy control individuals without the condition, but management of traditional cardiovascular risk factors and prolonged clinical remission can successfully mitigate it.

METHODOLOGY:

• Researchers performed a prospective study to assess the progression of subclinical atherosclerosis plaques and the development of cardiovascular events in patients with SLE over a 10-year follow-up period.
• They included 111 patients with SLE (mean age, 43 years; 91% women) and 94 matched healthy control individuals without prior atherosclerotic cardiovascular disease (CVD), active malignancy, pregnancy, or diabetes mellitus who underwent carotid ultrasound measurements.
• A total of 738 carotid measurements were analyzed from baseline to 3-, 7-, and 10-year follow-up periods for assessing new carotid plaque development; incident CVD events were also analyzed during follow-up.
• Disease remission was evaluated based on the Definition of Remission in SLE criteria.
• Target for management of cardiovascular risk factors was based on standard recommendations.
•  

TAKEAWAY:

• During the 10-year follow-up, patients with SLE showed a 2.3-fold higher risk for plaque progression than healthy control participants (adjusted incidence rate ratio [aIRR], 2.26; P = .002).
• Achieving risk reduction target for each standard cardiovascular risk factor (blood pressure, lipids, smoking, body weight, and physical activity) was associated with a 32% reduction in the risk for plaque progression (aIRR, 0.68; P = .004).
• Staying in remission for ≥ 75% of the follow-up period was significantly associated with a 43% reduction in the risk for plaque progression (aIRR, 0.57; P = .033).
• Patients with SLE also had a higher incidence of CVD events than healthy control participants (permutation-based log-rank P = .036).
•  

IN PRACTICE:

“These findings support the importance of prioritizing sustained remission rather than a low disease activity state for the prevention of atherosclerosis development and progression in SLE,” the authors wrote.

SOURCE:

The study was led by Nikolaos Papazoglou, MD, First Department of Propaedeutic Internal Medicine, Joint Academic Rheumatology Program, School of Medicine, National and Kapodistrian University of Athens in Greece. It was published online on December 25, 2024, in Arthritis & Rheumatology.

LIMITATIONS:

The study had limited statistical power to perform a multivariate analysis of incident CVD events due to low event rates. The cohort consisted solely of White Europeans, possibly limiting the generalizability of the findings to more ethnically diverse populations. Because antiphospholipid antibodies are known to be associated with CVD events in the general population, the lack of testing for antiphospholipid antibody positivity in healthy control participants could be another limitation.

DISCLOSURES:

The study did not receive any funding from public, commercial, or not-for-profit sectors. The authors reported no competing interests.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

Patients with systemic lupus erythematosus (SLE) face more than double the risk for atherosclerotic plaque progression than healthy control individuals without the condition, but management of traditional cardiovascular risk factors and prolonged clinical remission can successfully mitigate it.

METHODOLOGY:

• Researchers performed a prospective study to assess the progression of subclinical atherosclerosis plaques and the development of cardiovascular events in patients with SLE over a 10-year follow-up period.
• They included 111 patients with SLE (mean age, 43 years; 91% women) and 94 matched healthy control individuals without prior atherosclerotic cardiovascular disease (CVD), active malignancy, pregnancy, or diabetes mellitus who underwent carotid ultrasound measurements.
• A total of 738 carotid measurements were analyzed from baseline to 3-, 7-, and 10-year follow-up periods for assessing new carotid plaque development; incident CVD events were also analyzed during follow-up.
• Disease remission was evaluated based on the Definition of Remission in SLE criteria.
• Target for management of cardiovascular risk factors was based on standard recommendations.
•  

TAKEAWAY:

• During the 10-year follow-up, patients with SLE showed a 2.3-fold higher risk for plaque progression than healthy control participants (adjusted incidence rate ratio [aIRR], 2.26; P = .002).
• Achieving risk reduction target for each standard cardiovascular risk factor (blood pressure, lipids, smoking, body weight, and physical activity) was associated with a 32% reduction in the risk for plaque progression (aIRR, 0.68; P = .004).
• Staying in remission for ≥ 75% of the follow-up period was significantly associated with a 43% reduction in the risk for plaque progression (aIRR, 0.57; P = .033).
• Patients with SLE also had a higher incidence of CVD events than healthy control participants (permutation-based log-rank P = .036).
•  

IN PRACTICE:

“These findings support the importance of prioritizing sustained remission rather than a low disease activity state for the prevention of atherosclerosis development and progression in SLE,” the authors wrote.

SOURCE:

The study was led by Nikolaos Papazoglou, MD, First Department of Propaedeutic Internal Medicine, Joint Academic Rheumatology Program, School of Medicine, National and Kapodistrian University of Athens in Greece. It was published online on December 25, 2024, in Arthritis & Rheumatology.

LIMITATIONS:

The study had limited statistical power to perform a multivariate analysis of incident CVD events due to low event rates. The cohort consisted solely of White Europeans, possibly limiting the generalizability of the findings to more ethnically diverse populations. Because antiphospholipid antibodies are known to be associated with CVD events in the general population, the lack of testing for antiphospholipid antibody positivity in healthy control participants could be another limitation.

DISCLOSURES:

The study did not receive any funding from public, commercial, or not-for-profit sectors. The authors reported no competing interests.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

Patients with systemic lupus erythematosus (SLE) face more than double the risk for atherosclerotic plaque progression than healthy control individuals without the condition, but management of traditional cardiovascular risk factors and prolonged clinical remission can successfully mitigate it.

METHODOLOGY:

• Researchers performed a prospective study to assess the progression of subclinical atherosclerosis plaques and the development of cardiovascular events in patients with SLE over a 10-year follow-up period.
• They included 111 patients with SLE (mean age, 43 years; 91% women) and 94 matched healthy control individuals without prior atherosclerotic cardiovascular disease (CVD), active malignancy, pregnancy, or diabetes mellitus who underwent carotid ultrasound measurements.
• A total of 738 carotid measurements were analyzed from baseline to 3-, 7-, and 10-year follow-up periods for assessing new carotid plaque development; incident CVD events were also analyzed during follow-up.
• Disease remission was evaluated based on the Definition of Remission in SLE criteria.
• Target for management of cardiovascular risk factors was based on standard recommendations.
•  

TAKEAWAY:

• During the 10-year follow-up, patients with SLE showed a 2.3-fold higher risk for plaque progression than healthy control participants (adjusted incidence rate ratio [aIRR], 2.26; P = .002).
• Achieving risk reduction target for each standard cardiovascular risk factor (blood pressure, lipids, smoking, body weight, and physical activity) was associated with a 32% reduction in the risk for plaque progression (aIRR, 0.68; P = .004).
• Staying in remission for ≥ 75% of the follow-up period was significantly associated with a 43% reduction in the risk for plaque progression (aIRR, 0.57; P = .033).
• Patients with SLE also had a higher incidence of CVD events than healthy control participants (permutation-based log-rank P = .036).
•  

IN PRACTICE:

“These findings support the importance of prioritizing sustained remission rather than a low disease activity state for the prevention of atherosclerosis development and progression in SLE,” the authors wrote.

SOURCE:

The study was led by Nikolaos Papazoglou, MD, First Department of Propaedeutic Internal Medicine, Joint Academic Rheumatology Program, School of Medicine, National and Kapodistrian University of Athens in Greece. It was published online on December 25, 2024, in Arthritis & Rheumatology.

LIMITATIONS:

The study had limited statistical power to perform a multivariate analysis of incident CVD events due to low event rates. The cohort consisted solely of White Europeans, possibly limiting the generalizability of the findings to more ethnically diverse populations. Because antiphospholipid antibodies are known to be associated with CVD events in the general population, the lack of testing for antiphospholipid antibody positivity in healthy control participants could be another limitation.

DISCLOSURES:

The study did not receive any funding from public, commercial, or not-for-profit sectors. The authors reported no competing interests.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

The newer biologics — interleukin (IL)–17, IL-12/23, and IL-23 inhibitors — demonstrate comparable cardiovascular safety profiles to tumor necrosis factor (TNF) inhibitors in biologic-naive patients with psoriasis or psoriatic arthritis (PsA).

METHODOLOGY:

• In a retrospective cohort study, researchers conducted an emulated target trial analysis using data of 32,098 biologic-naive patients with psoriasis or PsA who were treated with one of the newer biologics (infliximab, adalimumab, etanercept, certolizumab pegol, secukinumab, ixekizumab, brodalumab, ustekinumab, risankizumab, guselkumab, and tildrakizumab) from the TriNetX Research Network between 2014 and 2022.
• Patients received TNF inhibitors (n = 20,314), IL-17 inhibitors (n = 5073), IL-12/23 inhibitors (n = 3573), or IL-23 inhibitors (n = 3138).
• A propensity-matched analysis compared each class of newer biologics with TNF inhibitors, adjusting for demographics, comorbidities, and medication use.
• The primary outcomes were major adverse cardiovascular events (MACE; myocardial infarction and stroke) or venous thromboembolic events (VTE).

TAKEAWAY:

• Compared with patients who received TNF inhibitors, the risk for MACE was not significantly different between patients who received IL-17 inhibitors (incidence rate ratio [IRR], 1.14; 95% CI, 0.86-1.52), IL-12/23 inhibitors (IRR, 1.24; 95% CI, 0.84-1.78), or IL-23 inhibitors (IRR, 0.93; 95% CI, 0.61-1.38)
• The VTE risk was also not significantly different between patients who received IL-17 inhibitors (IRR, 1.12; 95% CI, 0.63-2.08), IL-12/23 inhibitors (IRR, 1.51; 95% CI, 0.73-3.19), or IL-23 inhibitors (IRR, 1.42; 95% CI, 0.64-3.25) compared with those who received TNF inhibitors.
• Subgroup analyses for psoriasis or psoriatic arthritis alone confirmed consistent findings.
• Patients with preexisting hyperlipidemia and diabetes mellitus showed lower risks for MACE and VTE with newer biologics compared with TNF inhibitors. 

IN PRACTICE:

“No significant MACE and VTE risk differences were detected in patients with psoriasis or PsA between those receiving IL-17, IL-12/23, and IL-23 inhibitors and those with TNF inhibitors,” the authors concluded. These findings, they added “can be considered by physicians and patients when making treatment decisions” and also provide “evidence for future pharmacovigilance studies.”

SOURCE:

The study was led by Tai-Li Chen, MD, of the Department of Dermatology, Taipei Veterans General Hospital in Taipei, Taiwan. It was published online on December 27, 2024, in the Journal of the American Academy of Dermatology.

LIMITATIONS:

Study limitations included potential residual confounding factors, lack of information on disease severity, and inclusion of predominantly White individuals.

DISCLOSURES:

The study received support from Taipei Veterans General Hospital and Ministry of Science and Technology, Taiwan. The authors reported no conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

The newer biologics — interleukin (IL)–17, IL-12/23, and IL-23 inhibitors — demonstrate comparable cardiovascular safety profiles to tumor necrosis factor (TNF) inhibitors in biologic-naive patients with psoriasis or psoriatic arthritis (PsA).

METHODOLOGY:

• In a retrospective cohort study, researchers conducted an emulated target trial analysis using data of 32,098 biologic-naive patients with psoriasis or PsA who were treated with one of the newer biologics (infliximab, adalimumab, etanercept, certolizumab pegol, secukinumab, ixekizumab, brodalumab, ustekinumab, risankizumab, guselkumab, and tildrakizumab) from the TriNetX Research Network between 2014 and 2022.
• Patients received TNF inhibitors (n = 20,314), IL-17 inhibitors (n = 5073), IL-12/23 inhibitors (n = 3573), or IL-23 inhibitors (n = 3138).
• A propensity-matched analysis compared each class of newer biologics with TNF inhibitors, adjusting for demographics, comorbidities, and medication use.
• The primary outcomes were major adverse cardiovascular events (MACE; myocardial infarction and stroke) or venous thromboembolic events (VTE).

TAKEAWAY:

• Compared with patients who received TNF inhibitors, the risk for MACE was not significantly different between patients who received IL-17 inhibitors (incidence rate ratio [IRR], 1.14; 95% CI, 0.86-1.52), IL-12/23 inhibitors (IRR, 1.24; 95% CI, 0.84-1.78), or IL-23 inhibitors (IRR, 0.93; 95% CI, 0.61-1.38)
• The VTE risk was also not significantly different between patients who received IL-17 inhibitors (IRR, 1.12; 95% CI, 0.63-2.08), IL-12/23 inhibitors (IRR, 1.51; 95% CI, 0.73-3.19), or IL-23 inhibitors (IRR, 1.42; 95% CI, 0.64-3.25) compared with those who received TNF inhibitors.
• Subgroup analyses for psoriasis or psoriatic arthritis alone confirmed consistent findings.
• Patients with preexisting hyperlipidemia and diabetes mellitus showed lower risks for MACE and VTE with newer biologics compared with TNF inhibitors. 

IN PRACTICE:

“No significant MACE and VTE risk differences were detected in patients with psoriasis or PsA between those receiving IL-17, IL-12/23, and IL-23 inhibitors and those with TNF inhibitors,” the authors concluded. These findings, they added “can be considered by physicians and patients when making treatment decisions” and also provide “evidence for future pharmacovigilance studies.”

SOURCE:

The study was led by Tai-Li Chen, MD, of the Department of Dermatology, Taipei Veterans General Hospital in Taipei, Taiwan. It was published online on December 27, 2024, in the Journal of the American Academy of Dermatology.

LIMITATIONS:

Study limitations included potential residual confounding factors, lack of information on disease severity, and inclusion of predominantly White individuals.

DISCLOSURES:

The study received support from Taipei Veterans General Hospital and Ministry of Science and Technology, Taiwan. The authors reported no conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

The newer biologics — interleukin (IL)–17, IL-12/23, and IL-23 inhibitors — demonstrate comparable cardiovascular safety profiles to tumor necrosis factor (TNF) inhibitors in biologic-naive patients with psoriasis or psoriatic arthritis (PsA).

METHODOLOGY:

• In a retrospective cohort study, researchers conducted an emulated target trial analysis using data of 32,098 biologic-naive patients with psoriasis or PsA who were treated with one of the newer biologics (infliximab, adalimumab, etanercept, certolizumab pegol, secukinumab, ixekizumab, brodalumab, ustekinumab, risankizumab, guselkumab, and tildrakizumab) from the TriNetX Research Network between 2014 and 2022.
• Patients received TNF inhibitors (n = 20,314), IL-17 inhibitors (n = 5073), IL-12/23 inhibitors (n = 3573), or IL-23 inhibitors (n = 3138).
• A propensity-matched analysis compared each class of newer biologics with TNF inhibitors, adjusting for demographics, comorbidities, and medication use.
• The primary outcomes were major adverse cardiovascular events (MACE; myocardial infarction and stroke) or venous thromboembolic events (VTE).

TAKEAWAY:

• Compared with patients who received TNF inhibitors, the risk for MACE was not significantly different between patients who received IL-17 inhibitors (incidence rate ratio [IRR], 1.14; 95% CI, 0.86-1.52), IL-12/23 inhibitors (IRR, 1.24; 95% CI, 0.84-1.78), or IL-23 inhibitors (IRR, 0.93; 95% CI, 0.61-1.38)
• The VTE risk was also not significantly different between patients who received IL-17 inhibitors (IRR, 1.12; 95% CI, 0.63-2.08), IL-12/23 inhibitors (IRR, 1.51; 95% CI, 0.73-3.19), or IL-23 inhibitors (IRR, 1.42; 95% CI, 0.64-3.25) compared with those who received TNF inhibitors.
• Subgroup analyses for psoriasis or psoriatic arthritis alone confirmed consistent findings.
• Patients with preexisting hyperlipidemia and diabetes mellitus showed lower risks for MACE and VTE with newer biologics compared with TNF inhibitors. 

IN PRACTICE:

“No significant MACE and VTE risk differences were detected in patients with psoriasis or PsA between those receiving IL-17, IL-12/23, and IL-23 inhibitors and those with TNF inhibitors,” the authors concluded. These findings, they added “can be considered by physicians and patients when making treatment decisions” and also provide “evidence for future pharmacovigilance studies.”

SOURCE:

The study was led by Tai-Li Chen, MD, of the Department of Dermatology, Taipei Veterans General Hospital in Taipei, Taiwan. It was published online on December 27, 2024, in the Journal of the American Academy of Dermatology.

LIMITATIONS:

Study limitations included potential residual confounding factors, lack of information on disease severity, and inclusion of predominantly White individuals.

DISCLOSURES:

The study received support from Taipei Veterans General Hospital and Ministry of Science and Technology, Taiwan. The authors reported no conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Patients with rheumatoid arthritis (RA) face a higher risk for heart failure (HF) than those without the condition, with the elevated risk primarily driven by HF with preserved ejection fraction (HFpEF).

METHODOLOGY:

• The researchers conducted a retrospective cohort study using data from the Mass General Brigham Biobank to investigate the risk for overall HF and its subtypes, particularly HF with reduced EF (HFrEF) and HFpEF, in patients with RA.
• They included 1445 patients newly diagnosed with RA (mean age, 51.4 years; 78.7% women) and 4335 matched comparators without RA.
• Patients with RA were identified using diagnosis codes and RA-related natural language processing concepts.
• HFpEF and HFrEF were defined as HF with an EF ≥ 50% and ≤ 40%, respectively; incidences for overall HF, HFpEF, and HFrEF were calculated per 1000 person-years.

TAKEAWAY:

• The study identified 92 incident HF cases in the RA cohort and 157 in the non-RA cohort over a median follow-up of 10.3 years per patient.
• HFpEF was the predominant HF subtype in both cohorts, with a higher incidence in patients with RA than in those without the condition (4.33 vs 2.11 per 1000 person-years).
• Patients with RA showed a 79% higher risk for HF than those without the condition (adjusted hazard ratio [aHR], 1.79; 95% CI, 1.38-2.32).
• Among the HF subtypes, patients with RA had a significantly increased risk for HFpEF (aHR, 1.99; 95% CI, 1.43-2.77) but not for HFrEF.

IN PRACTICE:

“RA can be considered a human model for inflammation, and findings from this study support the notion that chronic inflammation increases risk for HFpEF,” the authors wrote.

SOURCE:

This study was led by Yumeko Kawano, MD, Brigham and Women’s Hospital, Boston, Massachusetts, and was published online in Arthritis Care & Research.

LIMITATIONS:

This study was conducted within an academic tertiary hospital system and involved participants from a biobank, which may have introduced selection bias and limited generalizability. The study did not account for post-baseline variables that could mediate the observed associations, such as the chronic use of nonsteroidal anti-inflammatory drugs, steroids, or specific disease-modifying antirheumatic drugs. The study relied on the availability of clinically performed cardiology studies for HF subtyping, possibly introducing misclassification of HF.

DISCLOSURES:

This study was supported by grants from the National Institute of Arthritis and Musculoskeletal and Skin Diseases. One author received support from the Ruth L. Kirschstein Institutional National Research Service Award, National Institutes of Health.

This article was created using several editorial tools, including artificial intelligence, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

Patients with rheumatoid arthritis (RA) face a higher risk for heart failure (HF) than those without the condition, with the elevated risk primarily driven by HF with preserved ejection fraction (HFpEF).

METHODOLOGY:

• The researchers conducted a retrospective cohort study using data from the Mass General Brigham Biobank to investigate the risk for overall HF and its subtypes, particularly HF with reduced EF (HFrEF) and HFpEF, in patients with RA.
• They included 1445 patients newly diagnosed with RA (mean age, 51.4 years; 78.7% women) and 4335 matched comparators without RA.
• Patients with RA were identified using diagnosis codes and RA-related natural language processing concepts.
• HFpEF and HFrEF were defined as HF with an EF ≥ 50% and ≤ 40%, respectively; incidences for overall HF, HFpEF, and HFrEF were calculated per 1000 person-years.

TAKEAWAY:

• The study identified 92 incident HF cases in the RA cohort and 157 in the non-RA cohort over a median follow-up of 10.3 years per patient.
• HFpEF was the predominant HF subtype in both cohorts, with a higher incidence in patients with RA than in those without the condition (4.33 vs 2.11 per 1000 person-years).
• Patients with RA showed a 79% higher risk for HF than those without the condition (adjusted hazard ratio [aHR], 1.79; 95% CI, 1.38-2.32).
• Among the HF subtypes, patients with RA had a significantly increased risk for HFpEF (aHR, 1.99; 95% CI, 1.43-2.77) but not for HFrEF.

IN PRACTICE:

“RA can be considered a human model for inflammation, and findings from this study support the notion that chronic inflammation increases risk for HFpEF,” the authors wrote.

SOURCE:

This study was led by Yumeko Kawano, MD, Brigham and Women’s Hospital, Boston, Massachusetts, and was published online in Arthritis Care & Research.

LIMITATIONS:

This study was conducted within an academic tertiary hospital system and involved participants from a biobank, which may have introduced selection bias and limited generalizability. The study did not account for post-baseline variables that could mediate the observed associations, such as the chronic use of nonsteroidal anti-inflammatory drugs, steroids, or specific disease-modifying antirheumatic drugs. The study relied on the availability of clinically performed cardiology studies for HF subtyping, possibly introducing misclassification of HF.

DISCLOSURES:

This study was supported by grants from the National Institute of Arthritis and Musculoskeletal and Skin Diseases. One author received support from the Ruth L. Kirschstein Institutional National Research Service Award, National Institutes of Health.

This article was created using several editorial tools, including artificial intelligence, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

Patients with rheumatoid arthritis (RA) face a higher risk for heart failure (HF) than those without the condition, with the elevated risk primarily driven by HF with preserved ejection fraction (HFpEF).

METHODOLOGY:

• The researchers conducted a retrospective cohort study using data from the Mass General Brigham Biobank to investigate the risk for overall HF and its subtypes, particularly HF with reduced EF (HFrEF) and HFpEF, in patients with RA.
• They included 1445 patients newly diagnosed with RA (mean age, 51.4 years; 78.7% women) and 4335 matched comparators without RA.
• Patients with RA were identified using diagnosis codes and RA-related natural language processing concepts.
• HFpEF and HFrEF were defined as HF with an EF ≥ 50% and ≤ 40%, respectively; incidences for overall HF, HFpEF, and HFrEF were calculated per 1000 person-years.

TAKEAWAY:

• The study identified 92 incident HF cases in the RA cohort and 157 in the non-RA cohort over a median follow-up of 10.3 years per patient.
• HFpEF was the predominant HF subtype in both cohorts, with a higher incidence in patients with RA than in those without the condition (4.33 vs 2.11 per 1000 person-years).
• Patients with RA showed a 79% higher risk for HF than those without the condition (adjusted hazard ratio [aHR], 1.79; 95% CI, 1.38-2.32).
• Among the HF subtypes, patients with RA had a significantly increased risk for HFpEF (aHR, 1.99; 95% CI, 1.43-2.77) but not for HFrEF.

IN PRACTICE:

“RA can be considered a human model for inflammation, and findings from this study support the notion that chronic inflammation increases risk for HFpEF,” the authors wrote.

SOURCE:

This study was led by Yumeko Kawano, MD, Brigham and Women’s Hospital, Boston, Massachusetts, and was published online in Arthritis Care & Research.

LIMITATIONS:

This study was conducted within an academic tertiary hospital system and involved participants from a biobank, which may have introduced selection bias and limited generalizability. The study did not account for post-baseline variables that could mediate the observed associations, such as the chronic use of nonsteroidal anti-inflammatory drugs, steroids, or specific disease-modifying antirheumatic drugs. The study relied on the availability of clinically performed cardiology studies for HF subtyping, possibly introducing misclassification of HF.

DISCLOSURES:

This study was supported by grants from the National Institute of Arthritis and Musculoskeletal and Skin Diseases. One author received support from the Ruth L. Kirschstein Institutional National Research Service Award, National Institutes of Health.

This article was created using several editorial tools, including artificial intelligence, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

NEW YORK CITY — Rheumatologists, dermatologists, drug manufacturers, and researchers do not pay enough attention to the role sex and gender play in the pathogenesis and presentation of psoriatic arthritis (PsA), Lihi Eder, MD, PhD, said at the Tenth Annual NYU Langone Advanced Seminar in Psoriasis and Psoriatic Arthritis. Being mindful that the disease and treatments affect men and women differently makes patient management more personalized and effective, she noted.

“We tend to ignore sex and gender when we manage our patients in our approach to psoriatic arthritis as well as other rheumatic diseases,” Eder said. “We have to start thinking about sex of the patient as a biomarker that can potentially help us personalize care and move from a gender-blinded to a gender-specific approach.”

Eder, the Canada Research Chair in Inflammatory Rheumatic Diseases at the Women’s College Hospital of the University of Toronto, in Ontario, Canada, said much of the obfuscation of the role gender plays in PsA begins with research. “There’s very little research into sex differences in PsA,” she said. A meta-analysis published last year by her group found that while 51% of participants in 54 PsA trials were women, only nine (17%) reported baseline characteristics by sex, 18 (33%) reported efficacy by sex, and two (4%) reported safety endpoints by sex.

Eder said sex is a biological factor, whereas gender is a “more complex” factor based on social and cultural aspects of men and women.

 

PsA Differences in Women vs Men

Although the prevalence of PsA in men and women is similar, sex affects the risk of developing rheumatic disease. For example, Eder cited a host of studies that showed Sjögren’s syndrome and systemic lupus erythematosus have a 9:1 and 7:1 prevalence in women vs men, whereas gout has a 1:4 prevalence.

Her group’s 2013 study, along with a 2023 study from Italy, found significant differences in how PsA disease activity and quality of life differ between the two sexes.

“Females tend to have a higher tender joint count and more clinical entheses,” Eder said. “They also have worse patient-reported outcomes when it comes to pain, fatigue, and physical dysfunction, and these are things that would influence quality of life.

“On the other hand, when we look at male patients, they tend to have higher CRP [C-reactive protein] levels, they tend to have more severe restriction in the spine, and they also tend to have more severe psoriasis.”

She added that women are less likely than men to develop joint damage that’s picked up on x-rays.

 

Questioning Drug Development 

A gender gap exists across four phases of drug development, Eder said. Preclinical studies tend to rely on single-sex models, phase 1 clinical trials target a standard 70-kg healthy male, and phase 2 and 3 trials as well as postmarketing surveillance do not consider gender in study design and have limited reporting of sex-specific endpoints, she said.

“So, it’s very hard to pick up these signals, and this may explain why most of the drugs that are withdrawn from the market pose a greater risk for women than for men,” she said, citing a 2001 Government Accountability Office report that found that 80% of prescription drugs withdrawn from the market pose a greater risk for women.

That gender bias also carries over to drug commercialization, she said. The sleeping pill zolpidem remains one of the few drugs for which the Food and Drug Administration has approved sex-specific dosing, Eder noted.

Her group’s 2023 meta-analysis showed that men and women respond differently to approved biological disease-modifying antirheumatic drugs. That research, which included a subanalysis of 18 trials and 6821 patients, found that men had a better American College of Rheumatology 20 response to tumor necrosis factor (TNF), interleukin-17 (IL-17), and IL-23 inhibitors, but there was no difference between the sexes in response to Janus-activated kinase (JAK) and tyrosine kinase 2 inhibitors. The same subanalysis also found no difference in the placebo response between men and women in those trials.

“So this raises the question: Should we consider the sex of the patient when we select treatments?” Eder said.

A French study last year reported that men had higher rates of persistence after 1 year: 62% vs 52% for women for TNF inhibitor, IL-17 inhibitor, and IL-23 inhibitor agents, but persistence rates for JAK inhibitors were similar between sexes.

“People ask me should we start favoring JAK inhibitors for females,” Eder said. “I think it’s premature. We need to do more research, but it does raise the question.”

A study by Eder and her group reported that women were more likely than men to discontinue their medications because their symptoms did not improve or the side effects were intolerable.

Another sex-differentiating factor of PsA that clinicians should take into account, Eder said, is the way men and women experience pain. “Women tend to report higher levels of pain across different rheumatic conditions,” she said, citing her own group’s 2022 study and a 2020 Dutch study. Cultural differences in how the sexes approach pain may also come into play, with men expected to be more tolerant and women more susceptible to it, Eder added. 

 

Evidence Is Mounting, but More Is Needed

The evidence that explains why these apparent differences exist between men and women with PsA is still lacking, Eder said in an interview with Medscape Medical News. “It’s very hard now because we don’t know the differences,” she said. “It’s very hard to know the solutions when you don’t know why things are happening.”

Nonetheless, she said, in her own practice she tries to be attuned to pain in women and is trying to stay unbiased when her patients talk about pain.

“I’ve also started asking females as they go into menopause or around the age of the mid-40s — those that complain about pain — about other menopausal-related symptoms, which I didn’t do before,” Eder said. She said she counsels patients whose pain might be driven by potentially menopausal transition, especially if they’re taking hormone-replacement therapy. She added that she is also using objective measures to differentiate PsA-related pain from other causes, such as fibromyalgia or depression.

Asked to comment on this topic, Iannis Adamopoulos, PhD, associate professor of medicine and director of the Arthritis Program and Head of the Osteoimmunology Laboratory at Beth Israel Deaconess Medical Center, Boston, told Medscape Medical News, “the science is now building” to better understand how sex and gender influence PsA. He noted that the National Institutes of Health already mandates sex-specific mouse studies in any research it funds.

Human studies, however, must take into account a host of variables, Adamopoulos said. “You have more variation within the groups because you don’t control 100% of people; you don’t put them in cages,” he said.

In her presentation, Eder noted that her group’s research into sex dimorphisms in the proteomic profile in PsA found that men have 20 times more sex-specific differentially expressed proteins than women. But Adamopoulos said that “there are no male and female proteins at all. There could be different levels but not different proteins.”

The research into sex differences in PsA is nascent, he said, adding, “There’s still a lot to uncover.” 

Eder disclosed financial relationships with AbbVie, Eli Lilly, Pfizer, Novartis, Johnson & Johnson, Bristol Myers Squibb, UCB, Fresenius Kabi, and Sandoz. Adamopoulos had no relevant financial disclosures.

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

NEW YORK CITY — Rheumatologists, dermatologists, drug manufacturers, and researchers do not pay enough attention to the role sex and gender play in the pathogenesis and presentation of psoriatic arthritis (PsA), Lihi Eder, MD, PhD, said at the Tenth Annual NYU Langone Advanced Seminar in Psoriasis and Psoriatic Arthritis. Being mindful that the disease and treatments affect men and women differently makes patient management more personalized and effective, she noted.

“We tend to ignore sex and gender when we manage our patients in our approach to psoriatic arthritis as well as other rheumatic diseases,” Eder said. “We have to start thinking about sex of the patient as a biomarker that can potentially help us personalize care and move from a gender-blinded to a gender-specific approach.”

Eder, the Canada Research Chair in Inflammatory Rheumatic Diseases at the Women’s College Hospital of the University of Toronto, in Ontario, Canada, said much of the obfuscation of the role gender plays in PsA begins with research. “There’s very little research into sex differences in PsA,” she said. A meta-analysis published last year by her group found that while 51% of participants in 54 PsA trials were women, only nine (17%) reported baseline characteristics by sex, 18 (33%) reported efficacy by sex, and two (4%) reported safety endpoints by sex.

Eder said sex is a biological factor, whereas gender is a “more complex” factor based on social and cultural aspects of men and women.

 

PsA Differences in Women vs Men

Although the prevalence of PsA in men and women is similar, sex affects the risk of developing rheumatic disease. For example, Eder cited a host of studies that showed Sjögren’s syndrome and systemic lupus erythematosus have a 9:1 and 7:1 prevalence in women vs men, whereas gout has a 1:4 prevalence.

Her group’s 2013 study, along with a 2023 study from Italy, found significant differences in how PsA disease activity and quality of life differ between the two sexes.

“Females tend to have a higher tender joint count and more clinical entheses,” Eder said. “They also have worse patient-reported outcomes when it comes to pain, fatigue, and physical dysfunction, and these are things that would influence quality of life.

“On the other hand, when we look at male patients, they tend to have higher CRP [C-reactive protein] levels, they tend to have more severe restriction in the spine, and they also tend to have more severe psoriasis.”

She added that women are less likely than men to develop joint damage that’s picked up on x-rays.

 

Questioning Drug Development 

A gender gap exists across four phases of drug development, Eder said. Preclinical studies tend to rely on single-sex models, phase 1 clinical trials target a standard 70-kg healthy male, and phase 2 and 3 trials as well as postmarketing surveillance do not consider gender in study design and have limited reporting of sex-specific endpoints, she said.

“So, it’s very hard to pick up these signals, and this may explain why most of the drugs that are withdrawn from the market pose a greater risk for women than for men,” she said, citing a 2001 Government Accountability Office report that found that 80% of prescription drugs withdrawn from the market pose a greater risk for women.

That gender bias also carries over to drug commercialization, she said. The sleeping pill zolpidem remains one of the few drugs for which the Food and Drug Administration has approved sex-specific dosing, Eder noted.

Her group’s 2023 meta-analysis showed that men and women respond differently to approved biological disease-modifying antirheumatic drugs. That research, which included a subanalysis of 18 trials and 6821 patients, found that men had a better American College of Rheumatology 20 response to tumor necrosis factor (TNF), interleukin-17 (IL-17), and IL-23 inhibitors, but there was no difference between the sexes in response to Janus-activated kinase (JAK) and tyrosine kinase 2 inhibitors. The same subanalysis also found no difference in the placebo response between men and women in those trials.

“So this raises the question: Should we consider the sex of the patient when we select treatments?” Eder said.

A French study last year reported that men had higher rates of persistence after 1 year: 62% vs 52% for women for TNF inhibitor, IL-17 inhibitor, and IL-23 inhibitor agents, but persistence rates for JAK inhibitors were similar between sexes.

“People ask me should we start favoring JAK inhibitors for females,” Eder said. “I think it’s premature. We need to do more research, but it does raise the question.”

A study by Eder and her group reported that women were more likely than men to discontinue their medications because their symptoms did not improve or the side effects were intolerable.

Another sex-differentiating factor of PsA that clinicians should take into account, Eder said, is the way men and women experience pain. “Women tend to report higher levels of pain across different rheumatic conditions,” she said, citing her own group’s 2022 study and a 2020 Dutch study. Cultural differences in how the sexes approach pain may also come into play, with men expected to be more tolerant and women more susceptible to it, Eder added. 

 

Evidence Is Mounting, but More Is Needed

The evidence that explains why these apparent differences exist between men and women with PsA is still lacking, Eder said in an interview with Medscape Medical News. “It’s very hard now because we don’t know the differences,” she said. “It’s very hard to know the solutions when you don’t know why things are happening.”

Nonetheless, she said, in her own practice she tries to be attuned to pain in women and is trying to stay unbiased when her patients talk about pain.

“I’ve also started asking females as they go into menopause or around the age of the mid-40s — those that complain about pain — about other menopausal-related symptoms, which I didn’t do before,” Eder said. She said she counsels patients whose pain might be driven by potentially menopausal transition, especially if they’re taking hormone-replacement therapy. She added that she is also using objective measures to differentiate PsA-related pain from other causes, such as fibromyalgia or depression.

Asked to comment on this topic, Iannis Adamopoulos, PhD, associate professor of medicine and director of the Arthritis Program and Head of the Osteoimmunology Laboratory at Beth Israel Deaconess Medical Center, Boston, told Medscape Medical News, “the science is now building” to better understand how sex and gender influence PsA. He noted that the National Institutes of Health already mandates sex-specific mouse studies in any research it funds.

Human studies, however, must take into account a host of variables, Adamopoulos said. “You have more variation within the groups because you don’t control 100% of people; you don’t put them in cages,” he said.

In her presentation, Eder noted that her group’s research into sex dimorphisms in the proteomic profile in PsA found that men have 20 times more sex-specific differentially expressed proteins than women. But Adamopoulos said that “there are no male and female proteins at all. There could be different levels but not different proteins.”

The research into sex differences in PsA is nascent, he said, adding, “There’s still a lot to uncover.” 

Eder disclosed financial relationships with AbbVie, Eli Lilly, Pfizer, Novartis, Johnson & Johnson, Bristol Myers Squibb, UCB, Fresenius Kabi, and Sandoz. Adamopoulos had no relevant financial disclosures.

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

NEW YORK CITY — Rheumatologists, dermatologists, drug manufacturers, and researchers do not pay enough attention to the role sex and gender play in the pathogenesis and presentation of psoriatic arthritis (PsA), Lihi Eder, MD, PhD, said at the Tenth Annual NYU Langone Advanced Seminar in Psoriasis and Psoriatic Arthritis. Being mindful that the disease and treatments affect men and women differently makes patient management more personalized and effective, she noted.

“We tend to ignore sex and gender when we manage our patients in our approach to psoriatic arthritis as well as other rheumatic diseases,” Eder said. “We have to start thinking about sex of the patient as a biomarker that can potentially help us personalize care and move from a gender-blinded to a gender-specific approach.”

Eder, the Canada Research Chair in Inflammatory Rheumatic Diseases at the Women’s College Hospital of the University of Toronto, in Ontario, Canada, said much of the obfuscation of the role gender plays in PsA begins with research. “There’s very little research into sex differences in PsA,” she said. A meta-analysis published last year by her group found that while 51% of participants in 54 PsA trials were women, only nine (17%) reported baseline characteristics by sex, 18 (33%) reported efficacy by sex, and two (4%) reported safety endpoints by sex.

Eder said sex is a biological factor, whereas gender is a “more complex” factor based on social and cultural aspects of men and women.

 

PsA Differences in Women vs Men

Although the prevalence of PsA in men and women is similar, sex affects the risk of developing rheumatic disease. For example, Eder cited a host of studies that showed Sjögren’s syndrome and systemic lupus erythematosus have a 9:1 and 7:1 prevalence in women vs men, whereas gout has a 1:4 prevalence.

Her group’s 2013 study, along with a 2023 study from Italy, found significant differences in how PsA disease activity and quality of life differ between the two sexes.

“Females tend to have a higher tender joint count and more clinical entheses,” Eder said. “They also have worse patient-reported outcomes when it comes to pain, fatigue, and physical dysfunction, and these are things that would influence quality of life.

“On the other hand, when we look at male patients, they tend to have higher CRP [C-reactive protein] levels, they tend to have more severe restriction in the spine, and they also tend to have more severe psoriasis.”

She added that women are less likely than men to develop joint damage that’s picked up on x-rays.

 

Questioning Drug Development 

A gender gap exists across four phases of drug development, Eder said. Preclinical studies tend to rely on single-sex models, phase 1 clinical trials target a standard 70-kg healthy male, and phase 2 and 3 trials as well as postmarketing surveillance do not consider gender in study design and have limited reporting of sex-specific endpoints, she said.

“So, it’s very hard to pick up these signals, and this may explain why most of the drugs that are withdrawn from the market pose a greater risk for women than for men,” she said, citing a 2001 Government Accountability Office report that found that 80% of prescription drugs withdrawn from the market pose a greater risk for women.

That gender bias also carries over to drug commercialization, she said. The sleeping pill zolpidem remains one of the few drugs for which the Food and Drug Administration has approved sex-specific dosing, Eder noted.

Her group’s 2023 meta-analysis showed that men and women respond differently to approved biological disease-modifying antirheumatic drugs. That research, which included a subanalysis of 18 trials and 6821 patients, found that men had a better American College of Rheumatology 20 response to tumor necrosis factor (TNF), interleukin-17 (IL-17), and IL-23 inhibitors, but there was no difference between the sexes in response to Janus-activated kinase (JAK) and tyrosine kinase 2 inhibitors. The same subanalysis also found no difference in the placebo response between men and women in those trials.

“So this raises the question: Should we consider the sex of the patient when we select treatments?” Eder said.

A French study last year reported that men had higher rates of persistence after 1 year: 62% vs 52% for women for TNF inhibitor, IL-17 inhibitor, and IL-23 inhibitor agents, but persistence rates for JAK inhibitors were similar between sexes.

“People ask me should we start favoring JAK inhibitors for females,” Eder said. “I think it’s premature. We need to do more research, but it does raise the question.”

A study by Eder and her group reported that women were more likely than men to discontinue their medications because their symptoms did not improve or the side effects were intolerable.

Another sex-differentiating factor of PsA that clinicians should take into account, Eder said, is the way men and women experience pain. “Women tend to report higher levels of pain across different rheumatic conditions,” she said, citing her own group’s 2022 study and a 2020 Dutch study. Cultural differences in how the sexes approach pain may also come into play, with men expected to be more tolerant and women more susceptible to it, Eder added. 

 

Evidence Is Mounting, but More Is Needed

The evidence that explains why these apparent differences exist between men and women with PsA is still lacking, Eder said in an interview with Medscape Medical News. “It’s very hard now because we don’t know the differences,” she said. “It’s very hard to know the solutions when you don’t know why things are happening.”

Nonetheless, she said, in her own practice she tries to be attuned to pain in women and is trying to stay unbiased when her patients talk about pain.

“I’ve also started asking females as they go into menopause or around the age of the mid-40s — those that complain about pain — about other menopausal-related symptoms, which I didn’t do before,” Eder said. She said she counsels patients whose pain might be driven by potentially menopausal transition, especially if they’re taking hormone-replacement therapy. She added that she is also using objective measures to differentiate PsA-related pain from other causes, such as fibromyalgia or depression.

Asked to comment on this topic, Iannis Adamopoulos, PhD, associate professor of medicine and director of the Arthritis Program and Head of the Osteoimmunology Laboratory at Beth Israel Deaconess Medical Center, Boston, told Medscape Medical News, “the science is now building” to better understand how sex and gender influence PsA. He noted that the National Institutes of Health already mandates sex-specific mouse studies in any research it funds.

Human studies, however, must take into account a host of variables, Adamopoulos said. “You have more variation within the groups because you don’t control 100% of people; you don’t put them in cages,” he said.

In her presentation, Eder noted that her group’s research into sex dimorphisms in the proteomic profile in PsA found that men have 20 times more sex-specific differentially expressed proteins than women. But Adamopoulos said that “there are no male and female proteins at all. There could be different levels but not different proteins.”

The research into sex differences in PsA is nascent, he said, adding, “There’s still a lot to uncover.” 

Eder disclosed financial relationships with AbbVie, Eli Lilly, Pfizer, Novartis, Johnson & Johnson, Bristol Myers Squibb, UCB, Fresenius Kabi, and Sandoz. Adamopoulos had no relevant financial disclosures.

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

NEW YORK CITY — The idea of having dermatologists and rheumatologists under one roof to see patients with psoriasis prone to psoriatic arthritis (PsA) — a concept known as combined clinics — has been around for more than a decade, and the idea of personalized medicine for these patients even longer than that, yet both approaches to care have encountered a host of obstacles, a longtime research rheumatologist said.

“It’s important that we work together, but there is a problem in terms of staffing — managing the meetings with patients together — and in the states in particular it’s a matter of who’s charging for what,” Dafna Gladman, MD, a rheumatologist at the University of Toronto, in Ontario, Canada, told attendees at the annual New York University (NYU) Langone Advanced Seminar in Psoriasis and Psoriatic Arthritis. Her institution has one of the 44 worldwide combined clinics registered in the Psoriasis & Psoriatic Arthritis Clinics Multicenter Advancement Network (PPACMAN), of which Gladman is an advisory board member.

 

Barriers to Combined Clinics

“Some of the barriers are physical in the sense that, for the dermatologists and rheumatologists to work at the same time, you need the right space, and in many places, you just don’t have the space to have the two specialists sitting at the same time,” Gladman told Medscape Medical News.

Some centers get around this by having the dermatology and rheumatology clinics next to or near each other. “So these two specialists are close enough to be able to go from room to room,” she added.

Another challenge facing combined clinics lies in the nature of how dermatologists and rheumatologists see patients. “The dermatologist sees patients a lot faster than the rheumatologist, so if the dermatologist and rheumatologist are sitting together, the dermatologist may not see as many patients as they would otherwise and therefore may not get reimbursed properly,” Gladman said.

To overcome these challenges, different models have emerged, Gladman said. If space allows, the ideal model is to have both specialties in one clinic, she said, while compensating for the different pace at which dermatologists and rheumatologists see patients.

The other model is to locate the two clinics close enough so that a person with suspected PsA can get to the rheumatology clinic soon after their dermatologic consult, or the rheumatologist can go to the dermatology clinic, Gladman said. Or the situation may be reversed when the rheumatologist needs a dermatology consult, she added.

When that’s not possible, a virtual visit may be the solution, Gladman said. She noted that PPACMAN offers ways to overcome the challenges of running a combined clinic.

Whatever combined clinic model a center chooses, clinicians must be mindful of preventing patients from falling through the cracks, Gladman said.

“When you treat patients separately, the patient sees the rheumatologist, and the rheumatologist wants to do one thing; then they go to the dermatologist and the dermatologist wants to do another thing, and the patient doesn’t do anything because they don’t know what to choose,” she said.

The combined clinic allows the patient to get the opinions of both specialists and avoid the uncertainty about the course of treatment, Gladman added.

Some combined clinics may also house other specialists, such as gastroenterologists, cardiologists, and nurse practitioners, noted Jose U. Scher, MD, director of the Arthritis Clinic and Psoriatic Arthritis Center at NYU Langone Health in New York City. Such centers are typically in academic centers “given challenges with space, scheduling, and reimbursement,” he told Medscape Medical News. NYU has a PPACMAN-registered combined clinic.

Regardless of how combined clinics are organized, Scher said, “We have found that the most important aspect of combined clinics is the open communication and integration of care between and amongst specialists and patients.”

 

The Potential of Personalized Medicine

“Personalized medicine is where we need to get to,” Gladman told seminar attendees. She said she had hoped it would be further along by now and be more integrated into the care of patients with psoriasis and PsA. “The idea is to identify psoriasis patients that are destined to develop psoriatic arthritis,” she said.

Besides that, identifying biomarkers is key to advancing personalized medicine for psoriasis, Gladman noted.

“In the skin, it’s easy; even the patient can assess their psoriasis,” she said. “But in the joints, it’s very difficult, so it would be nice to have some kind of biomarker, whether it’s the blood or an imaging modality. We want to identify the biomarkers for drug response or lack thereof so we know what drugs would be appropriate for the individual patient, and therefore, we can provide the right drug for the right person and fortunately at the right time.”

In explaining why personalized medicine isn’t further along in dermatology and rheumatology, Gladman told Medscape Medical News, “It’s a matter of finding the right things; we haven’t solved the mystery.” She cited a previous discussion at the seminar about the pathogenesis of PsA. “One person thinks it’s the bone marrow and another thinks it’s the T cells, so we haven’t quite put it all together to have a definitive answer.”

Personalized medicine in psoriasis and PsA is a “key unmet need,” Scher said. “Multiomics” — a biological analysis approach that uses multiple “omes,” such as the genome and microbiome — digital features, and wearables “can unlock novel diagnostic and therapeutic pathways that are desperately needed to enhance clinical response in PsA,” he said.

Also emerging are humanized animal models for laboratory research, which Scher called “potentially very useful tools to personalize approaches to PsA pathogenesis and treatment.”

Gladman disclosed financial relationships with AbbVie, Amgen, Bristol Myers Squibb, Eli Lilly, Galapagos, Gilead, Janssen, Novartis, Pfizer, and UCB. Scher had no relevant financial relationships.

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

NEW YORK CITY — The idea of having dermatologists and rheumatologists under one roof to see patients with psoriasis prone to psoriatic arthritis (PsA) — a concept known as combined clinics — has been around for more than a decade, and the idea of personalized medicine for these patients even longer than that, yet both approaches to care have encountered a host of obstacles, a longtime research rheumatologist said.

“It’s important that we work together, but there is a problem in terms of staffing — managing the meetings with patients together — and in the states in particular it’s a matter of who’s charging for what,” Dafna Gladman, MD, a rheumatologist at the University of Toronto, in Ontario, Canada, told attendees at the annual New York University (NYU) Langone Advanced Seminar in Psoriasis and Psoriatic Arthritis. Her institution has one of the 44 worldwide combined clinics registered in the Psoriasis & Psoriatic Arthritis Clinics Multicenter Advancement Network (PPACMAN), of which Gladman is an advisory board member.

 

Barriers to Combined Clinics

“Some of the barriers are physical in the sense that, for the dermatologists and rheumatologists to work at the same time, you need the right space, and in many places, you just don’t have the space to have the two specialists sitting at the same time,” Gladman told Medscape Medical News.

Some centers get around this by having the dermatology and rheumatology clinics next to or near each other. “So these two specialists are close enough to be able to go from room to room,” she added.

Another challenge facing combined clinics lies in the nature of how dermatologists and rheumatologists see patients. “The dermatologist sees patients a lot faster than the rheumatologist, so if the dermatologist and rheumatologist are sitting together, the dermatologist may not see as many patients as they would otherwise and therefore may not get reimbursed properly,” Gladman said.

To overcome these challenges, different models have emerged, Gladman said. If space allows, the ideal model is to have both specialties in one clinic, she said, while compensating for the different pace at which dermatologists and rheumatologists see patients.

The other model is to locate the two clinics close enough so that a person with suspected PsA can get to the rheumatology clinic soon after their dermatologic consult, or the rheumatologist can go to the dermatology clinic, Gladman said. Or the situation may be reversed when the rheumatologist needs a dermatology consult, she added.

When that’s not possible, a virtual visit may be the solution, Gladman said. She noted that PPACMAN offers ways to overcome the challenges of running a combined clinic.

Whatever combined clinic model a center chooses, clinicians must be mindful of preventing patients from falling through the cracks, Gladman said.

“When you treat patients separately, the patient sees the rheumatologist, and the rheumatologist wants to do one thing; then they go to the dermatologist and the dermatologist wants to do another thing, and the patient doesn’t do anything because they don’t know what to choose,” she said.

The combined clinic allows the patient to get the opinions of both specialists and avoid the uncertainty about the course of treatment, Gladman added.

Some combined clinics may also house other specialists, such as gastroenterologists, cardiologists, and nurse practitioners, noted Jose U. Scher, MD, director of the Arthritis Clinic and Psoriatic Arthritis Center at NYU Langone Health in New York City. Such centers are typically in academic centers “given challenges with space, scheduling, and reimbursement,” he told Medscape Medical News. NYU has a PPACMAN-registered combined clinic.

Regardless of how combined clinics are organized, Scher said, “We have found that the most important aspect of combined clinics is the open communication and integration of care between and amongst specialists and patients.”

 

The Potential of Personalized Medicine

“Personalized medicine is where we need to get to,” Gladman told seminar attendees. She said she had hoped it would be further along by now and be more integrated into the care of patients with psoriasis and PsA. “The idea is to identify psoriasis patients that are destined to develop psoriatic arthritis,” she said.

Besides that, identifying biomarkers is key to advancing personalized medicine for psoriasis, Gladman noted.

“In the skin, it’s easy; even the patient can assess their psoriasis,” she said. “But in the joints, it’s very difficult, so it would be nice to have some kind of biomarker, whether it’s the blood or an imaging modality. We want to identify the biomarkers for drug response or lack thereof so we know what drugs would be appropriate for the individual patient, and therefore, we can provide the right drug for the right person and fortunately at the right time.”

In explaining why personalized medicine isn’t further along in dermatology and rheumatology, Gladman told Medscape Medical News, “It’s a matter of finding the right things; we haven’t solved the mystery.” She cited a previous discussion at the seminar about the pathogenesis of PsA. “One person thinks it’s the bone marrow and another thinks it’s the T cells, so we haven’t quite put it all together to have a definitive answer.”

Personalized medicine in psoriasis and PsA is a “key unmet need,” Scher said. “Multiomics” — a biological analysis approach that uses multiple “omes,” such as the genome and microbiome — digital features, and wearables “can unlock novel diagnostic and therapeutic pathways that are desperately needed to enhance clinical response in PsA,” he said.

Also emerging are humanized animal models for laboratory research, which Scher called “potentially very useful tools to personalize approaches to PsA pathogenesis and treatment.”

Gladman disclosed financial relationships with AbbVie, Amgen, Bristol Myers Squibb, Eli Lilly, Galapagos, Gilead, Janssen, Novartis, Pfizer, and UCB. Scher had no relevant financial relationships.

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

NEW YORK CITY — The idea of having dermatologists and rheumatologists under one roof to see patients with psoriasis prone to psoriatic arthritis (PsA) — a concept known as combined clinics — has been around for more than a decade, and the idea of personalized medicine for these patients even longer than that, yet both approaches to care have encountered a host of obstacles, a longtime research rheumatologist said.

“It’s important that we work together, but there is a problem in terms of staffing — managing the meetings with patients together — and in the states in particular it’s a matter of who’s charging for what,” Dafna Gladman, MD, a rheumatologist at the University of Toronto, in Ontario, Canada, told attendees at the annual New York University (NYU) Langone Advanced Seminar in Psoriasis and Psoriatic Arthritis. Her institution has one of the 44 worldwide combined clinics registered in the Psoriasis & Psoriatic Arthritis Clinics Multicenter Advancement Network (PPACMAN), of which Gladman is an advisory board member.

 

Barriers to Combined Clinics

“Some of the barriers are physical in the sense that, for the dermatologists and rheumatologists to work at the same time, you need the right space, and in many places, you just don’t have the space to have the two specialists sitting at the same time,” Gladman told Medscape Medical News.

Some centers get around this by having the dermatology and rheumatology clinics next to or near each other. “So these two specialists are close enough to be able to go from room to room,” she added.

Another challenge facing combined clinics lies in the nature of how dermatologists and rheumatologists see patients. “The dermatologist sees patients a lot faster than the rheumatologist, so if the dermatologist and rheumatologist are sitting together, the dermatologist may not see as many patients as they would otherwise and therefore may not get reimbursed properly,” Gladman said.

To overcome these challenges, different models have emerged, Gladman said. If space allows, the ideal model is to have both specialties in one clinic, she said, while compensating for the different pace at which dermatologists and rheumatologists see patients.

The other model is to locate the two clinics close enough so that a person with suspected PsA can get to the rheumatology clinic soon after their dermatologic consult, or the rheumatologist can go to the dermatology clinic, Gladman said. Or the situation may be reversed when the rheumatologist needs a dermatology consult, she added.

When that’s not possible, a virtual visit may be the solution, Gladman said. She noted that PPACMAN offers ways to overcome the challenges of running a combined clinic.

Whatever combined clinic model a center chooses, clinicians must be mindful of preventing patients from falling through the cracks, Gladman said.

“When you treat patients separately, the patient sees the rheumatologist, and the rheumatologist wants to do one thing; then they go to the dermatologist and the dermatologist wants to do another thing, and the patient doesn’t do anything because they don’t know what to choose,” she said.

The combined clinic allows the patient to get the opinions of both specialists and avoid the uncertainty about the course of treatment, Gladman added.

Some combined clinics may also house other specialists, such as gastroenterologists, cardiologists, and nurse practitioners, noted Jose U. Scher, MD, director of the Arthritis Clinic and Psoriatic Arthritis Center at NYU Langone Health in New York City. Such centers are typically in academic centers “given challenges with space, scheduling, and reimbursement,” he told Medscape Medical News. NYU has a PPACMAN-registered combined clinic.

Regardless of how combined clinics are organized, Scher said, “We have found that the most important aspect of combined clinics is the open communication and integration of care between and amongst specialists and patients.”

 

The Potential of Personalized Medicine

“Personalized medicine is where we need to get to,” Gladman told seminar attendees. She said she had hoped it would be further along by now and be more integrated into the care of patients with psoriasis and PsA. “The idea is to identify psoriasis patients that are destined to develop psoriatic arthritis,” she said.

Besides that, identifying biomarkers is key to advancing personalized medicine for psoriasis, Gladman noted.

“In the skin, it’s easy; even the patient can assess their psoriasis,” she said. “But in the joints, it’s very difficult, so it would be nice to have some kind of biomarker, whether it’s the blood or an imaging modality. We want to identify the biomarkers for drug response or lack thereof so we know what drugs would be appropriate for the individual patient, and therefore, we can provide the right drug for the right person and fortunately at the right time.”

In explaining why personalized medicine isn’t further along in dermatology and rheumatology, Gladman told Medscape Medical News, “It’s a matter of finding the right things; we haven’t solved the mystery.” She cited a previous discussion at the seminar about the pathogenesis of PsA. “One person thinks it’s the bone marrow and another thinks it’s the T cells, so we haven’t quite put it all together to have a definitive answer.”

Personalized medicine in psoriasis and PsA is a “key unmet need,” Scher said. “Multiomics” — a biological analysis approach that uses multiple “omes,” such as the genome and microbiome — digital features, and wearables “can unlock novel diagnostic and therapeutic pathways that are desperately needed to enhance clinical response in PsA,” he said.

Also emerging are humanized animal models for laboratory research, which Scher called “potentially very useful tools to personalize approaches to PsA pathogenesis and treatment.”

Gladman disclosed financial relationships with AbbVie, Amgen, Bristol Myers Squibb, Eli Lilly, Galapagos, Gilead, Janssen, Novartis, Pfizer, and UCB. Scher had no relevant financial relationships.

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