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Novel x-ray score distinguishes psoriatic arthritis from osteoarthritis of the hand
LIVERPOOL, ENGLAND – A novel radiologic scoring system differentiated psoriatic arthritis (PsA) from nodal osteoarthritis (OA) of the hand in a pilot study.
“It’s a dilemma that’s faced, perhaps every couple of weeks, by most [rheumatologists]: Is it osteoarthritis or is it early psoriatic arthritis?” said Sardar Bahadur, MD, at the British Society for Rheumatology annual conference.
Both conditions are seen in daily practice, although the prevalence of hand OA is less frequent than knee OA. Approximately one in five of all adults in the United Kingdom have OA and 1%-2% have psoriasis. Of these, the prevalence of hand OA is about 11% and 0.1%-0.3% have psoriatic arthritis.
Being able to differentiate between the two conditions has important consequences for treatment, Dr. Bahadur said.
“Getting the diagnosis wrong could have major implications,” he said. “If you miss psoriatic arthritis, then potentially you are going to find irreversible joint damage causing pain and disability, and the opposite is also true, with misdiagnosis of osteoarthritis, with overuse of immunosuppression and all the cost implications as well as medicolegal consequences.”
Dr. Bahadur of the department of rehabilitation medicine and rheumatology at the Defence Medical Rehabilitation Centre Headley Court, in Epsom, England, added: “So early diagnosis is very important, it means early treatment, it means better care, potentially preventing serious and irreversible damage.”
Together with researchers at Guy’s and St Thomas’ NHS Trust, London, Dr. Bahadur hypothesized that changes in hand x-rays were distinct and could be reliably used to differentiate between the two conditions. They developed a scoring system for hand radiographs that looked at the differences in the interphalangeal joints, soft tissue, and bone features of patients with known OA or PsA.
Dr. Bahadur noted that the aim was to focus on plain film radiographs of the hands because these were inexpensive, universally accessible, did not rely on radiologists’ interpretation, and changes in the hands were known to occur in both OA and PsA.
A total of 99 sets of hand x-rays taken between 2008 and 2016 from 50 patients with OA and 49 patients with PsA were obtained. These were anonymized and then analyzed by a musculoskeletal radiologist using the scoring system the team had developed. The radiologist was unaware of the patients’ clinical status. The results were then compared to the clinical diagnosis.
The novel method of scoring each x-ray was then taught to two rheumatology and one radiology trainee during a 1-hour training session and were then asked to score the same radiographs.
Dr. Bahadur reported that the radiologist reported normal hand radiographs in five patients and, of the remaining 94 sets of left- and right-hand radiographs, the scoring system correctly allocated 100% of images to either PsA, OA, or rheumatoid arthritis (RA).
Of note was that the radiologist correctly identified two patients with nodal hand OA who later developed PsA several years later, and one patient with RA who was initially thought to have PsA.
“The system could be successfully used by nonradiologists,” Dr. Bahadur proposed. There was good agreement between the scoring system results and the clinical diagnosis then used by the trainees, with 88% and 67% of the radiographs correctly matched to the clinical diagnosis by the rheumatology trainees, and 70% for the radiology trainee.
Dr. Bahadur noted that the features that were consistently identified as being different between hand OA and PsA patients were soft tissue changes, such as dactylitis, as well as erosions, new bone formation, and other features such as subchondral surface changes and cysts.
The results of this single-center study show that the novel radiologic scoring system of hand radiographs was effective at differentiating patients with PsA from nodal OA.
“The ambition is to make this usable by nonradiologists,” Dr. Bahadur said. A multicenter trial would be the next step to look at the use of the scoring system.
Dr. Bahadur had no conflicts of interest to disclose.
SOURCE: Bahadur S et al. Rheumatology. 2018;57[Suppl. 3]:key075.184
LIVERPOOL, ENGLAND – A novel radiologic scoring system differentiated psoriatic arthritis (PsA) from nodal osteoarthritis (OA) of the hand in a pilot study.
“It’s a dilemma that’s faced, perhaps every couple of weeks, by most [rheumatologists]: Is it osteoarthritis or is it early psoriatic arthritis?” said Sardar Bahadur, MD, at the British Society for Rheumatology annual conference.
Both conditions are seen in daily practice, although the prevalence of hand OA is less frequent than knee OA. Approximately one in five of all adults in the United Kingdom have OA and 1%-2% have psoriasis. Of these, the prevalence of hand OA is about 11% and 0.1%-0.3% have psoriatic arthritis.
Being able to differentiate between the two conditions has important consequences for treatment, Dr. Bahadur said.
“Getting the diagnosis wrong could have major implications,” he said. “If you miss psoriatic arthritis, then potentially you are going to find irreversible joint damage causing pain and disability, and the opposite is also true, with misdiagnosis of osteoarthritis, with overuse of immunosuppression and all the cost implications as well as medicolegal consequences.”
Dr. Bahadur of the department of rehabilitation medicine and rheumatology at the Defence Medical Rehabilitation Centre Headley Court, in Epsom, England, added: “So early diagnosis is very important, it means early treatment, it means better care, potentially preventing serious and irreversible damage.”
Together with researchers at Guy’s and St Thomas’ NHS Trust, London, Dr. Bahadur hypothesized that changes in hand x-rays were distinct and could be reliably used to differentiate between the two conditions. They developed a scoring system for hand radiographs that looked at the differences in the interphalangeal joints, soft tissue, and bone features of patients with known OA or PsA.
Dr. Bahadur noted that the aim was to focus on plain film radiographs of the hands because these were inexpensive, universally accessible, did not rely on radiologists’ interpretation, and changes in the hands were known to occur in both OA and PsA.
A total of 99 sets of hand x-rays taken between 2008 and 2016 from 50 patients with OA and 49 patients with PsA were obtained. These were anonymized and then analyzed by a musculoskeletal radiologist using the scoring system the team had developed. The radiologist was unaware of the patients’ clinical status. The results were then compared to the clinical diagnosis.
The novel method of scoring each x-ray was then taught to two rheumatology and one radiology trainee during a 1-hour training session and were then asked to score the same radiographs.
Dr. Bahadur reported that the radiologist reported normal hand radiographs in five patients and, of the remaining 94 sets of left- and right-hand radiographs, the scoring system correctly allocated 100% of images to either PsA, OA, or rheumatoid arthritis (RA).
Of note was that the radiologist correctly identified two patients with nodal hand OA who later developed PsA several years later, and one patient with RA who was initially thought to have PsA.
“The system could be successfully used by nonradiologists,” Dr. Bahadur proposed. There was good agreement between the scoring system results and the clinical diagnosis then used by the trainees, with 88% and 67% of the radiographs correctly matched to the clinical diagnosis by the rheumatology trainees, and 70% for the radiology trainee.
Dr. Bahadur noted that the features that were consistently identified as being different between hand OA and PsA patients were soft tissue changes, such as dactylitis, as well as erosions, new bone formation, and other features such as subchondral surface changes and cysts.
The results of this single-center study show that the novel radiologic scoring system of hand radiographs was effective at differentiating patients with PsA from nodal OA.
“The ambition is to make this usable by nonradiologists,” Dr. Bahadur said. A multicenter trial would be the next step to look at the use of the scoring system.
Dr. Bahadur had no conflicts of interest to disclose.
SOURCE: Bahadur S et al. Rheumatology. 2018;57[Suppl. 3]:key075.184
LIVERPOOL, ENGLAND – A novel radiologic scoring system differentiated psoriatic arthritis (PsA) from nodal osteoarthritis (OA) of the hand in a pilot study.
“It’s a dilemma that’s faced, perhaps every couple of weeks, by most [rheumatologists]: Is it osteoarthritis or is it early psoriatic arthritis?” said Sardar Bahadur, MD, at the British Society for Rheumatology annual conference.
Both conditions are seen in daily practice, although the prevalence of hand OA is less frequent than knee OA. Approximately one in five of all adults in the United Kingdom have OA and 1%-2% have psoriasis. Of these, the prevalence of hand OA is about 11% and 0.1%-0.3% have psoriatic arthritis.
Being able to differentiate between the two conditions has important consequences for treatment, Dr. Bahadur said.
“Getting the diagnosis wrong could have major implications,” he said. “If you miss psoriatic arthritis, then potentially you are going to find irreversible joint damage causing pain and disability, and the opposite is also true, with misdiagnosis of osteoarthritis, with overuse of immunosuppression and all the cost implications as well as medicolegal consequences.”
Dr. Bahadur of the department of rehabilitation medicine and rheumatology at the Defence Medical Rehabilitation Centre Headley Court, in Epsom, England, added: “So early diagnosis is very important, it means early treatment, it means better care, potentially preventing serious and irreversible damage.”
Together with researchers at Guy’s and St Thomas’ NHS Trust, London, Dr. Bahadur hypothesized that changes in hand x-rays were distinct and could be reliably used to differentiate between the two conditions. They developed a scoring system for hand radiographs that looked at the differences in the interphalangeal joints, soft tissue, and bone features of patients with known OA or PsA.
Dr. Bahadur noted that the aim was to focus on plain film radiographs of the hands because these were inexpensive, universally accessible, did not rely on radiologists’ interpretation, and changes in the hands were known to occur in both OA and PsA.
A total of 99 sets of hand x-rays taken between 2008 and 2016 from 50 patients with OA and 49 patients with PsA were obtained. These were anonymized and then analyzed by a musculoskeletal radiologist using the scoring system the team had developed. The radiologist was unaware of the patients’ clinical status. The results were then compared to the clinical diagnosis.
The novel method of scoring each x-ray was then taught to two rheumatology and one radiology trainee during a 1-hour training session and were then asked to score the same radiographs.
Dr. Bahadur reported that the radiologist reported normal hand radiographs in five patients and, of the remaining 94 sets of left- and right-hand radiographs, the scoring system correctly allocated 100% of images to either PsA, OA, or rheumatoid arthritis (RA).
Of note was that the radiologist correctly identified two patients with nodal hand OA who later developed PsA several years later, and one patient with RA who was initially thought to have PsA.
“The system could be successfully used by nonradiologists,” Dr. Bahadur proposed. There was good agreement between the scoring system results and the clinical diagnosis then used by the trainees, with 88% and 67% of the radiographs correctly matched to the clinical diagnosis by the rheumatology trainees, and 70% for the radiology trainee.
Dr. Bahadur noted that the features that were consistently identified as being different between hand OA and PsA patients were soft tissue changes, such as dactylitis, as well as erosions, new bone formation, and other features such as subchondral surface changes and cysts.
The results of this single-center study show that the novel radiologic scoring system of hand radiographs was effective at differentiating patients with PsA from nodal OA.
“The ambition is to make this usable by nonradiologists,” Dr. Bahadur said. A multicenter trial would be the next step to look at the use of the scoring system.
Dr. Bahadur had no conflicts of interest to disclose.
SOURCE: Bahadur S et al. Rheumatology. 2018;57[Suppl. 3]:key075.184
REPORTING FROM RHEUMATOLOGY 2018
Key clinical point:
Major finding: Using the scoring system, 100% of images were correctly allocated to PsA, OA, or RA.
Study details: Single center pilot study assessing 99 x-rays of both hands taken between 2008 and 2016 of patients with OA (n = 50) or PsA (n = 49).
Disclosures: Dr. Bahadur had no conflicts of interest to disclose.
Source: Bahadur S et al., Rheumatology. 2018;57[Suppl. 3]:key075.184
Methotrexate-induced pulmonary fibrosis risk examined in 10-year study
LIVERPOOL, ENGLAND – A 10-year follow up of patients with inflammatory arthritis has shown that methotrexate does not appear to increase the risk of pulmonary fibrosis.
“As rheumatologists, it’s a really important message that methotrexate does not cause chronic pulmonary fibrosis and it should not be stopped because of pulmonary fibrosis,” Julie Dawson, MD, said in an interview at the British Society for Rheumatology annual conference. “It’s the rheumatoid arthritis. It’s not the methotrexate.”
Dr. Dawson, of St. Helens and Knowsley Teaching Hospitals NHS Trust, St. Helens, England, added that the current findings were consistent with her team’s prior research looking at earlier time periods. There was also no correlation between the duration or dose of methotrexate used and the development of the lung disease, she said.
“If anything, the suggestion is you’d be more symptomatic if you delay using methotrexate,” Dr. Dawson observed. If patients are not doing well on methotrexate, then perhaps adjusting therapy or changing to another drug would of course be the next step, but if patients are well controlled then “stopping it is the worst thing to do” for their arthritis, she said.
“This is of great clinical interest, and we can be reassured now about this, I think. This is really good, long-term data,” said Devesh Mewar, MD, of Royal Liverpool and Broadgreen University Hospitals NHS Trust, Liverpool, England, who was not involved in the research.
“We know that methotrexate is associated with a pneumonitis reaction, but there is no high-quality evidence that methotrexate is associated with a chronic pulmonary fibrosis” Dr. Dawson said, explaining the rationale for the current study she presented during a poster session. Previous studies considered data for up to 5 years, she added, so the aim of the current study, therefore, was to look at the longer-term effect of methotrexate use on the incidence of pulmonary fibrosis.
Data on 129 patients who had started treatment with methotrexate from 2004 to 2007 were analyzed, of whom 63 (49%) had stayed on methotrexate for 10 or more years. Most (82%) had been given methotrexate to treat rheumatoid arthritis (RA), with other indications including inflammatory arthritis (5.4%) and psoriatic arthritis (4.7%).
“Practice was different 10 years ago, so just 56% of patients commenced methotrexate within the first year of the diagnosis of rheumatoid arthritis,” Dr. Dawson reported.
Only four cases of symptomatic pulmonary fibrosis were seen, all in the RA patients, and three of these were in patients who had started methotrexate over 1 year after their diagnosis. The incidence of 3.8% seen in the study matches the expected incidence of pulmonary fibrosis in RA and was actually “at the lower end of the expected incidence,” Dr. Dawson said. Previous studies have suggested an incidence rate of RA-associated interstitial lung disease of about 3%-7%.
All of the pulmonary fibrosis cases had occurred in men and 75% were seropositive for rheumatoid factor. The mean duration of RA at the time of onset of pulmonary fibrosis was 7.8 years and the usual interstitial pattern of fibrosis was seen. The 125 patients without pulmonary fibrosis had taken methotrexate for a mean of 8 years at a mean final weekly dose of 16.3 mg, compared with a mean of 6 years at a mean dose of 18.1 mg per week in the 4 patients with pulmonary fibrosis.
One of the next steps is to look at cases where methotrexate has been stopped and the effects of that on pulmonary fibrosis and disease activity. In Dr. Dawson’s experience, stopping methotrexate just affects the management of the arthritis and had no difference to the progression of pulmonary fibrosis.
If patients start to experience any lung symptoms while continuing methotrexate, such as shortness of breath, then they would need to be assessed and undergo lung function tests to monitor their condition. Treating the fibrosis using an antifibrotic drug, such as pirfenidone, is something that might be possible in the future, but this needs investigation in inflammatory arthritis as the drug is currently only licensed for use in idiopathic cases.
This is something the British Rheumatoid Interstitial Lung network plans to investigate in a placebo-controlled study of RA patients with fibrotic lung disease. “We’re looking to see if antifibrotic agents are going to slow the disease as it does in idiopathic pulmonary fibrosis, which is obviously quite exciting when it’s such a hard condition to treat,” said Dr. Dawson, who will be one of the study’s investigators.
Dr. Dawson had no conflicts of interest to disclose. Dr. Mewar was not involved in the study and had nothing to disclose.
SOURCE: Dawson J et al. Rheumatology. 2018;57[Suppl. 3]:key075.470.
The subject of this retrospective study is of great interest. The authors point out that pulmonary fibrosis (as opposed to acute allergic reaction, which is extremely rare) is also extremely uncommon in patients using methotrexate over the long haul. Over 10 years, their data points to a 3.1% incidence of symptomatic pulmonary fibrosis.
The issue here is its generalizability. There were 63 patients who used methotrexate for 10 years or more and 88 who used it for 5 years or more, according to the poster. This must represent a highly selected population. For example, what percent of the total RA/psoriatic arthritis/”inflammatory arthritis” population do these patients represent, i.e., what is the denominator here? The authors stated that the 63 patients who stayed on methotrexate for 10 or more years represent 49% of the 129 patients on methotrexate overall in the study. This is a highly unusual datum, as most of the literature indicates that only 40% or less of patients stay on methotrexate for even 5 years. And this completely ignores the issue of adherence over this long a period; these patients must represent a truly minuscule percentage of the total if they actually stayed on methotrexate with even moderate adherence for 10 years.
Importantly, the authors point out that they had only four cases of symptomatic pulmonary fibrosis. Once more, this points to the highly selective group of patients seen, as this study does not examine patients with asymptomatic pulmonary fibrosis, including those with fibrosis on high-resolution CT of the lungs or chest film or evidence of abnormalities on pulmonary function tests, but who do not have sufficient symptoms ascribed to methotrexate to bring them to medical attention.
This is a nice hypothesis-generating study, but the actual incidence of methotrexate-induced lung fibrosis remains completely unknown. I heartily applaud their intention to start a prospective study to answer this interesting question.
Daniel E. Furst, MD, is professor of rheumatology at the University of Washington, Seattle, who also is affiliated with the University of California, Los Angeles, and the University of Florence, Italy. He was not involved with the study.
The subject of this retrospective study is of great interest. The authors point out that pulmonary fibrosis (as opposed to acute allergic reaction, which is extremely rare) is also extremely uncommon in patients using methotrexate over the long haul. Over 10 years, their data points to a 3.1% incidence of symptomatic pulmonary fibrosis.
The issue here is its generalizability. There were 63 patients who used methotrexate for 10 years or more and 88 who used it for 5 years or more, according to the poster. This must represent a highly selected population. For example, what percent of the total RA/psoriatic arthritis/”inflammatory arthritis” population do these patients represent, i.e., what is the denominator here? The authors stated that the 63 patients who stayed on methotrexate for 10 or more years represent 49% of the 129 patients on methotrexate overall in the study. This is a highly unusual datum, as most of the literature indicates that only 40% or less of patients stay on methotrexate for even 5 years. And this completely ignores the issue of adherence over this long a period; these patients must represent a truly minuscule percentage of the total if they actually stayed on methotrexate with even moderate adherence for 10 years.
Importantly, the authors point out that they had only four cases of symptomatic pulmonary fibrosis. Once more, this points to the highly selective group of patients seen, as this study does not examine patients with asymptomatic pulmonary fibrosis, including those with fibrosis on high-resolution CT of the lungs or chest film or evidence of abnormalities on pulmonary function tests, but who do not have sufficient symptoms ascribed to methotrexate to bring them to medical attention.
This is a nice hypothesis-generating study, but the actual incidence of methotrexate-induced lung fibrosis remains completely unknown. I heartily applaud their intention to start a prospective study to answer this interesting question.
Daniel E. Furst, MD, is professor of rheumatology at the University of Washington, Seattle, who also is affiliated with the University of California, Los Angeles, and the University of Florence, Italy. He was not involved with the study.
The subject of this retrospective study is of great interest. The authors point out that pulmonary fibrosis (as opposed to acute allergic reaction, which is extremely rare) is also extremely uncommon in patients using methotrexate over the long haul. Over 10 years, their data points to a 3.1% incidence of symptomatic pulmonary fibrosis.
The issue here is its generalizability. There were 63 patients who used methotrexate for 10 years or more and 88 who used it for 5 years or more, according to the poster. This must represent a highly selected population. For example, what percent of the total RA/psoriatic arthritis/”inflammatory arthritis” population do these patients represent, i.e., what is the denominator here? The authors stated that the 63 patients who stayed on methotrexate for 10 or more years represent 49% of the 129 patients on methotrexate overall in the study. This is a highly unusual datum, as most of the literature indicates that only 40% or less of patients stay on methotrexate for even 5 years. And this completely ignores the issue of adherence over this long a period; these patients must represent a truly minuscule percentage of the total if they actually stayed on methotrexate with even moderate adherence for 10 years.
Importantly, the authors point out that they had only four cases of symptomatic pulmonary fibrosis. Once more, this points to the highly selective group of patients seen, as this study does not examine patients with asymptomatic pulmonary fibrosis, including those with fibrosis on high-resolution CT of the lungs or chest film or evidence of abnormalities on pulmonary function tests, but who do not have sufficient symptoms ascribed to methotrexate to bring them to medical attention.
This is a nice hypothesis-generating study, but the actual incidence of methotrexate-induced lung fibrosis remains completely unknown. I heartily applaud their intention to start a prospective study to answer this interesting question.
Daniel E. Furst, MD, is professor of rheumatology at the University of Washington, Seattle, who also is affiliated with the University of California, Los Angeles, and the University of Florence, Italy. He was not involved with the study.
LIVERPOOL, ENGLAND – A 10-year follow up of patients with inflammatory arthritis has shown that methotrexate does not appear to increase the risk of pulmonary fibrosis.
“As rheumatologists, it’s a really important message that methotrexate does not cause chronic pulmonary fibrosis and it should not be stopped because of pulmonary fibrosis,” Julie Dawson, MD, said in an interview at the British Society for Rheumatology annual conference. “It’s the rheumatoid arthritis. It’s not the methotrexate.”
Dr. Dawson, of St. Helens and Knowsley Teaching Hospitals NHS Trust, St. Helens, England, added that the current findings were consistent with her team’s prior research looking at earlier time periods. There was also no correlation between the duration or dose of methotrexate used and the development of the lung disease, she said.
“If anything, the suggestion is you’d be more symptomatic if you delay using methotrexate,” Dr. Dawson observed. If patients are not doing well on methotrexate, then perhaps adjusting therapy or changing to another drug would of course be the next step, but if patients are well controlled then “stopping it is the worst thing to do” for their arthritis, she said.
“This is of great clinical interest, and we can be reassured now about this, I think. This is really good, long-term data,” said Devesh Mewar, MD, of Royal Liverpool and Broadgreen University Hospitals NHS Trust, Liverpool, England, who was not involved in the research.
“We know that methotrexate is associated with a pneumonitis reaction, but there is no high-quality evidence that methotrexate is associated with a chronic pulmonary fibrosis” Dr. Dawson said, explaining the rationale for the current study she presented during a poster session. Previous studies considered data for up to 5 years, she added, so the aim of the current study, therefore, was to look at the longer-term effect of methotrexate use on the incidence of pulmonary fibrosis.
Data on 129 patients who had started treatment with methotrexate from 2004 to 2007 were analyzed, of whom 63 (49%) had stayed on methotrexate for 10 or more years. Most (82%) had been given methotrexate to treat rheumatoid arthritis (RA), with other indications including inflammatory arthritis (5.4%) and psoriatic arthritis (4.7%).
“Practice was different 10 years ago, so just 56% of patients commenced methotrexate within the first year of the diagnosis of rheumatoid arthritis,” Dr. Dawson reported.
Only four cases of symptomatic pulmonary fibrosis were seen, all in the RA patients, and three of these were in patients who had started methotrexate over 1 year after their diagnosis. The incidence of 3.8% seen in the study matches the expected incidence of pulmonary fibrosis in RA and was actually “at the lower end of the expected incidence,” Dr. Dawson said. Previous studies have suggested an incidence rate of RA-associated interstitial lung disease of about 3%-7%.
All of the pulmonary fibrosis cases had occurred in men and 75% were seropositive for rheumatoid factor. The mean duration of RA at the time of onset of pulmonary fibrosis was 7.8 years and the usual interstitial pattern of fibrosis was seen. The 125 patients without pulmonary fibrosis had taken methotrexate for a mean of 8 years at a mean final weekly dose of 16.3 mg, compared with a mean of 6 years at a mean dose of 18.1 mg per week in the 4 patients with pulmonary fibrosis.
One of the next steps is to look at cases where methotrexate has been stopped and the effects of that on pulmonary fibrosis and disease activity. In Dr. Dawson’s experience, stopping methotrexate just affects the management of the arthritis and had no difference to the progression of pulmonary fibrosis.
If patients start to experience any lung symptoms while continuing methotrexate, such as shortness of breath, then they would need to be assessed and undergo lung function tests to monitor their condition. Treating the fibrosis using an antifibrotic drug, such as pirfenidone, is something that might be possible in the future, but this needs investigation in inflammatory arthritis as the drug is currently only licensed for use in idiopathic cases.
This is something the British Rheumatoid Interstitial Lung network plans to investigate in a placebo-controlled study of RA patients with fibrotic lung disease. “We’re looking to see if antifibrotic agents are going to slow the disease as it does in idiopathic pulmonary fibrosis, which is obviously quite exciting when it’s such a hard condition to treat,” said Dr. Dawson, who will be one of the study’s investigators.
Dr. Dawson had no conflicts of interest to disclose. Dr. Mewar was not involved in the study and had nothing to disclose.
SOURCE: Dawson J et al. Rheumatology. 2018;57[Suppl. 3]:key075.470.
LIVERPOOL, ENGLAND – A 10-year follow up of patients with inflammatory arthritis has shown that methotrexate does not appear to increase the risk of pulmonary fibrosis.
“As rheumatologists, it’s a really important message that methotrexate does not cause chronic pulmonary fibrosis and it should not be stopped because of pulmonary fibrosis,” Julie Dawson, MD, said in an interview at the British Society for Rheumatology annual conference. “It’s the rheumatoid arthritis. It’s not the methotrexate.”
Dr. Dawson, of St. Helens and Knowsley Teaching Hospitals NHS Trust, St. Helens, England, added that the current findings were consistent with her team’s prior research looking at earlier time periods. There was also no correlation between the duration or dose of methotrexate used and the development of the lung disease, she said.
“If anything, the suggestion is you’d be more symptomatic if you delay using methotrexate,” Dr. Dawson observed. If patients are not doing well on methotrexate, then perhaps adjusting therapy or changing to another drug would of course be the next step, but if patients are well controlled then “stopping it is the worst thing to do” for their arthritis, she said.
“This is of great clinical interest, and we can be reassured now about this, I think. This is really good, long-term data,” said Devesh Mewar, MD, of Royal Liverpool and Broadgreen University Hospitals NHS Trust, Liverpool, England, who was not involved in the research.
“We know that methotrexate is associated with a pneumonitis reaction, but there is no high-quality evidence that methotrexate is associated with a chronic pulmonary fibrosis” Dr. Dawson said, explaining the rationale for the current study she presented during a poster session. Previous studies considered data for up to 5 years, she added, so the aim of the current study, therefore, was to look at the longer-term effect of methotrexate use on the incidence of pulmonary fibrosis.
Data on 129 patients who had started treatment with methotrexate from 2004 to 2007 were analyzed, of whom 63 (49%) had stayed on methotrexate for 10 or more years. Most (82%) had been given methotrexate to treat rheumatoid arthritis (RA), with other indications including inflammatory arthritis (5.4%) and psoriatic arthritis (4.7%).
“Practice was different 10 years ago, so just 56% of patients commenced methotrexate within the first year of the diagnosis of rheumatoid arthritis,” Dr. Dawson reported.
Only four cases of symptomatic pulmonary fibrosis were seen, all in the RA patients, and three of these were in patients who had started methotrexate over 1 year after their diagnosis. The incidence of 3.8% seen in the study matches the expected incidence of pulmonary fibrosis in RA and was actually “at the lower end of the expected incidence,” Dr. Dawson said. Previous studies have suggested an incidence rate of RA-associated interstitial lung disease of about 3%-7%.
All of the pulmonary fibrosis cases had occurred in men and 75% were seropositive for rheumatoid factor. The mean duration of RA at the time of onset of pulmonary fibrosis was 7.8 years and the usual interstitial pattern of fibrosis was seen. The 125 patients without pulmonary fibrosis had taken methotrexate for a mean of 8 years at a mean final weekly dose of 16.3 mg, compared with a mean of 6 years at a mean dose of 18.1 mg per week in the 4 patients with pulmonary fibrosis.
One of the next steps is to look at cases where methotrexate has been stopped and the effects of that on pulmonary fibrosis and disease activity. In Dr. Dawson’s experience, stopping methotrexate just affects the management of the arthritis and had no difference to the progression of pulmonary fibrosis.
If patients start to experience any lung symptoms while continuing methotrexate, such as shortness of breath, then they would need to be assessed and undergo lung function tests to monitor their condition. Treating the fibrosis using an antifibrotic drug, such as pirfenidone, is something that might be possible in the future, but this needs investigation in inflammatory arthritis as the drug is currently only licensed for use in idiopathic cases.
This is something the British Rheumatoid Interstitial Lung network plans to investigate in a placebo-controlled study of RA patients with fibrotic lung disease. “We’re looking to see if antifibrotic agents are going to slow the disease as it does in idiopathic pulmonary fibrosis, which is obviously quite exciting when it’s such a hard condition to treat,” said Dr. Dawson, who will be one of the study’s investigators.
Dr. Dawson had no conflicts of interest to disclose. Dr. Mewar was not involved in the study and had nothing to disclose.
SOURCE: Dawson J et al. Rheumatology. 2018;57[Suppl. 3]:key075.470.
REPORTING FROM RHEUMATOLOGY 2018
Key clinical point:
Major finding: At 10 years’ follow-up, four patients (3.1%) developed pulmonary fibrosis.
Study details: Retrospective analysis of 129 patients with inflammatory arthritis treated with methotrexate for up to 10 years.
Disclosures: Dr. Dawson had no conflicts of interest to disclose. Dr. Mewar was not involved in the study and had nothing to disclose.
Source: Dawson J et al. Rheumatology. 2018;57[Suppl. 3]:key075.470.
Heart disease in GPA exacts high toll in year 2 and beyond
LIVERPOOL, ENGLAND – Cardiovascular disease was the predominant cause of death of patients with granulomatosis with polyangiitis 1-5 years after a diagnosis in a study by U.K. researchers, suggesting that this could be a target for future intervention.
While active disease was the No. 1 cause of death within the first year of diagnosis in 40% of patients with granulomatosis with polyangiitis (GPA), it was overtaken by cardiovascular disease (CVD) as the main cause of death in 37.5% of patients in the next 4 years from diagnosis.
Nevertheless, active disease remained an important cause of death, accounting for 10% of deaths at 1-5 years, 18.2% at 5-10 years, and 16.7% at 10-15 years.
“The idea for this study came from patients with vasculitis who were polled by Vasculitis UK,” Fiona A. Pearce, MBBS, explained at the British Society for Rheumatology annual conference.
“Further research into mortality was one of their top priorities as patients want to know the honest truth about what is going to happen to them,” added Dr. Pearce, of the division of epidemiology and public health at the University of Nottingham (England).
GPA is a rare type of vasculitis that is estimated to occur in around 1,350 people every year in the United Kingdom. Mortality is known to be high, with around 11%-14% of patients dying in the first year of diagnosis, but there are few data on what happens over a longer term.
The aim of the study was therefore to examine patient survival in the long term – what were the mortality rates several years post diagnosis? Did the risk of death remain high throughout this time and did the causes of death change?
“Of course, the important clinical question was, “Can we then improve things?’ ” Dr. Pearce said.
Two U.K. databases – Clinical Practice Research Datalink and Hospital Episode Statistics – were used to identify patients with GPA diagnosed between 1998 and 2014 and match each case to 10 controls based on age, gender, and family practice. Data on the cause and date of any deaths were then obtained from the Office of National Statistics.
Overall, 465 cases of GPA were matched to 4,610 controls. The median age of participants was 61 years and 57% were male. There were 50 cases with more than 10 years of follow-up data available and data on 139 deaths could be analyzed.
A survival analysis showed that there was a significant reduction in cases versus controls, “but it’s not a constant,” Dr. Pearce noted.
“In the time immediately after diagnosis, the risk of death in people with GPA is very high, and over the first 6 months it tails off.” Then the mortalities are very similar, albeit much lower, to those of controls, but with another dip around 8 years.
The number at risk of death in the second year was 310 for GPA vs. 3,543 for controls and 230 vs. 2,622 at 4 years, 138 vs. 1,704 at 6 years, 93 vs. 1,136 at 8 years, and 49 vs. 658 at 10 years.
Looking at the data another way, the hazard ratios for death comparing GPA cases to controls was 24.5 in the first month, 14.6 in months 1-2, 7.5 by 2-3 months, 4.3 at 3-6 months, 1.6 at 6 months to 8 years, and 3.2 at 8-10 years.
Mortality seems to have improved with time. Splitting the cohort into two time periods based on their diagnosis, those diagnosed between 2008 and 2014 had a lower risk of death than did those diagnosed between 1998 and 2007, although it was still more than four times higher than the background population.
The leading cause of death in patients with GPA 5-10 years after diagnosis was cancer (30.3% of cases), but when this was compared against the general population, the risk was no greater (hazard ratio, 1.0).
GPA cases were also 2.9 times more likely than controls to die as a result of an infection, suggesting that this together with CVD could be a target for mortality reduction strategies.
“We can’t get away from the fact that although this is a large study, there are still small numbers of patients because this is rare disease,” Dr. Pearce observed. “We also don’t have detailed clinical information on each patient, so we can’t look for associations or clinical phenotypes at diagnosis, and there are no biomarkers.”
From a clinical perspective, she noted, it is important to remember that deaths in the first year are mainly from active disease and to continue to try to diagnose and treat the condition as early as possible.
Arthritis Research UK funded the trial. Dr. Pearce had nothing to disclose.
SOURCE: Pearce F et al. Rheumatology. 2018;57(Suppl. 3):key075.204.
LIVERPOOL, ENGLAND – Cardiovascular disease was the predominant cause of death of patients with granulomatosis with polyangiitis 1-5 years after a diagnosis in a study by U.K. researchers, suggesting that this could be a target for future intervention.
While active disease was the No. 1 cause of death within the first year of diagnosis in 40% of patients with granulomatosis with polyangiitis (GPA), it was overtaken by cardiovascular disease (CVD) as the main cause of death in 37.5% of patients in the next 4 years from diagnosis.
Nevertheless, active disease remained an important cause of death, accounting for 10% of deaths at 1-5 years, 18.2% at 5-10 years, and 16.7% at 10-15 years.
“The idea for this study came from patients with vasculitis who were polled by Vasculitis UK,” Fiona A. Pearce, MBBS, explained at the British Society for Rheumatology annual conference.
“Further research into mortality was one of their top priorities as patients want to know the honest truth about what is going to happen to them,” added Dr. Pearce, of the division of epidemiology and public health at the University of Nottingham (England).
GPA is a rare type of vasculitis that is estimated to occur in around 1,350 people every year in the United Kingdom. Mortality is known to be high, with around 11%-14% of patients dying in the first year of diagnosis, but there are few data on what happens over a longer term.
The aim of the study was therefore to examine patient survival in the long term – what were the mortality rates several years post diagnosis? Did the risk of death remain high throughout this time and did the causes of death change?
“Of course, the important clinical question was, “Can we then improve things?’ ” Dr. Pearce said.
Two U.K. databases – Clinical Practice Research Datalink and Hospital Episode Statistics – were used to identify patients with GPA diagnosed between 1998 and 2014 and match each case to 10 controls based on age, gender, and family practice. Data on the cause and date of any deaths were then obtained from the Office of National Statistics.
Overall, 465 cases of GPA were matched to 4,610 controls. The median age of participants was 61 years and 57% were male. There were 50 cases with more than 10 years of follow-up data available and data on 139 deaths could be analyzed.
A survival analysis showed that there was a significant reduction in cases versus controls, “but it’s not a constant,” Dr. Pearce noted.
“In the time immediately after diagnosis, the risk of death in people with GPA is very high, and over the first 6 months it tails off.” Then the mortalities are very similar, albeit much lower, to those of controls, but with another dip around 8 years.
The number at risk of death in the second year was 310 for GPA vs. 3,543 for controls and 230 vs. 2,622 at 4 years, 138 vs. 1,704 at 6 years, 93 vs. 1,136 at 8 years, and 49 vs. 658 at 10 years.
Looking at the data another way, the hazard ratios for death comparing GPA cases to controls was 24.5 in the first month, 14.6 in months 1-2, 7.5 by 2-3 months, 4.3 at 3-6 months, 1.6 at 6 months to 8 years, and 3.2 at 8-10 years.
Mortality seems to have improved with time. Splitting the cohort into two time periods based on their diagnosis, those diagnosed between 2008 and 2014 had a lower risk of death than did those diagnosed between 1998 and 2007, although it was still more than four times higher than the background population.
The leading cause of death in patients with GPA 5-10 years after diagnosis was cancer (30.3% of cases), but when this was compared against the general population, the risk was no greater (hazard ratio, 1.0).
GPA cases were also 2.9 times more likely than controls to die as a result of an infection, suggesting that this together with CVD could be a target for mortality reduction strategies.
“We can’t get away from the fact that although this is a large study, there are still small numbers of patients because this is rare disease,” Dr. Pearce observed. “We also don’t have detailed clinical information on each patient, so we can’t look for associations or clinical phenotypes at diagnosis, and there are no biomarkers.”
From a clinical perspective, she noted, it is important to remember that deaths in the first year are mainly from active disease and to continue to try to diagnose and treat the condition as early as possible.
Arthritis Research UK funded the trial. Dr. Pearce had nothing to disclose.
SOURCE: Pearce F et al. Rheumatology. 2018;57(Suppl. 3):key075.204.
LIVERPOOL, ENGLAND – Cardiovascular disease was the predominant cause of death of patients with granulomatosis with polyangiitis 1-5 years after a diagnosis in a study by U.K. researchers, suggesting that this could be a target for future intervention.
While active disease was the No. 1 cause of death within the first year of diagnosis in 40% of patients with granulomatosis with polyangiitis (GPA), it was overtaken by cardiovascular disease (CVD) as the main cause of death in 37.5% of patients in the next 4 years from diagnosis.
Nevertheless, active disease remained an important cause of death, accounting for 10% of deaths at 1-5 years, 18.2% at 5-10 years, and 16.7% at 10-15 years.
“The idea for this study came from patients with vasculitis who were polled by Vasculitis UK,” Fiona A. Pearce, MBBS, explained at the British Society for Rheumatology annual conference.
“Further research into mortality was one of their top priorities as patients want to know the honest truth about what is going to happen to them,” added Dr. Pearce, of the division of epidemiology and public health at the University of Nottingham (England).
GPA is a rare type of vasculitis that is estimated to occur in around 1,350 people every year in the United Kingdom. Mortality is known to be high, with around 11%-14% of patients dying in the first year of diagnosis, but there are few data on what happens over a longer term.
The aim of the study was therefore to examine patient survival in the long term – what were the mortality rates several years post diagnosis? Did the risk of death remain high throughout this time and did the causes of death change?
“Of course, the important clinical question was, “Can we then improve things?’ ” Dr. Pearce said.
Two U.K. databases – Clinical Practice Research Datalink and Hospital Episode Statistics – were used to identify patients with GPA diagnosed between 1998 and 2014 and match each case to 10 controls based on age, gender, and family practice. Data on the cause and date of any deaths were then obtained from the Office of National Statistics.
Overall, 465 cases of GPA were matched to 4,610 controls. The median age of participants was 61 years and 57% were male. There were 50 cases with more than 10 years of follow-up data available and data on 139 deaths could be analyzed.
A survival analysis showed that there was a significant reduction in cases versus controls, “but it’s not a constant,” Dr. Pearce noted.
“In the time immediately after diagnosis, the risk of death in people with GPA is very high, and over the first 6 months it tails off.” Then the mortalities are very similar, albeit much lower, to those of controls, but with another dip around 8 years.
The number at risk of death in the second year was 310 for GPA vs. 3,543 for controls and 230 vs. 2,622 at 4 years, 138 vs. 1,704 at 6 years, 93 vs. 1,136 at 8 years, and 49 vs. 658 at 10 years.
Looking at the data another way, the hazard ratios for death comparing GPA cases to controls was 24.5 in the first month, 14.6 in months 1-2, 7.5 by 2-3 months, 4.3 at 3-6 months, 1.6 at 6 months to 8 years, and 3.2 at 8-10 years.
Mortality seems to have improved with time. Splitting the cohort into two time periods based on their diagnosis, those diagnosed between 2008 and 2014 had a lower risk of death than did those diagnosed between 1998 and 2007, although it was still more than four times higher than the background population.
The leading cause of death in patients with GPA 5-10 years after diagnosis was cancer (30.3% of cases), but when this was compared against the general population, the risk was no greater (hazard ratio, 1.0).
GPA cases were also 2.9 times more likely than controls to die as a result of an infection, suggesting that this together with CVD could be a target for mortality reduction strategies.
“We can’t get away from the fact that although this is a large study, there are still small numbers of patients because this is rare disease,” Dr. Pearce observed. “We also don’t have detailed clinical information on each patient, so we can’t look for associations or clinical phenotypes at diagnosis, and there are no biomarkers.”
From a clinical perspective, she noted, it is important to remember that deaths in the first year are mainly from active disease and to continue to try to diagnose and treat the condition as early as possible.
Arthritis Research UK funded the trial. Dr. Pearce had nothing to disclose.
SOURCE: Pearce F et al. Rheumatology. 2018;57(Suppl. 3):key075.204.
REPORTING FROM RHEUMATOLOGY 2018
Key clinical point:
Major finding: The main cause of death changed from active disease (40% of all cases) within the first year to cardiovascular disease at years 1-5 (37.5%).
Study details: Retrospective cohort study of 465 individuals newly diagnosed with granulomatosis with polyangiitis matched to 4,610 controls from the general U.K. primary care population.
Disclosures: Arthritis Research UK funded the trial. Dr. Pearce had nothing to disclose.
Source: Pearce F et al. Rheumatology. 2018;57(Suppl. 3):key075.204.
Aim for remission, not low disease activity, in rheumatoid arthritis
LIVERPOOL, ENGLAND – , according to the conclusion of a study presented at the British Society for Rheumatology annual conference.
The study showed clear differences in functional and quality of life outcomes over time when comparing patients who achieved remission with those who achieved low disease activity.
Not only were better scores on the Health Assessment Questionnaire (HAQ) seen if remission were achieved rather than low disease activity, but also better scores were recorded using the Short Form–36 (SF-36) mental component and physical components.
Indeed, from baseline assessments to 12 months follow-up, HAQ scores fell from an average of about 0.8 for those in remission and 0.9 for those with a low disease activity index to approximately 0.4 and 0.6, respectively.
The physical component score of the SF-36 also improved from around 35 and 30 at baseline in the remission and low disease activity groups to just above 40 and just under 35, respectively, at 12 months.
Baseline SF-36 mental component scores were around 51 and 49 in each group, respectively, at baseline but improved to around 55 with remission and remained steady in the low disease activity group at 12 months.
“This is something you often don’t see,” observed Sam Norton, PhD, who presented the findings on behalf of the lead author Elena Nikiphorou, MD. Dr. Norton is a senior lecturer in the department of health psychology at King’s College London whose research interests lie in studying the psychological well-being and illness outcomes in rheumatoid arthritis and other chronic physical illnesses.
“Of course, there could be a bit of reverse causality with people with good mental health being more likely to hit remission, which is why you can see there is a gap at baseline as well,” Dr. Norton suggested.
The researchers used data on 2,701 patients who were enrolled in the Early Rheumatoid Arthritis Network (ERAN) and Early Rheumatoid Arthritis Study (ERAS) cohorts. The research question was whether achieving low disease activity was an acceptable target in rheumatoid arthritis, and if disease outcomes made a difference to those who achieved remission.
The mean age of participants was 55 years in ERAS and 57 years in ERAN, with a similar percentage of female participants (67%), and slightly better baseline HAQ and Disease Activity Scale scores in the ERAN cohort, which is to be expected, Dr. Norton said, as this was a later-recruited population of patients (2002-2013 vs. 1986-2000 for ERAS).
Disease activity was categorized in three ways: firstly, remission or low disease activity over 1-5 years were defined as mean DAS28 score of less than 2.6 and a score of 2.6-3.2, respectively. Secondly, sustained low disease activity or remission was considered over 1-2 years, and thirdly, Boolean remission over 1-2 years, which are strict criteria of remission to meet.
Overall, 23.4% of patients achieved remission and 13.7% achieved low disease activity, and a respective 10.3% and 13.7% met criteria for sustained remission or sustained low disease activity. Just 3.4% met Boolean criteria for remission.
“The key messages are: There is a really important difference between remission and low disease activity score categories and that treating people to a remission target means they will do better in terms of quality of life outcomes over time compared to just stopping at a low disease activity,” Dr. Norton noted.
There was an important caveat to stating that remission should be the primary treat-to-target goal, in that there will likely be a relatively small proportion of patients that will achieve the strictest definition of remission, he added. Perhaps different targets need to be set for those with comorbidities or who are older.
“So, while remission should be a primary target there should be other targets considered alongside that,” he proposed.
Dr. Norton and his coauthors had nothing to disclose.
SOURCE: Nikiphorou E et al. Rheumatology. 2018;57[Suppl. 3]:key075.189.
LIVERPOOL, ENGLAND – , according to the conclusion of a study presented at the British Society for Rheumatology annual conference.
The study showed clear differences in functional and quality of life outcomes over time when comparing patients who achieved remission with those who achieved low disease activity.
Not only were better scores on the Health Assessment Questionnaire (HAQ) seen if remission were achieved rather than low disease activity, but also better scores were recorded using the Short Form–36 (SF-36) mental component and physical components.
Indeed, from baseline assessments to 12 months follow-up, HAQ scores fell from an average of about 0.8 for those in remission and 0.9 for those with a low disease activity index to approximately 0.4 and 0.6, respectively.
The physical component score of the SF-36 also improved from around 35 and 30 at baseline in the remission and low disease activity groups to just above 40 and just under 35, respectively, at 12 months.
Baseline SF-36 mental component scores were around 51 and 49 in each group, respectively, at baseline but improved to around 55 with remission and remained steady in the low disease activity group at 12 months.
“This is something you often don’t see,” observed Sam Norton, PhD, who presented the findings on behalf of the lead author Elena Nikiphorou, MD. Dr. Norton is a senior lecturer in the department of health psychology at King’s College London whose research interests lie in studying the psychological well-being and illness outcomes in rheumatoid arthritis and other chronic physical illnesses.
“Of course, there could be a bit of reverse causality with people with good mental health being more likely to hit remission, which is why you can see there is a gap at baseline as well,” Dr. Norton suggested.
The researchers used data on 2,701 patients who were enrolled in the Early Rheumatoid Arthritis Network (ERAN) and Early Rheumatoid Arthritis Study (ERAS) cohorts. The research question was whether achieving low disease activity was an acceptable target in rheumatoid arthritis, and if disease outcomes made a difference to those who achieved remission.
The mean age of participants was 55 years in ERAS and 57 years in ERAN, with a similar percentage of female participants (67%), and slightly better baseline HAQ and Disease Activity Scale scores in the ERAN cohort, which is to be expected, Dr. Norton said, as this was a later-recruited population of patients (2002-2013 vs. 1986-2000 for ERAS).
Disease activity was categorized in three ways: firstly, remission or low disease activity over 1-5 years were defined as mean DAS28 score of less than 2.6 and a score of 2.6-3.2, respectively. Secondly, sustained low disease activity or remission was considered over 1-2 years, and thirdly, Boolean remission over 1-2 years, which are strict criteria of remission to meet.
Overall, 23.4% of patients achieved remission and 13.7% achieved low disease activity, and a respective 10.3% and 13.7% met criteria for sustained remission or sustained low disease activity. Just 3.4% met Boolean criteria for remission.
“The key messages are: There is a really important difference between remission and low disease activity score categories and that treating people to a remission target means they will do better in terms of quality of life outcomes over time compared to just stopping at a low disease activity,” Dr. Norton noted.
There was an important caveat to stating that remission should be the primary treat-to-target goal, in that there will likely be a relatively small proportion of patients that will achieve the strictest definition of remission, he added. Perhaps different targets need to be set for those with comorbidities or who are older.
“So, while remission should be a primary target there should be other targets considered alongside that,” he proposed.
Dr. Norton and his coauthors had nothing to disclose.
SOURCE: Nikiphorou E et al. Rheumatology. 2018;57[Suppl. 3]:key075.189.
LIVERPOOL, ENGLAND – , according to the conclusion of a study presented at the British Society for Rheumatology annual conference.
The study showed clear differences in functional and quality of life outcomes over time when comparing patients who achieved remission with those who achieved low disease activity.
Not only were better scores on the Health Assessment Questionnaire (HAQ) seen if remission were achieved rather than low disease activity, but also better scores were recorded using the Short Form–36 (SF-36) mental component and physical components.
Indeed, from baseline assessments to 12 months follow-up, HAQ scores fell from an average of about 0.8 for those in remission and 0.9 for those with a low disease activity index to approximately 0.4 and 0.6, respectively.
The physical component score of the SF-36 also improved from around 35 and 30 at baseline in the remission and low disease activity groups to just above 40 and just under 35, respectively, at 12 months.
Baseline SF-36 mental component scores were around 51 and 49 in each group, respectively, at baseline but improved to around 55 with remission and remained steady in the low disease activity group at 12 months.
“This is something you often don’t see,” observed Sam Norton, PhD, who presented the findings on behalf of the lead author Elena Nikiphorou, MD. Dr. Norton is a senior lecturer in the department of health psychology at King’s College London whose research interests lie in studying the psychological well-being and illness outcomes in rheumatoid arthritis and other chronic physical illnesses.
“Of course, there could be a bit of reverse causality with people with good mental health being more likely to hit remission, which is why you can see there is a gap at baseline as well,” Dr. Norton suggested.
The researchers used data on 2,701 patients who were enrolled in the Early Rheumatoid Arthritis Network (ERAN) and Early Rheumatoid Arthritis Study (ERAS) cohorts. The research question was whether achieving low disease activity was an acceptable target in rheumatoid arthritis, and if disease outcomes made a difference to those who achieved remission.
The mean age of participants was 55 years in ERAS and 57 years in ERAN, with a similar percentage of female participants (67%), and slightly better baseline HAQ and Disease Activity Scale scores in the ERAN cohort, which is to be expected, Dr. Norton said, as this was a later-recruited population of patients (2002-2013 vs. 1986-2000 for ERAS).
Disease activity was categorized in three ways: firstly, remission or low disease activity over 1-5 years were defined as mean DAS28 score of less than 2.6 and a score of 2.6-3.2, respectively. Secondly, sustained low disease activity or remission was considered over 1-2 years, and thirdly, Boolean remission over 1-2 years, which are strict criteria of remission to meet.
Overall, 23.4% of patients achieved remission and 13.7% achieved low disease activity, and a respective 10.3% and 13.7% met criteria for sustained remission or sustained low disease activity. Just 3.4% met Boolean criteria for remission.
“The key messages are: There is a really important difference between remission and low disease activity score categories and that treating people to a remission target means they will do better in terms of quality of life outcomes over time compared to just stopping at a low disease activity,” Dr. Norton noted.
There was an important caveat to stating that remission should be the primary treat-to-target goal, in that there will likely be a relatively small proportion of patients that will achieve the strictest definition of remission, he added. Perhaps different targets need to be set for those with comorbidities or who are older.
“So, while remission should be a primary target there should be other targets considered alongside that,” he proposed.
Dr. Norton and his coauthors had nothing to disclose.
SOURCE: Nikiphorou E et al. Rheumatology. 2018;57[Suppl. 3]:key075.189.
REPORTING FROM RHEUMATOLOGY 2018
Key clinical point: Better outcomes were achieved if patients with rheumatoid arthritis met criteria for remission rather than low disease activity.
Major finding: The study showed clear differences in functional and quality of life outcomes over time when comparing patients who achieved remission with those who achieved low disease activity.
Study details: A prospective study of 2,701 patients enrolled in two early rheumatoid arthritis cohorts.
Disclosures: Dr. Norton and his coauthors had nothing to disclose.
Source: Nikiphorou E et al. Rheumatology. 2018;57[Suppl. 3]:key075.189.