Osteoarthritis

Updated EULAR recommendations on the management of hand osteoarthritis include five overarching principles as well as two new recommendations that reflect new research in the field.

Astrid860/Getty Images

The task force, led by Margreet Kloppenburg, MD, PhD, of the department of rheumatology at Leiden (the Netherlands) University Medical Center, noted that a decade had passed since the first recommendations were published in 2007.

“It was timely to update the recommendations, as many new studies had emerged during this period. In light of this new evidence, many of the 2007 recommendations were modified and new recommendations were added,” wrote Dr. Kloppenburg and her colleagues. The recommendations were published online in Annals of the Rheumatic Diseases.

They noted that the recommendations were targeted to all health professionals across primary and secondary care but also aimed to inform patients about their disease to “support shared decision making.”

In line with other EULAR sets of management recommendations, the update included five overarching principles that cover treatment goals, information and education for patients, individualization of treatment, shared decision making between clinicians and patients, and the need to take into consideration a multidisciplinary and multimodal (pharmacologic and nonpharmacologic) treatment approach.

The authors noted that for a long time hand OA was a “forgotten disease” and this was reflected by the paucity of clinical trials in the area. As a direct consequence, previous recommendations were based on expert opinion rather than evidence.

However, new data allowed the task force to recommend not to treat patients with hand OA with conventional synthetic or biologic disease-modifying antirheumatic drugs (DMARDs). The recommendation achieved the strongest level of evidence and a high level of agreement from the 19-member expert panel, which included 2 patient research partners. The authors said the recommendation was based on newer studies that demonstrated a lack of efficacy of csDMARDs and bDMARDs.

The authors also advised adapting the long-term follow-up of patients with hand OA to individual needs, although they noted this was based on expert opinion alone and that in the absence of a disease-modifying treatment, the goal of follow-up differs from that of many other rheumatic diseases. Individual needs will dictate the degree of follow-up required, based on the severity of symptoms, presence of erosive disease, reevaluation of the use of pharmacologic therapy, and a patient’s wishes and expectations. They also noted that “for most patients, standard radiographic follow-up is not useful at this moment” and that “follow-up does not necessarily have to be performed by a rheumatologist.

“Follow-up will likely increase adherence to nonpharmacological therapies like exercise or orthoses, and provides an opportunity for reevaluation of treatment,” they wrote.

The recommendations advise offering education and training in ergonomic principles and exercises to patients to improve function and muscle strength, as well as considering the use of orthoses in some patients.

Treatment recommendations suggested preferring topical treatments over systemic treatments and that oral analgesics, particularly NSAIDs, should be considered for a limited duration. The authors advised that chondroitin sulfate may be used in patients for pain relief and improvement in functioning and that intra-articular glucocorticoids should not generally be used but may be considered in patients with painful interphalangeal joints. Surgery should be considered for patients with structural abnormalities when other treatment modalities have not been sufficiently effective in relieving pain.

The recommendations were funded by EULAR. Several of the authors reported receiving consultancy fees and/or honoraria as well as research funding from industry.

SOURCE: Kloppenburg M et al. Ann Rheum Dis. 2018 Aug 28. doi: 10.1136/annrheumdis-2018-213826.

Updated EULAR recommendations on the management of hand osteoarthritis include five overarching principles as well as two new recommendations that reflect new research in the field.

Astrid860/Getty Images

The task force, led by Margreet Kloppenburg, MD, PhD, of the department of rheumatology at Leiden (the Netherlands) University Medical Center, noted that a decade had passed since the first recommendations were published in 2007.

“It was timely to update the recommendations, as many new studies had emerged during this period. In light of this new evidence, many of the 2007 recommendations were modified and new recommendations were added,” wrote Dr. Kloppenburg and her colleagues. The recommendations were published online in Annals of the Rheumatic Diseases.

They noted that the recommendations were targeted to all health professionals across primary and secondary care but also aimed to inform patients about their disease to “support shared decision making.”

In line with other EULAR sets of management recommendations, the update included five overarching principles that cover treatment goals, information and education for patients, individualization of treatment, shared decision making between clinicians and patients, and the need to take into consideration a multidisciplinary and multimodal (pharmacologic and nonpharmacologic) treatment approach.

The authors noted that for a long time hand OA was a “forgotten disease” and this was reflected by the paucity of clinical trials in the area. As a direct consequence, previous recommendations were based on expert opinion rather than evidence.

However, new data allowed the task force to recommend not to treat patients with hand OA with conventional synthetic or biologic disease-modifying antirheumatic drugs (DMARDs). The recommendation achieved the strongest level of evidence and a high level of agreement from the 19-member expert panel, which included 2 patient research partners. The authors said the recommendation was based on newer studies that demonstrated a lack of efficacy of csDMARDs and bDMARDs.

The authors also advised adapting the long-term follow-up of patients with hand OA to individual needs, although they noted this was based on expert opinion alone and that in the absence of a disease-modifying treatment, the goal of follow-up differs from that of many other rheumatic diseases. Individual needs will dictate the degree of follow-up required, based on the severity of symptoms, presence of erosive disease, reevaluation of the use of pharmacologic therapy, and a patient’s wishes and expectations. They also noted that “for most patients, standard radiographic follow-up is not useful at this moment” and that “follow-up does not necessarily have to be performed by a rheumatologist.

“Follow-up will likely increase adherence to nonpharmacological therapies like exercise or orthoses, and provides an opportunity for reevaluation of treatment,” they wrote.

The recommendations advise offering education and training in ergonomic principles and exercises to patients to improve function and muscle strength, as well as considering the use of orthoses in some patients.

Treatment recommendations suggested preferring topical treatments over systemic treatments and that oral analgesics, particularly NSAIDs, should be considered for a limited duration. The authors advised that chondroitin sulfate may be used in patients for pain relief and improvement in functioning and that intra-articular glucocorticoids should not generally be used but may be considered in patients with painful interphalangeal joints. Surgery should be considered for patients with structural abnormalities when other treatment modalities have not been sufficiently effective in relieving pain.

The recommendations were funded by EULAR. Several of the authors reported receiving consultancy fees and/or honoraria as well as research funding from industry.

SOURCE: Kloppenburg M et al. Ann Rheum Dis. 2018 Aug 28. doi: 10.1136/annrheumdis-2018-213826.

Updated EULAR recommendations on the management of hand osteoarthritis include five overarching principles as well as two new recommendations that reflect new research in the field.

Astrid860/Getty Images

The task force, led by Margreet Kloppenburg, MD, PhD, of the department of rheumatology at Leiden (the Netherlands) University Medical Center, noted that a decade had passed since the first recommendations were published in 2007.

“It was timely to update the recommendations, as many new studies had emerged during this period. In light of this new evidence, many of the 2007 recommendations were modified and new recommendations were added,” wrote Dr. Kloppenburg and her colleagues. The recommendations were published online in Annals of the Rheumatic Diseases.

They noted that the recommendations were targeted to all health professionals across primary and secondary care but also aimed to inform patients about their disease to “support shared decision making.”

In line with other EULAR sets of management recommendations, the update included five overarching principles that cover treatment goals, information and education for patients, individualization of treatment, shared decision making between clinicians and patients, and the need to take into consideration a multidisciplinary and multimodal (pharmacologic and nonpharmacologic) treatment approach.

The authors noted that for a long time hand OA was a “forgotten disease” and this was reflected by the paucity of clinical trials in the area. As a direct consequence, previous recommendations were based on expert opinion rather than evidence.

However, new data allowed the task force to recommend not to treat patients with hand OA with conventional synthetic or biologic disease-modifying antirheumatic drugs (DMARDs). The recommendation achieved the strongest level of evidence and a high level of agreement from the 19-member expert panel, which included 2 patient research partners. The authors said the recommendation was based on newer studies that demonstrated a lack of efficacy of csDMARDs and bDMARDs.

The authors also advised adapting the long-term follow-up of patients with hand OA to individual needs, although they noted this was based on expert opinion alone and that in the absence of a disease-modifying treatment, the goal of follow-up differs from that of many other rheumatic diseases. Individual needs will dictate the degree of follow-up required, based on the severity of symptoms, presence of erosive disease, reevaluation of the use of pharmacologic therapy, and a patient’s wishes and expectations. They also noted that “for most patients, standard radiographic follow-up is not useful at this moment” and that “follow-up does not necessarily have to be performed by a rheumatologist.

“Follow-up will likely increase adherence to nonpharmacological therapies like exercise or orthoses, and provides an opportunity for reevaluation of treatment,” they wrote.

The recommendations advise offering education and training in ergonomic principles and exercises to patients to improve function and muscle strength, as well as considering the use of orthoses in some patients.

Treatment recommendations suggested preferring topical treatments over systemic treatments and that oral analgesics, particularly NSAIDs, should be considered for a limited duration. The authors advised that chondroitin sulfate may be used in patients for pain relief and improvement in functioning and that intra-articular glucocorticoids should not generally be used but may be considered in patients with painful interphalangeal joints. Surgery should be considered for patients with structural abnormalities when other treatment modalities have not been sufficiently effective in relieving pain.

The recommendations were funded by EULAR. Several of the authors reported receiving consultancy fees and/or honoraria as well as research funding from industry.

SOURCE: Kloppenburg M et al. Ann Rheum Dis. 2018 Aug 28. doi: 10.1136/annrheumdis-2018-213826.

In the largest analysis ever of cardiovascular risk associated with the initiation of nonsteroidal anti-inflammatory drugs (NSAIDs), diclofenac emerged as a clear culprit in higher risk for adverse cardiovascular outcomes.

Those beginning diclofenac had a 50% increased 30-day risk for a composite outcome of major adverse cardiovascular events (MACE) compared with individuals who didn’t initiate an NSAID or acetaminophen (95% confidence interval for incidence rate ratio, 1.4-1.7).

The risk was still significantly elevated when the study’s first author, Morten Schmidt, MD, and his colleagues compared diclofenac initiation with beginning other NSAIDs or acetaminophen. Compared with those starting ibuprofen or acetaminophen, the MACE risk was elevated 20% in diclofenac initiators (95% CI, 1.1-1.3 for both). Initiating diclofenac was associated with 30% greater risk for MACE compared with initiating naproxen (95% CI, 1.1-1.5).

“Diclofenac is the most frequently used NSAID in low-, middle-, and high-income countries and is available over the counter in most countries; therefore, its cardiovascular risk profile is of major clinical and public health importance,” wrote Dr. Schmidt and his coauthors.

In all, the study included 1,370,832 individuals who initiated diclofenac, 3,878,454 ibuprofen initiators, 291,490 naproxen initiators, and 764,781 acetaminophen initiators. Those starting diclofenac were compared with those starting other medications, and with 1,303,209 individuals who sought health care but did not start one of the medications.

The researchers used the longstanding and complete Danish health registry system to their advantage in designing a cohort trial that was modeled to resemble a clinical trial. For each month, beginning in 1996 and continuing through 2016, Dr. Schmidt and his collaborators assembled propensity-matched cohorts of individuals to compare each study group. The study design achieved many of the aims of a clinical trial while working within the ethical constraints of studying medications now known to elevate cardiovascular risk.

For each 30-day period, the investigators were then able to track and compare cardiovascular outcomes for each group. Each month, data for a new cohort were collected, beginning a new “clinical trial.” Individuals could be included in more than one month’s worth of “trial” data as long as they continued to meet inclusion criteria.

The completeness of Danish health data meant that the researchers were confident in data about comorbidities, other prescription medications, and outcomes.

Dr. Schmidt and his colleagues performed subgroup and sensitivity analyses to look at the extent to which preexisting risks for cardiovascular disease mediated MACE risk on diclofenac initiation. They found that diclofenac initiators in the highest risk group had up to 40 excess cardiovascular events per year – about half of them fatal – that were attributable to starting the medication. Although that group had the highest absolute risk, however, “the relative risks were highest in those with the lowest baseline risk,” wrote the investigators.

In addition to looking at rates of MACE, secondary outcomes for the study included evaluating the association between medication use or non-use and each individual component of the composite primary outcome. These included first-time occurrences of the nonfatal endpoints of atrial fibrillation or flutter, ischemic (but not hemorrhagic) stroke, heart failure, and myocardial infarction. Cardiac death was death from any cardiac cause.

“Supporting use of a combined endpoint, event rates consistently increased for all individual outcomes” for diclofenac initiators compared with those who did not start an NSAID, wrote Dr. Schmidt and his colleagues.

Individuals were excluded if they had known cardiovascular, kidney, liver, or ulcer disease, and if they had malignancy or serious mental health diagnoses such as dementia or schizophrenia. Participants, aged a mean 48-56 years, had to be at least 18 years of age and could not have filled a prescription for an NSAID within the previous 12 months. Men made up 36.6%-46.3% of the cohorts.

Dr. Schmidt, of Aarhus (Denmark) University, and his collaborators said that in comparison with other NSAIDs, the short half-life of diclofenac means that a supratherapeutic plasma concentration of diclofenac soon after initiation achieves not just cyclooxygenase-2 (COX-2), but also COX-1 inhibition. However, after those high levels fall, patients taking diclofenac spend a substantial period of time with unopposed COX-2 inhibition, a state that is known to be prothrombotic, and also associated with blood pressure elevation, atherogenesis, and worsening of heart failure.

Diclofenac and ibuprofen had similar gastrointestinal bleeding risks, and both medications were associated with a higher risk of bleeding than were ibuprofen, acetaminophen, or no medication.

“Comparing diclofenac initiation with no NSAID initiation, the consistency between our results and those of previous meta-analyses of both trial and observational data provides strong evidence to guide clinical decision making,” said Dr. Schmidt and his coauthors.

“Considering its cardiovascular and gastrointestinal risks, however, there is little justification to initiate diclofenac treatment before other traditional NSAIDs,” noted the investigators. “It is time to acknowledge the potential health risk of diclofenac and to reduce its use.”

The study was funded by the Department of Clinical Epidemiology Research Foundation, University of Aarhus, and by the Program for Clinical Research Infrastructure, funded by the Lundbeck Foundation, Novo Nordisk Foundation, and the Danish Research Council. The authors reported that they had no relevant conflicts of interest.
 

[email protected]

SOURCE: Schmidt M et al. BMJ 2018;362:k3426

In the largest analysis ever of cardiovascular risk associated with the initiation of nonsteroidal anti-inflammatory drugs (NSAIDs), diclofenac emerged as a clear culprit in higher risk for adverse cardiovascular outcomes.

Those beginning diclofenac had a 50% increased 30-day risk for a composite outcome of major adverse cardiovascular events (MACE) compared with individuals who didn’t initiate an NSAID or acetaminophen (95% confidence interval for incidence rate ratio, 1.4-1.7).

The risk was still significantly elevated when the study’s first author, Morten Schmidt, MD, and his colleagues compared diclofenac initiation with beginning other NSAIDs or acetaminophen. Compared with those starting ibuprofen or acetaminophen, the MACE risk was elevated 20% in diclofenac initiators (95% CI, 1.1-1.3 for both). Initiating diclofenac was associated with 30% greater risk for MACE compared with initiating naproxen (95% CI, 1.1-1.5).

“Diclofenac is the most frequently used NSAID in low-, middle-, and high-income countries and is available over the counter in most countries; therefore, its cardiovascular risk profile is of major clinical and public health importance,” wrote Dr. Schmidt and his coauthors.

In all, the study included 1,370,832 individuals who initiated diclofenac, 3,878,454 ibuprofen initiators, 291,490 naproxen initiators, and 764,781 acetaminophen initiators. Those starting diclofenac were compared with those starting other medications, and with 1,303,209 individuals who sought health care but did not start one of the medications.

The researchers used the longstanding and complete Danish health registry system to their advantage in designing a cohort trial that was modeled to resemble a clinical trial. For each month, beginning in 1996 and continuing through 2016, Dr. Schmidt and his collaborators assembled propensity-matched cohorts of individuals to compare each study group. The study design achieved many of the aims of a clinical trial while working within the ethical constraints of studying medications now known to elevate cardiovascular risk.

For each 30-day period, the investigators were then able to track and compare cardiovascular outcomes for each group. Each month, data for a new cohort were collected, beginning a new “clinical trial.” Individuals could be included in more than one month’s worth of “trial” data as long as they continued to meet inclusion criteria.

The completeness of Danish health data meant that the researchers were confident in data about comorbidities, other prescription medications, and outcomes.

Dr. Schmidt and his colleagues performed subgroup and sensitivity analyses to look at the extent to which preexisting risks for cardiovascular disease mediated MACE risk on diclofenac initiation. They found that diclofenac initiators in the highest risk group had up to 40 excess cardiovascular events per year – about half of them fatal – that were attributable to starting the medication. Although that group had the highest absolute risk, however, “the relative risks were highest in those with the lowest baseline risk,” wrote the investigators.

In addition to looking at rates of MACE, secondary outcomes for the study included evaluating the association between medication use or non-use and each individual component of the composite primary outcome. These included first-time occurrences of the nonfatal endpoints of atrial fibrillation or flutter, ischemic (but not hemorrhagic) stroke, heart failure, and myocardial infarction. Cardiac death was death from any cardiac cause.

“Supporting use of a combined endpoint, event rates consistently increased for all individual outcomes” for diclofenac initiators compared with those who did not start an NSAID, wrote Dr. Schmidt and his colleagues.

Individuals were excluded if they had known cardiovascular, kidney, liver, or ulcer disease, and if they had malignancy or serious mental health diagnoses such as dementia or schizophrenia. Participants, aged a mean 48-56 years, had to be at least 18 years of age and could not have filled a prescription for an NSAID within the previous 12 months. Men made up 36.6%-46.3% of the cohorts.

Dr. Schmidt, of Aarhus (Denmark) University, and his collaborators said that in comparison with other NSAIDs, the short half-life of diclofenac means that a supratherapeutic plasma concentration of diclofenac soon after initiation achieves not just cyclooxygenase-2 (COX-2), but also COX-1 inhibition. However, after those high levels fall, patients taking diclofenac spend a substantial period of time with unopposed COX-2 inhibition, a state that is known to be prothrombotic, and also associated with blood pressure elevation, atherogenesis, and worsening of heart failure.

Diclofenac and ibuprofen had similar gastrointestinal bleeding risks, and both medications were associated with a higher risk of bleeding than were ibuprofen, acetaminophen, or no medication.

“Comparing diclofenac initiation with no NSAID initiation, the consistency between our results and those of previous meta-analyses of both trial and observational data provides strong evidence to guide clinical decision making,” said Dr. Schmidt and his coauthors.

“Considering its cardiovascular and gastrointestinal risks, however, there is little justification to initiate diclofenac treatment before other traditional NSAIDs,” noted the investigators. “It is time to acknowledge the potential health risk of diclofenac and to reduce its use.”

The study was funded by the Department of Clinical Epidemiology Research Foundation, University of Aarhus, and by the Program for Clinical Research Infrastructure, funded by the Lundbeck Foundation, Novo Nordisk Foundation, and the Danish Research Council. The authors reported that they had no relevant conflicts of interest.
 

[email protected]

SOURCE: Schmidt M et al. BMJ 2018;362:k3426

In the largest analysis ever of cardiovascular risk associated with the initiation of nonsteroidal anti-inflammatory drugs (NSAIDs), diclofenac emerged as a clear culprit in higher risk for adverse cardiovascular outcomes.

Those beginning diclofenac had a 50% increased 30-day risk for a composite outcome of major adverse cardiovascular events (MACE) compared with individuals who didn’t initiate an NSAID or acetaminophen (95% confidence interval for incidence rate ratio, 1.4-1.7).

The risk was still significantly elevated when the study’s first author, Morten Schmidt, MD, and his colleagues compared diclofenac initiation with beginning other NSAIDs or acetaminophen. Compared with those starting ibuprofen or acetaminophen, the MACE risk was elevated 20% in diclofenac initiators (95% CI, 1.1-1.3 for both). Initiating diclofenac was associated with 30% greater risk for MACE compared with initiating naproxen (95% CI, 1.1-1.5).

“Diclofenac is the most frequently used NSAID in low-, middle-, and high-income countries and is available over the counter in most countries; therefore, its cardiovascular risk profile is of major clinical and public health importance,” wrote Dr. Schmidt and his coauthors.

In all, the study included 1,370,832 individuals who initiated diclofenac, 3,878,454 ibuprofen initiators, 291,490 naproxen initiators, and 764,781 acetaminophen initiators. Those starting diclofenac were compared with those starting other medications, and with 1,303,209 individuals who sought health care but did not start one of the medications.

The researchers used the longstanding and complete Danish health registry system to their advantage in designing a cohort trial that was modeled to resemble a clinical trial. For each month, beginning in 1996 and continuing through 2016, Dr. Schmidt and his collaborators assembled propensity-matched cohorts of individuals to compare each study group. The study design achieved many of the aims of a clinical trial while working within the ethical constraints of studying medications now known to elevate cardiovascular risk.

For each 30-day period, the investigators were then able to track and compare cardiovascular outcomes for each group. Each month, data for a new cohort were collected, beginning a new “clinical trial.” Individuals could be included in more than one month’s worth of “trial” data as long as they continued to meet inclusion criteria.

The completeness of Danish health data meant that the researchers were confident in data about comorbidities, other prescription medications, and outcomes.

Dr. Schmidt and his colleagues performed subgroup and sensitivity analyses to look at the extent to which preexisting risks for cardiovascular disease mediated MACE risk on diclofenac initiation. They found that diclofenac initiators in the highest risk group had up to 40 excess cardiovascular events per year – about half of them fatal – that were attributable to starting the medication. Although that group had the highest absolute risk, however, “the relative risks were highest in those with the lowest baseline risk,” wrote the investigators.

In addition to looking at rates of MACE, secondary outcomes for the study included evaluating the association between medication use or non-use and each individual component of the composite primary outcome. These included first-time occurrences of the nonfatal endpoints of atrial fibrillation or flutter, ischemic (but not hemorrhagic) stroke, heart failure, and myocardial infarction. Cardiac death was death from any cardiac cause.

“Supporting use of a combined endpoint, event rates consistently increased for all individual outcomes” for diclofenac initiators compared with those who did not start an NSAID, wrote Dr. Schmidt and his colleagues.

Individuals were excluded if they had known cardiovascular, kidney, liver, or ulcer disease, and if they had malignancy or serious mental health diagnoses such as dementia or schizophrenia. Participants, aged a mean 48-56 years, had to be at least 18 years of age and could not have filled a prescription for an NSAID within the previous 12 months. Men made up 36.6%-46.3% of the cohorts.

Dr. Schmidt, of Aarhus (Denmark) University, and his collaborators said that in comparison with other NSAIDs, the short half-life of diclofenac means that a supratherapeutic plasma concentration of diclofenac soon after initiation achieves not just cyclooxygenase-2 (COX-2), but also COX-1 inhibition. However, after those high levels fall, patients taking diclofenac spend a substantial period of time with unopposed COX-2 inhibition, a state that is known to be prothrombotic, and also associated with blood pressure elevation, atherogenesis, and worsening of heart failure.

Diclofenac and ibuprofen had similar gastrointestinal bleeding risks, and both medications were associated with a higher risk of bleeding than were ibuprofen, acetaminophen, or no medication.

“Comparing diclofenac initiation with no NSAID initiation, the consistency between our results and those of previous meta-analyses of both trial and observational data provides strong evidence to guide clinical decision making,” said Dr. Schmidt and his coauthors.

“Considering its cardiovascular and gastrointestinal risks, however, there is little justification to initiate diclofenac treatment before other traditional NSAIDs,” noted the investigators. “It is time to acknowledge the potential health risk of diclofenac and to reduce its use.”

The study was funded by the Department of Clinical Epidemiology Research Foundation, University of Aarhus, and by the Program for Clinical Research Infrastructure, funded by the Lundbeck Foundation, Novo Nordisk Foundation, and the Danish Research Council. The authors reported that they had no relevant conflicts of interest.
 

[email protected]

SOURCE: Schmidt M et al. BMJ 2018;362:k3426

Two subcutaneous dosages of the nerve growth factor–inhibitor tanezumab showed significant benefits in patients with osteoarthritic joint pain in a multicenter, randomized, phase 3 trial of 698 patients run primarily at U.S. centers.

The 16-week responses to two subcutaneous injections with tanezumab spaced 8 weeks apart showed statistically significant improvements in pain, physical function, and patient global self assessment, compared with placebo, the primary endpoints for the study, Pfizer and Lilly jointly reported. The two companies together are developing tanezumab for an indication for osteoarthritic pain, as well as for chronic lower back pain and pain from cancer metastases.

The company announcement said that patients showed good tolerance to the tanezumab treatments, with no new safety signals and no osteonecrosis seen. About 1% of patients on tanezumab stopped treatment because of an adverse effect, and less than 1.5% of patients on the drug had progressive osteoarthritis during treatment, compared with no patients in the placebo group.

The study enrolled patients at any one of 98 centers in the United States, Puerto Rico, or Canada with confirmed moderate or severe osteoarthritis of the knee or hip that either produced pain refractory to conventional pain medications or involved patients unable to take these medications. The researchers randomized patients to receive two 2.5-mg doses of tanezumab, a 2.5-mg dose followed 8 weeks later by a 5-mg dose, or two placebo doses. The primary outcomes were changes from baseline when measured 16 weeks after the start of treatment in the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) pain subscale, the WOMAC physical function subscale, and patient’s global assessment of osteoarthritis. Both of the tested tanezumab regimens produced statistically significant improvements in each of the three measures, compared with the placebo control patients, the companies reported.

Tanezumab is a humanized monoclonal antibody that binds to and inhibits nerve growth factor. This inhibition may prevent pain signals from reaching the spinal cord and brain, according to the companies’ report. In June 2017, the two companies announced that development of tanezumab had received “Fast Track” designation from the Food and Drug Administration for the indications of treating chronic osteoarthritic pain and chronic lower back pain.

[email protected]

Two subcutaneous dosages of the nerve growth factor–inhibitor tanezumab showed significant benefits in patients with osteoarthritic joint pain in a multicenter, randomized, phase 3 trial of 698 patients run primarily at U.S. centers.

The 16-week responses to two subcutaneous injections with tanezumab spaced 8 weeks apart showed statistically significant improvements in pain, physical function, and patient global self assessment, compared with placebo, the primary endpoints for the study, Pfizer and Lilly jointly reported. The two companies together are developing tanezumab for an indication for osteoarthritic pain, as well as for chronic lower back pain and pain from cancer metastases.

The company announcement said that patients showed good tolerance to the tanezumab treatments, with no new safety signals and no osteonecrosis seen. About 1% of patients on tanezumab stopped treatment because of an adverse effect, and less than 1.5% of patients on the drug had progressive osteoarthritis during treatment, compared with no patients in the placebo group.

The study enrolled patients at any one of 98 centers in the United States, Puerto Rico, or Canada with confirmed moderate or severe osteoarthritis of the knee or hip that either produced pain refractory to conventional pain medications or involved patients unable to take these medications. The researchers randomized patients to receive two 2.5-mg doses of tanezumab, a 2.5-mg dose followed 8 weeks later by a 5-mg dose, or two placebo doses. The primary outcomes were changes from baseline when measured 16 weeks after the start of treatment in the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) pain subscale, the WOMAC physical function subscale, and patient’s global assessment of osteoarthritis. Both of the tested tanezumab regimens produced statistically significant improvements in each of the three measures, compared with the placebo control patients, the companies reported.

Tanezumab is a humanized monoclonal antibody that binds to and inhibits nerve growth factor. This inhibition may prevent pain signals from reaching the spinal cord and brain, according to the companies’ report. In June 2017, the two companies announced that development of tanezumab had received “Fast Track” designation from the Food and Drug Administration for the indications of treating chronic osteoarthritic pain and chronic lower back pain.

[email protected]

Two subcutaneous dosages of the nerve growth factor–inhibitor tanezumab showed significant benefits in patients with osteoarthritic joint pain in a multicenter, randomized, phase 3 trial of 698 patients run primarily at U.S. centers.

The 16-week responses to two subcutaneous injections with tanezumab spaced 8 weeks apart showed statistically significant improvements in pain, physical function, and patient global self assessment, compared with placebo, the primary endpoints for the study, Pfizer and Lilly jointly reported. The two companies together are developing tanezumab for an indication for osteoarthritic pain, as well as for chronic lower back pain and pain from cancer metastases.

The company announcement said that patients showed good tolerance to the tanezumab treatments, with no new safety signals and no osteonecrosis seen. About 1% of patients on tanezumab stopped treatment because of an adverse effect, and less than 1.5% of patients on the drug had progressive osteoarthritis during treatment, compared with no patients in the placebo group.

The study enrolled patients at any one of 98 centers in the United States, Puerto Rico, or Canada with confirmed moderate or severe osteoarthritis of the knee or hip that either produced pain refractory to conventional pain medications or involved patients unable to take these medications. The researchers randomized patients to receive two 2.5-mg doses of tanezumab, a 2.5-mg dose followed 8 weeks later by a 5-mg dose, or two placebo doses. The primary outcomes were changes from baseline when measured 16 weeks after the start of treatment in the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) pain subscale, the WOMAC physical function subscale, and patient’s global assessment of osteoarthritis. Both of the tested tanezumab regimens produced statistically significant improvements in each of the three measures, compared with the placebo control patients, the companies reported.

Tanezumab is a humanized monoclonal antibody that binds to and inhibits nerve growth factor. This inhibition may prevent pain signals from reaching the spinal cord and brain, according to the companies’ report. In June 2017, the two companies announced that development of tanezumab had received “Fast Track” designation from the Food and Drug Administration for the indications of treating chronic osteoarthritic pain and chronic lower back pain.

[email protected]

AMSTERDAM – Structural severity in OA is related to the onset of depressive symptoms while surgery “ameliorates” depression in RA, according to the results of two separate studies presented at the European Congress of Rheumatology.

Using data on more than 1,600 individuals with knee OA from the Osteoarthritis Initiative, Alan Rathbun, PhD, and his associates looked at the components of disease severity and how they might individually contribute to the development of depression. They found that the odds of having depression more than doubled as joint space width increased (odds ratio, 2.25) and gait speed decreased (OR, 2.08), and rose 60% as pain became more severe (OR, 1.60).

Sara Freeman/MDedge News

Worsening knee OA could set off depression

“Studies have consistently shown that depressive symptoms are associated with worse osteoarthritis disease severity, however, there is a lack of research focused on identifying the specific components that contribute to the onset of depressive symptoms in nondepressed OA patients,” said Dr. Rathbun in an interview ahead of his presentation.

Dr. Rathbun, a research associate in the departments of epidemiology and of public health and medicine at the University of Maryland, Baltimore, also said that while OA guidelines do advise on treating depression, there is no standardized way to manage comorbid depression in routine clinical practice.

“If OA disease severity contributes to the development and worsening of depressive symptoms, it may be necessary to intervene on both conditions simultaneously in order to successfully manage them,” he suggested.

“Depression is a frequently occurring comorbidity in persons with OA,” Dr. Rathbun later observed during a press conference. Around one in five people with knee OA have depression, he said. This is an important fact if you consider how common symptomatic knee OA is – affecting 10% of men and 13% of women aged over 60 years – and the impact that it has on people’s quality of life, healthcare utilization, and mortality.

Dr. Rathbun and colleagues examined data on 1,652 men and women who were part of the Osteoarthritis Initiative, a multicenter, prospective, longitudinal study of knee health sponsored by the National Institutes of Health. For inclusion in the study, participants had to have radiographic knee OA, no depressive symptoms, and complete data on the disease severity components of interest: minimum joint space width, 20-meter gait speed, and the pain subscale of the Western Ontario and McMaster Universities Osteoarthritis Index. Depression was assessed using the Center for Epidemiological Studies Depression Scale, with no depression ascribed a score of 16 or under. Data from three additional annual follow-up visits was also required.

“All three components of OA disease progression were associated with an increased risk for the onset of depressive symptoms in those with radiographic knee OA,” Dr. Rathbun said in the interview. While pain severity has previously been linked to depressive symptoms in OA, the finding of worsening structural disease is new.

“The clinical implications of our findings are that the onset of depressive symptoms in OA patients is related to worsening pain, physical function, and structural disease severity,” he added. They also mean that these components and depression need to be targeted at the same time.

“Future studies need to ascertain whether depressive symptoms modify clinical response to analgesic medications in OA patients,” Dr. Rathbun suggested. “Considering that analgesics are often the first-line treatment for OA patients and the high prevalence of depressive symptoms in this population, comorbid depression may be an important contributor to ineffective medical management in the many OA patients who undergo total joint replacement.”
 

Depression “ameliorated” by orthopedic surgery for RA

While the effects of analgesic medications might be something to look at in relation to depression in OA, research presented elsewhere at the congress suggested that appropriate surgical intervention might also be key to dealing with depressive symptoms, at least in patients with RA.

After a 1-year follow-up in patients with RA who underwent orthopedic surgery, the mean BDI-II score improved from 13.0 to 11.5 (P less than .01), and the percentage of patients with a BDI-II score of 14 or more fell from 43% to 35%. Improvements in other health assessments – the Japanese version of the Health Assessment Questionnaire and the EuroQol 5 dimensions instrument – were also seen.

The prospective, observational cohort study included 276 patients with structural damage caused by RA. The most common site of joint damage requiring elective surgery was the wrist (n = 74), followed by the hand (n = 63), knee (n = 50), forefoot (n = 50), elbow (n = 26), hand and wrist (n = 18), hip (n = 13), ankle (n = 12), and shoulder (n = 6).

Looking at the improvement in depression scores by surgical site revealed a significant difference from baseline for the elbow (P less than .001), wrist (P less than .001), and forefoot (P less than .05). The magnitude of decrease in the BDI-II scores was independently related to Steinbrocker stage and pain measured on a visual analog scale.

“Depression was ameliorated by surgical intervention in patients with RA,” Hajime Ishikawa, MD, PhD, of the department of rheumatology at Niigata Rheumatic Center in Shibata, Japan, and associates concluded in their poster presentation. They added that the psychological changes observed were “related to the preoperative severity of joint damage and pain in the affected joint.”

Dr. Rathbun’s work was supported by a Rheumatology Research Foundation Scientist Development Award. Dr. Ishikawa and associates stated they had no disclosures of interest.

SOURCES: Rathbun AM et al. Ann Rheum Dis. 2018;77(Suppl 2):50-1. Abstract OP0003; Ishikawa H et al. Ann Rheum Dis. 2018;77(Suppl 2):297-8. Abstract THU0156.

AMSTERDAM – Structural severity in OA is related to the onset of depressive symptoms while surgery “ameliorates” depression in RA, according to the results of two separate studies presented at the European Congress of Rheumatology.

Using data on more than 1,600 individuals with knee OA from the Osteoarthritis Initiative, Alan Rathbun, PhD, and his associates looked at the components of disease severity and how they might individually contribute to the development of depression. They found that the odds of having depression more than doubled as joint space width increased (odds ratio, 2.25) and gait speed decreased (OR, 2.08), and rose 60% as pain became more severe (OR, 1.60).

Sara Freeman/MDedge News

Worsening knee OA could set off depression

“Studies have consistently shown that depressive symptoms are associated with worse osteoarthritis disease severity, however, there is a lack of research focused on identifying the specific components that contribute to the onset of depressive symptoms in nondepressed OA patients,” said Dr. Rathbun in an interview ahead of his presentation.

Dr. Rathbun, a research associate in the departments of epidemiology and of public health and medicine at the University of Maryland, Baltimore, also said that while OA guidelines do advise on treating depression, there is no standardized way to manage comorbid depression in routine clinical practice.

“If OA disease severity contributes to the development and worsening of depressive symptoms, it may be necessary to intervene on both conditions simultaneously in order to successfully manage them,” he suggested.

“Depression is a frequently occurring comorbidity in persons with OA,” Dr. Rathbun later observed during a press conference. Around one in five people with knee OA have depression, he said. This is an important fact if you consider how common symptomatic knee OA is – affecting 10% of men and 13% of women aged over 60 years – and the impact that it has on people’s quality of life, healthcare utilization, and mortality.

Dr. Rathbun and colleagues examined data on 1,652 men and women who were part of the Osteoarthritis Initiative, a multicenter, prospective, longitudinal study of knee health sponsored by the National Institutes of Health. For inclusion in the study, participants had to have radiographic knee OA, no depressive symptoms, and complete data on the disease severity components of interest: minimum joint space width, 20-meter gait speed, and the pain subscale of the Western Ontario and McMaster Universities Osteoarthritis Index. Depression was assessed using the Center for Epidemiological Studies Depression Scale, with no depression ascribed a score of 16 or under. Data from three additional annual follow-up visits was also required.

“All three components of OA disease progression were associated with an increased risk for the onset of depressive symptoms in those with radiographic knee OA,” Dr. Rathbun said in the interview. While pain severity has previously been linked to depressive symptoms in OA, the finding of worsening structural disease is new.

“The clinical implications of our findings are that the onset of depressive symptoms in OA patients is related to worsening pain, physical function, and structural disease severity,” he added. They also mean that these components and depression need to be targeted at the same time.

“Future studies need to ascertain whether depressive symptoms modify clinical response to analgesic medications in OA patients,” Dr. Rathbun suggested. “Considering that analgesics are often the first-line treatment for OA patients and the high prevalence of depressive symptoms in this population, comorbid depression may be an important contributor to ineffective medical management in the many OA patients who undergo total joint replacement.”
 

Depression “ameliorated” by orthopedic surgery for RA

While the effects of analgesic medications might be something to look at in relation to depression in OA, research presented elsewhere at the congress suggested that appropriate surgical intervention might also be key to dealing with depressive symptoms, at least in patients with RA.

After a 1-year follow-up in patients with RA who underwent orthopedic surgery, the mean BDI-II score improved from 13.0 to 11.5 (P less than .01), and the percentage of patients with a BDI-II score of 14 or more fell from 43% to 35%. Improvements in other health assessments – the Japanese version of the Health Assessment Questionnaire and the EuroQol 5 dimensions instrument – were also seen.

The prospective, observational cohort study included 276 patients with structural damage caused by RA. The most common site of joint damage requiring elective surgery was the wrist (n = 74), followed by the hand (n = 63), knee (n = 50), forefoot (n = 50), elbow (n = 26), hand and wrist (n = 18), hip (n = 13), ankle (n = 12), and shoulder (n = 6).

Looking at the improvement in depression scores by surgical site revealed a significant difference from baseline for the elbow (P less than .001), wrist (P less than .001), and forefoot (P less than .05). The magnitude of decrease in the BDI-II scores was independently related to Steinbrocker stage and pain measured on a visual analog scale.

“Depression was ameliorated by surgical intervention in patients with RA,” Hajime Ishikawa, MD, PhD, of the department of rheumatology at Niigata Rheumatic Center in Shibata, Japan, and associates concluded in their poster presentation. They added that the psychological changes observed were “related to the preoperative severity of joint damage and pain in the affected joint.”

Dr. Rathbun’s work was supported by a Rheumatology Research Foundation Scientist Development Award. Dr. Ishikawa and associates stated they had no disclosures of interest.

SOURCES: Rathbun AM et al. Ann Rheum Dis. 2018;77(Suppl 2):50-1. Abstract OP0003; Ishikawa H et al. Ann Rheum Dis. 2018;77(Suppl 2):297-8. Abstract THU0156.

AMSTERDAM – Structural severity in OA is related to the onset of depressive symptoms while surgery “ameliorates” depression in RA, according to the results of two separate studies presented at the European Congress of Rheumatology.

Using data on more than 1,600 individuals with knee OA from the Osteoarthritis Initiative, Alan Rathbun, PhD, and his associates looked at the components of disease severity and how they might individually contribute to the development of depression. They found that the odds of having depression more than doubled as joint space width increased (odds ratio, 2.25) and gait speed decreased (OR, 2.08), and rose 60% as pain became more severe (OR, 1.60).

Sara Freeman/MDedge News

Worsening knee OA could set off depression

“Studies have consistently shown that depressive symptoms are associated with worse osteoarthritis disease severity, however, there is a lack of research focused on identifying the specific components that contribute to the onset of depressive symptoms in nondepressed OA patients,” said Dr. Rathbun in an interview ahead of his presentation.

Dr. Rathbun, a research associate in the departments of epidemiology and of public health and medicine at the University of Maryland, Baltimore, also said that while OA guidelines do advise on treating depression, there is no standardized way to manage comorbid depression in routine clinical practice.

“If OA disease severity contributes to the development and worsening of depressive symptoms, it may be necessary to intervene on both conditions simultaneously in order to successfully manage them,” he suggested.

“Depression is a frequently occurring comorbidity in persons with OA,” Dr. Rathbun later observed during a press conference. Around one in five people with knee OA have depression, he said. This is an important fact if you consider how common symptomatic knee OA is – affecting 10% of men and 13% of women aged over 60 years – and the impact that it has on people’s quality of life, healthcare utilization, and mortality.

Dr. Rathbun and colleagues examined data on 1,652 men and women who were part of the Osteoarthritis Initiative, a multicenter, prospective, longitudinal study of knee health sponsored by the National Institutes of Health. For inclusion in the study, participants had to have radiographic knee OA, no depressive symptoms, and complete data on the disease severity components of interest: minimum joint space width, 20-meter gait speed, and the pain subscale of the Western Ontario and McMaster Universities Osteoarthritis Index. Depression was assessed using the Center for Epidemiological Studies Depression Scale, with no depression ascribed a score of 16 or under. Data from three additional annual follow-up visits was also required.

“All three components of OA disease progression were associated with an increased risk for the onset of depressive symptoms in those with radiographic knee OA,” Dr. Rathbun said in the interview. While pain severity has previously been linked to depressive symptoms in OA, the finding of worsening structural disease is new.

“The clinical implications of our findings are that the onset of depressive symptoms in OA patients is related to worsening pain, physical function, and structural disease severity,” he added. They also mean that these components and depression need to be targeted at the same time.

“Future studies need to ascertain whether depressive symptoms modify clinical response to analgesic medications in OA patients,” Dr. Rathbun suggested. “Considering that analgesics are often the first-line treatment for OA patients and the high prevalence of depressive symptoms in this population, comorbid depression may be an important contributor to ineffective medical management in the many OA patients who undergo total joint replacement.”
 

Depression “ameliorated” by orthopedic surgery for RA

While the effects of analgesic medications might be something to look at in relation to depression in OA, research presented elsewhere at the congress suggested that appropriate surgical intervention might also be key to dealing with depressive symptoms, at least in patients with RA.

After a 1-year follow-up in patients with RA who underwent orthopedic surgery, the mean BDI-II score improved from 13.0 to 11.5 (P less than .01), and the percentage of patients with a BDI-II score of 14 or more fell from 43% to 35%. Improvements in other health assessments – the Japanese version of the Health Assessment Questionnaire and the EuroQol 5 dimensions instrument – were also seen.

The prospective, observational cohort study included 276 patients with structural damage caused by RA. The most common site of joint damage requiring elective surgery was the wrist (n = 74), followed by the hand (n = 63), knee (n = 50), forefoot (n = 50), elbow (n = 26), hand and wrist (n = 18), hip (n = 13), ankle (n = 12), and shoulder (n = 6).

Looking at the improvement in depression scores by surgical site revealed a significant difference from baseline for the elbow (P less than .001), wrist (P less than .001), and forefoot (P less than .05). The magnitude of decrease in the BDI-II scores was independently related to Steinbrocker stage and pain measured on a visual analog scale.

“Depression was ameliorated by surgical intervention in patients with RA,” Hajime Ishikawa, MD, PhD, of the department of rheumatology at Niigata Rheumatic Center in Shibata, Japan, and associates concluded in their poster presentation. They added that the psychological changes observed were “related to the preoperative severity of joint damage and pain in the affected joint.”

Dr. Rathbun’s work was supported by a Rheumatology Research Foundation Scientist Development Award. Dr. Ishikawa and associates stated they had no disclosures of interest.

SOURCES: Rathbun AM et al. Ann Rheum Dis. 2018;77(Suppl 2):50-1. Abstract OP0003; Ishikawa H et al. Ann Rheum Dis. 2018;77(Suppl 2):297-8. Abstract THU0156.

EULAR 2018’s scientific program in Amsterdam is packed with lectures, clinical and basic science symposia, workshops, and special interest sessions covering the full spectrum of rheumatic diseases, said Dr. Robert Landewé, chair of the Scientific Program Committee.

“More than 5,000 scientific abstracts were submitted, which is an absolute, all-time record,” Dr. Landewé said. Four experts scored each abstract, and only the top 7% were invited for oral presentation during abstract sessions or symposia, he explained in an interview.

Wednesday, June 13

A high point of the 2018 scientific program is Wednesday’s opening plenary session, which will feature abstracts that were handpicked by Dr. Landewé and Dr. Thomas Dörner, professor of rheumatology at Charite Universitätsmedizin, Berlin. “This session includes highly scored abstracts, including late-breakers, on current advances in therapeutics and disease classification,” said Dr. Dörner, who chaired this year’s Abstract Selection Committee.

The plenary abstract session will cover new findings on gout and cardiovascular disease from CANTOS (Canakinumab Anti-inflammatory Thrombosis Outcome Study), long-term mortality in patients with early RA from the COBRA (Combinatietherapie Bij Reumatoide Artritis) study, the use of zoledronic acid to treat knee osteoarthritis with bone lesions, and the relationship between bisphosphonate drug holidays and hip fracture risk. Researchers also will discuss baricitinib in systemic lupus erythematosus (SLE), the value of MRI when treating remitted RA to target, the validation of SLE classification criteria, and draft classification criteria for ANCA-associated vasculitides.

A notable clinical science session on Wednesday will cover cancer and inflammation, Dr. Landewé said. “This is a topic of increasing interest because cancer and inflammation share mutual pathways.”

Novel cancer therapies such as immune checkpoint inhibitors have improved outcomes across a range of tumor types, but also can induce rheumatic disease, he added. Accordingly, presenters will discuss inflammation as “friend” versus “foe” in cancer treatment, the role of tumor necrosis factor in cancer, and risk of malignancy among patients with RA.

Thursday, June 14

Topics in this session will include the use of estrogens and other hormonal therapies in patients with rheumatic disease, registry studies of rheumatologic conditions during pregnancy, and how clinicians can best discuss sexual concerns with their rheumatology patients.

Friday, June 15

For the first time, the scientific program also will include a clinical science session held jointly with the European Society of Musculoskeletal Radiology (ESSR). Dr. Joachim Sieper of Germany and ESSR President Dr. Monique Reijnierse of the Netherlands will cochair the Friday afternoon session on the role of MRI in rheumatology. Attendees from both organizations will learn when to use MRI in early and established RA and spondyloarthritis, and how to interpret the results, with abundant time built in for questions and answers. Dr. Landewé called the joint session “a test case” for exciting web-based interactions between EULAR and ESSR.

Another clinical science session on Friday afternoon will dive into the diagnosis of spondyloarthritis, which Dr. Landewé called “a matter of recognizing patterns, not ticking boxes on a list of criteria. This symposium leads you through the art of pattern recognition.”

Later on Friday afternoon, a session will explore advances in biologic therapy of small-vessel vasculitis, he added. “Biologic disease-modifying antirheumatic drugs [bDMARDs] are becoming more and more important in this area of expanding interest.” Experts will address complement inhibition in ANCA-associated vasculitis (AAV), the use of induction and maintenance rituximab in AAV, the evolving role of mepolizumab in eosinophilic granulomatosis with polyangiitis, survival in AAV, and the use of rituximab for treating children with granulomatosis with polyangiitis and microscopic polyangiitis.

Saturday, June 16

On Saturday, a bench-to-bedside session will cover gout and kidney function. “This is an area with important new insights,” Dr. Dörner said. Presenters will discuss the genetics of hyperuricemia, renal urate transporters, and the pros and cons of using xanthine oxidase inhibitors to treat chronic kidney disease. Researchers will also cover studies of impaired neutrophil chemotaxis in patients with chronic kidney disease and hyperuricemia, and the relationship between renal medullar hyperechogenicity and gout severity.

Also on Saturday, a clinical science session titled, “Rheumatoid arthritis: Is it all in your head?” will explore emerging data on the relationship between inflammation and depression. Patients with RA often face both clinical depression and social isolation, and these complex psychosocial conditions can worsen one another. “In addition to proper drug choice, treating RA effectively depends on how concomitant problems, such as nonspecific pain, depression, and social isolation, are coped with in a broad context,” Dr. Landewé said. “When it comes to optimal management, rheumatologists need to communicate and prescribe, not just prescribe.”

Christian Apfelbacher, PhD, of Germany will discuss prevention and treatment strategies and Dr. Jonathan Cavanagh of the United Kingdom will cover neuroimaging in RA. Researchers also will discuss new findings on pain, depression, and anxiety in patients recently diagnosed with RA.

Also on Saturday, a special session will cover EULAR’s initiatives to improve clinical approaches (ESSCA), Dr. Dörner noted. This effort has produced new or updated recommendations on topics such as vaccination, Sjögren’s syndrome, glucocorticoid therapy, and management of hand osteoarthritis, he said. “These recommendations follow a number of others and are expected to impact clinical science as well as clinical practice.”

EULAR 2018’s scientific program in Amsterdam is packed with lectures, clinical and basic science symposia, workshops, and special interest sessions covering the full spectrum of rheumatic diseases, said Dr. Robert Landewé, chair of the Scientific Program Committee.

“More than 5,000 scientific abstracts were submitted, which is an absolute, all-time record,” Dr. Landewé said. Four experts scored each abstract, and only the top 7% were invited for oral presentation during abstract sessions or symposia, he explained in an interview.

Wednesday, June 13

A high point of the 2018 scientific program is Wednesday’s opening plenary session, which will feature abstracts that were handpicked by Dr. Landewé and Dr. Thomas Dörner, professor of rheumatology at Charite Universitätsmedizin, Berlin. “This session includes highly scored abstracts, including late-breakers, on current advances in therapeutics and disease classification,” said Dr. Dörner, who chaired this year’s Abstract Selection Committee.

The plenary abstract session will cover new findings on gout and cardiovascular disease from CANTOS (Canakinumab Anti-inflammatory Thrombosis Outcome Study), long-term mortality in patients with early RA from the COBRA (Combinatietherapie Bij Reumatoide Artritis) study, the use of zoledronic acid to treat knee osteoarthritis with bone lesions, and the relationship between bisphosphonate drug holidays and hip fracture risk. Researchers also will discuss baricitinib in systemic lupus erythematosus (SLE), the value of MRI when treating remitted RA to target, the validation of SLE classification criteria, and draft classification criteria for ANCA-associated vasculitides.

A notable clinical science session on Wednesday will cover cancer and inflammation, Dr. Landewé said. “This is a topic of increasing interest because cancer and inflammation share mutual pathways.”

Novel cancer therapies such as immune checkpoint inhibitors have improved outcomes across a range of tumor types, but also can induce rheumatic disease, he added. Accordingly, presenters will discuss inflammation as “friend” versus “foe” in cancer treatment, the role of tumor necrosis factor in cancer, and risk of malignancy among patients with RA.

Thursday, June 14

Topics in this session will include the use of estrogens and other hormonal therapies in patients with rheumatic disease, registry studies of rheumatologic conditions during pregnancy, and how clinicians can best discuss sexual concerns with their rheumatology patients.

Friday, June 15

For the first time, the scientific program also will include a clinical science session held jointly with the European Society of Musculoskeletal Radiology (ESSR). Dr. Joachim Sieper of Germany and ESSR President Dr. Monique Reijnierse of the Netherlands will cochair the Friday afternoon session on the role of MRI in rheumatology. Attendees from both organizations will learn when to use MRI in early and established RA and spondyloarthritis, and how to interpret the results, with abundant time built in for questions and answers. Dr. Landewé called the joint session “a test case” for exciting web-based interactions between EULAR and ESSR.

Another clinical science session on Friday afternoon will dive into the diagnosis of spondyloarthritis, which Dr. Landewé called “a matter of recognizing patterns, not ticking boxes on a list of criteria. This symposium leads you through the art of pattern recognition.”

Later on Friday afternoon, a session will explore advances in biologic therapy of small-vessel vasculitis, he added. “Biologic disease-modifying antirheumatic drugs [bDMARDs] are becoming more and more important in this area of expanding interest.” Experts will address complement inhibition in ANCA-associated vasculitis (AAV), the use of induction and maintenance rituximab in AAV, the evolving role of mepolizumab in eosinophilic granulomatosis with polyangiitis, survival in AAV, and the use of rituximab for treating children with granulomatosis with polyangiitis and microscopic polyangiitis.

Saturday, June 16

On Saturday, a bench-to-bedside session will cover gout and kidney function. “This is an area with important new insights,” Dr. Dörner said. Presenters will discuss the genetics of hyperuricemia, renal urate transporters, and the pros and cons of using xanthine oxidase inhibitors to treat chronic kidney disease. Researchers will also cover studies of impaired neutrophil chemotaxis in patients with chronic kidney disease and hyperuricemia, and the relationship between renal medullar hyperechogenicity and gout severity.

Also on Saturday, a clinical science session titled, “Rheumatoid arthritis: Is it all in your head?” will explore emerging data on the relationship between inflammation and depression. Patients with RA often face both clinical depression and social isolation, and these complex psychosocial conditions can worsen one another. “In addition to proper drug choice, treating RA effectively depends on how concomitant problems, such as nonspecific pain, depression, and social isolation, are coped with in a broad context,” Dr. Landewé said. “When it comes to optimal management, rheumatologists need to communicate and prescribe, not just prescribe.”

Christian Apfelbacher, PhD, of Germany will discuss prevention and treatment strategies and Dr. Jonathan Cavanagh of the United Kingdom will cover neuroimaging in RA. Researchers also will discuss new findings on pain, depression, and anxiety in patients recently diagnosed with RA.

Also on Saturday, a special session will cover EULAR’s initiatives to improve clinical approaches (ESSCA), Dr. Dörner noted. This effort has produced new or updated recommendations on topics such as vaccination, Sjögren’s syndrome, glucocorticoid therapy, and management of hand osteoarthritis, he said. “These recommendations follow a number of others and are expected to impact clinical science as well as clinical practice.”

EULAR 2018’s scientific program in Amsterdam is packed with lectures, clinical and basic science symposia, workshops, and special interest sessions covering the full spectrum of rheumatic diseases, said Dr. Robert Landewé, chair of the Scientific Program Committee.

“More than 5,000 scientific abstracts were submitted, which is an absolute, all-time record,” Dr. Landewé said. Four experts scored each abstract, and only the top 7% were invited for oral presentation during abstract sessions or symposia, he explained in an interview.

Wednesday, June 13

A high point of the 2018 scientific program is Wednesday’s opening plenary session, which will feature abstracts that were handpicked by Dr. Landewé and Dr. Thomas Dörner, professor of rheumatology at Charite Universitätsmedizin, Berlin. “This session includes highly scored abstracts, including late-breakers, on current advances in therapeutics and disease classification,” said Dr. Dörner, who chaired this year’s Abstract Selection Committee.

The plenary abstract session will cover new findings on gout and cardiovascular disease from CANTOS (Canakinumab Anti-inflammatory Thrombosis Outcome Study), long-term mortality in patients with early RA from the COBRA (Combinatietherapie Bij Reumatoide Artritis) study, the use of zoledronic acid to treat knee osteoarthritis with bone lesions, and the relationship between bisphosphonate drug holidays and hip fracture risk. Researchers also will discuss baricitinib in systemic lupus erythematosus (SLE), the value of MRI when treating remitted RA to target, the validation of SLE classification criteria, and draft classification criteria for ANCA-associated vasculitides.

A notable clinical science session on Wednesday will cover cancer and inflammation, Dr. Landewé said. “This is a topic of increasing interest because cancer and inflammation share mutual pathways.”

Novel cancer therapies such as immune checkpoint inhibitors have improved outcomes across a range of tumor types, but also can induce rheumatic disease, he added. Accordingly, presenters will discuss inflammation as “friend” versus “foe” in cancer treatment, the role of tumor necrosis factor in cancer, and risk of malignancy among patients with RA.

Thursday, June 14

Topics in this session will include the use of estrogens and other hormonal therapies in patients with rheumatic disease, registry studies of rheumatologic conditions during pregnancy, and how clinicians can best discuss sexual concerns with their rheumatology patients.

Friday, June 15

For the first time, the scientific program also will include a clinical science session held jointly with the European Society of Musculoskeletal Radiology (ESSR). Dr. Joachim Sieper of Germany and ESSR President Dr. Monique Reijnierse of the Netherlands will cochair the Friday afternoon session on the role of MRI in rheumatology. Attendees from both organizations will learn when to use MRI in early and established RA and spondyloarthritis, and how to interpret the results, with abundant time built in for questions and answers. Dr. Landewé called the joint session “a test case” for exciting web-based interactions between EULAR and ESSR.

Another clinical science session on Friday afternoon will dive into the diagnosis of spondyloarthritis, which Dr. Landewé called “a matter of recognizing patterns, not ticking boxes on a list of criteria. This symposium leads you through the art of pattern recognition.”

Later on Friday afternoon, a session will explore advances in biologic therapy of small-vessel vasculitis, he added. “Biologic disease-modifying antirheumatic drugs [bDMARDs] are becoming more and more important in this area of expanding interest.” Experts will address complement inhibition in ANCA-associated vasculitis (AAV), the use of induction and maintenance rituximab in AAV, the evolving role of mepolizumab in eosinophilic granulomatosis with polyangiitis, survival in AAV, and the use of rituximab for treating children with granulomatosis with polyangiitis and microscopic polyangiitis.

Saturday, June 16

On Saturday, a bench-to-bedside session will cover gout and kidney function. “This is an area with important new insights,” Dr. Dörner said. Presenters will discuss the genetics of hyperuricemia, renal urate transporters, and the pros and cons of using xanthine oxidase inhibitors to treat chronic kidney disease. Researchers will also cover studies of impaired neutrophil chemotaxis in patients with chronic kidney disease and hyperuricemia, and the relationship between renal medullar hyperechogenicity and gout severity.

Also on Saturday, a clinical science session titled, “Rheumatoid arthritis: Is it all in your head?” will explore emerging data on the relationship between inflammation and depression. Patients with RA often face both clinical depression and social isolation, and these complex psychosocial conditions can worsen one another. “In addition to proper drug choice, treating RA effectively depends on how concomitant problems, such as nonspecific pain, depression, and social isolation, are coped with in a broad context,” Dr. Landewé said. “When it comes to optimal management, rheumatologists need to communicate and prescribe, not just prescribe.”

Christian Apfelbacher, PhD, of Germany will discuss prevention and treatment strategies and Dr. Jonathan Cavanagh of the United Kingdom will cover neuroimaging in RA. Researchers also will discuss new findings on pain, depression, and anxiety in patients recently diagnosed with RA.

Also on Saturday, a special session will cover EULAR’s initiatives to improve clinical approaches (ESSCA), Dr. Dörner noted. This effort has produced new or updated recommendations on topics such as vaccination, Sjögren’s syndrome, glucocorticoid therapy, and management of hand osteoarthritis, he said. “These recommendations follow a number of others and are expected to impact clinical science as well as clinical practice.”

LIVERPOOL, ENGLAND – Hip pain increases all-cause mortality in people with OA by a third, according to data obtained from a large, community-based study.

The hazard ratio for all-cause mortality was 1.33 (95% confidence interval, 1.17-1.51) in people who self-reported hip pain over the course of up to 25 years’ follow-up. The presence of hip pain also increased the risk of cardiovascular mortality (HR, 1.22; 95% CI, 0.99-1.50).

Sara Freeman/MDedge News

SOURCE: Cleveland RJ et al. Osteoarthritis Cartilage. 2018:26(1):S10-1. Abstract 1.

LIVERPOOL, ENGLAND – Hip pain increases all-cause mortality in people with OA by a third, according to data obtained from a large, community-based study.

The hazard ratio for all-cause mortality was 1.33 (95% confidence interval, 1.17-1.51) in people who self-reported hip pain over the course of up to 25 years’ follow-up. The presence of hip pain also increased the risk of cardiovascular mortality (HR, 1.22; 95% CI, 0.99-1.50).

Sara Freeman/MDedge News

SOURCE: Cleveland RJ et al. Osteoarthritis Cartilage. 2018:26(1):S10-1. Abstract 1.

LIVERPOOL, ENGLAND – Hip pain increases all-cause mortality in people with OA by a third, according to data obtained from a large, community-based study.

The hazard ratio for all-cause mortality was 1.33 (95% confidence interval, 1.17-1.51) in people who self-reported hip pain over the course of up to 25 years’ follow-up. The presence of hip pain also increased the risk of cardiovascular mortality (HR, 1.22; 95% CI, 0.99-1.50).

Sara Freeman/MDedge News

SOURCE: Cleveland RJ et al. Osteoarthritis Cartilage. 2018:26(1):S10-1. Abstract 1.

LIVERPOOL, ENGLAND – With a rising osteoarthritis prevalence and no cure, efforts need to shift towards disease prevention, especially among those with joint injuries,, Jackie Whittaker, PT, PhD, said at the World Congress of Osteoarthritis.

“We all know that the burden of this disease is enormous and it’s expanding at an alarming rate,” she said at the congress, sponsored by the Osteoarthritis Research Society International.

“The only way that we have at this moment to try to reduce the burden of this disease is to shift our approach to management upstream and focus on prevention,” said Dr. Whittaker, who is an associate professor and research director at the University of Alberta, Edmonton, Canada.

According to the World Health Organization, OA is expected to become the fourth leading cause of disability worldwide by 2020. Furthermore, there will be a projected rise in prevalence from 12% to 25% in North America by 2030.

Dr. Whittaker suggested that it was time to try to identify those at risk of developing OA, such as after a joint injury, and ran through some suggestions on how posttraumatic OA (PTOA) might be preventable.
 

Secondary prevention of posttraumatic osteoarthritis

The prevention of PTOA can be split into primary, secondary and tertiary prevention, with primary prevention trying to prevent injuries from occurring in the first place.

“Strategies aimed at identifying and slowing down the onset of symptomatic osteoarthritis in preclinical populations would be referred to as secondary prevention,” Dr. Whittaker explained, adding that tertiary prevention would then be strategies aimed at improving function and reducing disability in those who already have symptomatic PTOA.

While there are programs that address primary and tertiary prevention – such as Footy First, an exercise training program adopted by the Australian Football League to reduce the risk of common leg injuries and the Good Life with osteoArthritis in Denmark (GLA:D^®) education and supervised exercise program for those with symptomatic OA – there is more of a gap for secondary prevention.

Some of the first steps to developing a secondary prevention model would be to determine the extent of PTOA after joint injury and then identify risk factors or causal mechanisms. Then, prevention strategies could be developed and tested before implementation and effectiveness studies are performed.

Performing the necessary prospective cohort studies, however, is when things get challenging – PTOA can take 10–15 years to manifest and studies would potentially need to run for long periods of time, which comes at a cost. Other challenges are that there is no commonly agree definition. PTOA is multifactorial, and because people may be in their 20s, there could be other contributing factors to the disease course.
 

Identifying modifiable risk factors

There are a “fair number” of prospective and retrospective studies that have been done to try to identify patients at risk for OA after joint injury. Several have looked at unmodifiable risk factors, such as age and sex, and the type of injury. Others have looked at potentially modifiable factors such as the treatment approach and avoiding re-injury, joint mechanics and strength, body composition and aerobic fitness and behavioral characteristics such as physical activity and return to sport.

Data from the Alberta Youth PrE-OA Study, an ongoing longitudinal cohort study, have shown that structural changes consistent with OA are not unique to tears in the anterior cruciate ligament or to meniscal tears, which are known to up the risk of PTOA. Furthermore, the odds of having MRI-defined OA 3–10 years after a knee injury varies by the injury history, type, and surgery.

Other findings from the Alberta Youth PrE-OA Study data have shown that previously injured subjects have a 30% risk for re-injury, with weaker knee extensors and flexors and poorer dynamic balance than uninjured study participants. The results have also shown that there is reduced physical activity and avoidance in those who have been injured.
 

Who is the population at risk?

“Although the supporting evidence and the level of evidence for some of the risk factors is not as thorough as we would like it, there are some common themes across the literature, that are consistent to what we see in clinical practice, and what we know from primary and tertiary prevention,” Dr. Whittaker said. “Based upon that, we can start to hypothesize who’s at greatest risk of developing posttraumatic osteoarthritis and what we might start doing about it right now.”

Dr. Whittaker proposed the following risk factors could be used to “build a profile” of someone at risk of PTOA:

• Having sustained an anterior cruciate ligament (ACL) tear with or without a damaged meniscus
• Elevated body mass index (BMI) or adiposity, and low grade systemic inflammation
• Weak knee muscles, and poor dynamic balance
• Reduced or disengaged from physical activity
• Insufficient rehabilitation, pain or stiffness, or fear of movement

There is also an argument for nutrition being involved, Dr. Whittaker said, with levels of micronutrients such as vitamins D and K and calcium playing an integral role in bone health.
 

What could secondary prevention look like?

“So, with this risk profile, what can be done?” Dr. Whittaker asked rhetorically. Exercise therapy is key, and increasing the muscle strength of the knee and lower extremity are an important component of this strategy. Strength alone may not be enough, so exercise programs will need to increase the neuromuscular control of functional movements. Tackling people’s fear of movement will also be a priority. “I think it’s very important that we promote, if not implement, physical activity guidelines.”

Education is also going to be an important part of any secondary prevention program for PTOA, ensuring that people have realistic expectations about re-injury and their risk of developing osteoarthritis and the importance of remaining physically active. Balancing physical activity against their likelihood of flare-ups and learning how to avoid re-injury if at all possible. Weight control and diet will also be a component to include.

One final component is how clinicians work with patients to minimize their risk of PTOA. “We need to co-manage these patients,” Dr. Whittaker said. “We need to have difficult conversations with them and really balance giving them a picture of reality without over medicalizing the situation.”

Dr. Whitaker stated that she had no financial relationships or commercial interests to disclose.

SOURCE: Whittaker J, et al. Osteoarthritis Cartilage 2018:26(1):S7-8. Abstract I-22.

LIVERPOOL, ENGLAND – With a rising osteoarthritis prevalence and no cure, efforts need to shift towards disease prevention, especially among those with joint injuries,, Jackie Whittaker, PT, PhD, said at the World Congress of Osteoarthritis.

“We all know that the burden of this disease is enormous and it’s expanding at an alarming rate,” she said at the congress, sponsored by the Osteoarthritis Research Society International.

“The only way that we have at this moment to try to reduce the burden of this disease is to shift our approach to management upstream and focus on prevention,” said Dr. Whittaker, who is an associate professor and research director at the University of Alberta, Edmonton, Canada.

According to the World Health Organization, OA is expected to become the fourth leading cause of disability worldwide by 2020. Furthermore, there will be a projected rise in prevalence from 12% to 25% in North America by 2030.

Dr. Whittaker suggested that it was time to try to identify those at risk of developing OA, such as after a joint injury, and ran through some suggestions on how posttraumatic OA (PTOA) might be preventable.
 

Secondary prevention of posttraumatic osteoarthritis

The prevention of PTOA can be split into primary, secondary and tertiary prevention, with primary prevention trying to prevent injuries from occurring in the first place.

“Strategies aimed at identifying and slowing down the onset of symptomatic osteoarthritis in preclinical populations would be referred to as secondary prevention,” Dr. Whittaker explained, adding that tertiary prevention would then be strategies aimed at improving function and reducing disability in those who already have symptomatic PTOA.

While there are programs that address primary and tertiary prevention – such as Footy First, an exercise training program adopted by the Australian Football League to reduce the risk of common leg injuries and the Good Life with osteoArthritis in Denmark (GLA:D^®) education and supervised exercise program for those with symptomatic OA – there is more of a gap for secondary prevention.

Some of the first steps to developing a secondary prevention model would be to determine the extent of PTOA after joint injury and then identify risk factors or causal mechanisms. Then, prevention strategies could be developed and tested before implementation and effectiveness studies are performed.

Performing the necessary prospective cohort studies, however, is when things get challenging – PTOA can take 10–15 years to manifest and studies would potentially need to run for long periods of time, which comes at a cost. Other challenges are that there is no commonly agree definition. PTOA is multifactorial, and because people may be in their 20s, there could be other contributing factors to the disease course.
 

Identifying modifiable risk factors

There are a “fair number” of prospective and retrospective studies that have been done to try to identify patients at risk for OA after joint injury. Several have looked at unmodifiable risk factors, such as age and sex, and the type of injury. Others have looked at potentially modifiable factors such as the treatment approach and avoiding re-injury, joint mechanics and strength, body composition and aerobic fitness and behavioral characteristics such as physical activity and return to sport.

Data from the Alberta Youth PrE-OA Study, an ongoing longitudinal cohort study, have shown that structural changes consistent with OA are not unique to tears in the anterior cruciate ligament or to meniscal tears, which are known to up the risk of PTOA. Furthermore, the odds of having MRI-defined OA 3–10 years after a knee injury varies by the injury history, type, and surgery.

Other findings from the Alberta Youth PrE-OA Study data have shown that previously injured subjects have a 30% risk for re-injury, with weaker knee extensors and flexors and poorer dynamic balance than uninjured study participants. The results have also shown that there is reduced physical activity and avoidance in those who have been injured.
 

Who is the population at risk?

“Although the supporting evidence and the level of evidence for some of the risk factors is not as thorough as we would like it, there are some common themes across the literature, that are consistent to what we see in clinical practice, and what we know from primary and tertiary prevention,” Dr. Whittaker said. “Based upon that, we can start to hypothesize who’s at greatest risk of developing posttraumatic osteoarthritis and what we might start doing about it right now.”

Dr. Whittaker proposed the following risk factors could be used to “build a profile” of someone at risk of PTOA:

• Having sustained an anterior cruciate ligament (ACL) tear with or without a damaged meniscus
• Elevated body mass index (BMI) or adiposity, and low grade systemic inflammation
• Weak knee muscles, and poor dynamic balance
• Reduced or disengaged from physical activity
• Insufficient rehabilitation, pain or stiffness, or fear of movement

There is also an argument for nutrition being involved, Dr. Whittaker said, with levels of micronutrients such as vitamins D and K and calcium playing an integral role in bone health.
 

What could secondary prevention look like?

“So, with this risk profile, what can be done?” Dr. Whittaker asked rhetorically. Exercise therapy is key, and increasing the muscle strength of the knee and lower extremity are an important component of this strategy. Strength alone may not be enough, so exercise programs will need to increase the neuromuscular control of functional movements. Tackling people’s fear of movement will also be a priority. “I think it’s very important that we promote, if not implement, physical activity guidelines.”

Education is also going to be an important part of any secondary prevention program for PTOA, ensuring that people have realistic expectations about re-injury and their risk of developing osteoarthritis and the importance of remaining physically active. Balancing physical activity against their likelihood of flare-ups and learning how to avoid re-injury if at all possible. Weight control and diet will also be a component to include.

One final component is how clinicians work with patients to minimize their risk of PTOA. “We need to co-manage these patients,” Dr. Whittaker said. “We need to have difficult conversations with them and really balance giving them a picture of reality without over medicalizing the situation.”

Dr. Whitaker stated that she had no financial relationships or commercial interests to disclose.

SOURCE: Whittaker J, et al. Osteoarthritis Cartilage 2018:26(1):S7-8. Abstract I-22.

LIVERPOOL, ENGLAND – With a rising osteoarthritis prevalence and no cure, efforts need to shift towards disease prevention, especially among those with joint injuries,, Jackie Whittaker, PT, PhD, said at the World Congress of Osteoarthritis.

“We all know that the burden of this disease is enormous and it’s expanding at an alarming rate,” she said at the congress, sponsored by the Osteoarthritis Research Society International.

“The only way that we have at this moment to try to reduce the burden of this disease is to shift our approach to management upstream and focus on prevention,” said Dr. Whittaker, who is an associate professor and research director at the University of Alberta, Edmonton, Canada.

According to the World Health Organization, OA is expected to become the fourth leading cause of disability worldwide by 2020. Furthermore, there will be a projected rise in prevalence from 12% to 25% in North America by 2030.

Dr. Whittaker suggested that it was time to try to identify those at risk of developing OA, such as after a joint injury, and ran through some suggestions on how posttraumatic OA (PTOA) might be preventable.
 

Secondary prevention of posttraumatic osteoarthritis

The prevention of PTOA can be split into primary, secondary and tertiary prevention, with primary prevention trying to prevent injuries from occurring in the first place.

“Strategies aimed at identifying and slowing down the onset of symptomatic osteoarthritis in preclinical populations would be referred to as secondary prevention,” Dr. Whittaker explained, adding that tertiary prevention would then be strategies aimed at improving function and reducing disability in those who already have symptomatic PTOA.

While there are programs that address primary and tertiary prevention – such as Footy First, an exercise training program adopted by the Australian Football League to reduce the risk of common leg injuries and the Good Life with osteoArthritis in Denmark (GLA:D^®) education and supervised exercise program for those with symptomatic OA – there is more of a gap for secondary prevention.

Some of the first steps to developing a secondary prevention model would be to determine the extent of PTOA after joint injury and then identify risk factors or causal mechanisms. Then, prevention strategies could be developed and tested before implementation and effectiveness studies are performed.

Performing the necessary prospective cohort studies, however, is when things get challenging – PTOA can take 10–15 years to manifest and studies would potentially need to run for long periods of time, which comes at a cost. Other challenges are that there is no commonly agree definition. PTOA is multifactorial, and because people may be in their 20s, there could be other contributing factors to the disease course.
 

Identifying modifiable risk factors

There are a “fair number” of prospective and retrospective studies that have been done to try to identify patients at risk for OA after joint injury. Several have looked at unmodifiable risk factors, such as age and sex, and the type of injury. Others have looked at potentially modifiable factors such as the treatment approach and avoiding re-injury, joint mechanics and strength, body composition and aerobic fitness and behavioral characteristics such as physical activity and return to sport.

Data from the Alberta Youth PrE-OA Study, an ongoing longitudinal cohort study, have shown that structural changes consistent with OA are not unique to tears in the anterior cruciate ligament or to meniscal tears, which are known to up the risk of PTOA. Furthermore, the odds of having MRI-defined OA 3–10 years after a knee injury varies by the injury history, type, and surgery.

Other findings from the Alberta Youth PrE-OA Study data have shown that previously injured subjects have a 30% risk for re-injury, with weaker knee extensors and flexors and poorer dynamic balance than uninjured study participants. The results have also shown that there is reduced physical activity and avoidance in those who have been injured.
 

Who is the population at risk?

“Although the supporting evidence and the level of evidence for some of the risk factors is not as thorough as we would like it, there are some common themes across the literature, that are consistent to what we see in clinical practice, and what we know from primary and tertiary prevention,” Dr. Whittaker said. “Based upon that, we can start to hypothesize who’s at greatest risk of developing posttraumatic osteoarthritis and what we might start doing about it right now.”

Dr. Whittaker proposed the following risk factors could be used to “build a profile” of someone at risk of PTOA:

• Having sustained an anterior cruciate ligament (ACL) tear with or without a damaged meniscus
• Elevated body mass index (BMI) or adiposity, and low grade systemic inflammation
• Weak knee muscles, and poor dynamic balance
• Reduced or disengaged from physical activity
• Insufficient rehabilitation, pain or stiffness, or fear of movement

There is also an argument for nutrition being involved, Dr. Whittaker said, with levels of micronutrients such as vitamins D and K and calcium playing an integral role in bone health.
 

What could secondary prevention look like?

“So, with this risk profile, what can be done?” Dr. Whittaker asked rhetorically. Exercise therapy is key, and increasing the muscle strength of the knee and lower extremity are an important component of this strategy. Strength alone may not be enough, so exercise programs will need to increase the neuromuscular control of functional movements. Tackling people’s fear of movement will also be a priority. “I think it’s very important that we promote, if not implement, physical activity guidelines.”

Education is also going to be an important part of any secondary prevention program for PTOA, ensuring that people have realistic expectations about re-injury and their risk of developing osteoarthritis and the importance of remaining physically active. Balancing physical activity against their likelihood of flare-ups and learning how to avoid re-injury if at all possible. Weight control and diet will also be a component to include.

One final component is how clinicians work with patients to minimize their risk of PTOA. “We need to co-manage these patients,” Dr. Whittaker said. “We need to have difficult conversations with them and really balance giving them a picture of reality without over medicalizing the situation.”

Dr. Whitaker stated that she had no financial relationships or commercial interests to disclose.

SOURCE: Whittaker J, et al. Osteoarthritis Cartilage 2018:26(1):S7-8. Abstract I-22.

LIVERPOOL, ENGLAND – Individuals who have had a knee injury prior to developing osteoarthritis are a distinct subgroup of patients with knee OA,according to data from the Good Life with osteoArthritis in Denmark (GLA:D^®) Registry.

Clear differences in the clinical presentation can be observed between patients with knee OA who have and have not had a previous knee injury, researcher Paetur Mikal Holm reported at the World Congress on Osteoarthritis.

“These differences include being younger, being a male, having a lower BMI [body mass index], and being more physically active; also, we see reduced quality of life, longer symptom duration, and widespread pain” said Mr. Holm, a PhD fellow in the department of sports science and clinical biomechanics, musculoskeletal function, and physiotherapy at the University of Southern Denmark in Odense. “The last two characteristics in particular – widespread pain and symptom duration – may have an important impact on treatment,” he added.

Sara Freeman/MDedge News

SOURCE: Holm PM et al. Osteoarthr Cartil. 2018:26(1):S56.OARSI 2018 Abstract 84.

LIVERPOOL, ENGLAND – Individuals who have had a knee injury prior to developing osteoarthritis are a distinct subgroup of patients with knee OA,according to data from the Good Life with osteoArthritis in Denmark (GLA:D^®) Registry.

Clear differences in the clinical presentation can be observed between patients with knee OA who have and have not had a previous knee injury, researcher Paetur Mikal Holm reported at the World Congress on Osteoarthritis.

“These differences include being younger, being a male, having a lower BMI [body mass index], and being more physically active; also, we see reduced quality of life, longer symptom duration, and widespread pain” said Mr. Holm, a PhD fellow in the department of sports science and clinical biomechanics, musculoskeletal function, and physiotherapy at the University of Southern Denmark in Odense. “The last two characteristics in particular – widespread pain and symptom duration – may have an important impact on treatment,” he added.

Sara Freeman/MDedge News

SOURCE: Holm PM et al. Osteoarthr Cartil. 2018:26(1):S56.OARSI 2018 Abstract 84.

LIVERPOOL, ENGLAND – Individuals who have had a knee injury prior to developing osteoarthritis are a distinct subgroup of patients with knee OA,according to data from the Good Life with osteoArthritis in Denmark (GLA:D^®) Registry.

Clear differences in the clinical presentation can be observed between patients with knee OA who have and have not had a previous knee injury, researcher Paetur Mikal Holm reported at the World Congress on Osteoarthritis.

“These differences include being younger, being a male, having a lower BMI [body mass index], and being more physically active; also, we see reduced quality of life, longer symptom duration, and widespread pain” said Mr. Holm, a PhD fellow in the department of sports science and clinical biomechanics, musculoskeletal function, and physiotherapy at the University of Southern Denmark in Odense. “The last two characteristics in particular – widespread pain and symptom duration – may have an important impact on treatment,” he added.

Sara Freeman/MDedge News

SOURCE: Holm PM et al. Osteoarthr Cartil. 2018:26(1):S56.OARSI 2018 Abstract 84.

LIVERPOOL, ENGLAND – Osteoarthritis is associated with a “considerably higher disease burden” than rheumatoid arthritis 6 months after initial presentation, according to one expert’s analysis at the World Congress on Osteoarthritis.

This may partly be because of the improved treatments now available for rheumatoid arthritis, whereas there remain few treatments, and no disease-modifying therapy as yet, for osteoarthritis, Theodore Pincus, MD, suggested at the congress sponsored by the Osteoarthritis Research Society International.

The MDHAQ/RAPID3 is a simple assessment tool that consists of two pages and asks patients to rate items such as their physical function in activities of daily living and levels of pain in the past week. It also asks about levels of anxiety, depression, and quality of sleep, and it includes a self-reported joint count and a patient global assessment. Scores on RAPID3 range from 0 to 30, and comprise three 0-10 scores for physical function, pain, and patient global assessment subscales in which higher scores indicate greater disease burden.

“Using this tool, we’ve been able to obtain data on patients with OA and RA for at least 30 years,” Dr. Pincus said.

One of the issues with comparing the burden of the two diseases, he noted, is that there are few places that have used the same assessment tool.

Dr. Pincus and his associates at Rush University have also shown that the disease burden in OA remains high 6 months after first visit, while greater improvement is seen in RA over this period (Osteoarthritis Cartilage. 2018;26[1]:S260. Abstract 491).

In a study of 151 patients with OA and 202 with RA, they found the composite RAPID3 scores were equally high in patients with OA and RA at their first visit (16.0 vs. 15.5, respectively) but higher in OA patients at the 6-month reassessment (14.3 vs. 11.9; P less than .004).

“We can now say that at presentation, OA and RA are similar in MDHAQ/RAPID3 scores, which were adjusted for age and BMI,” Dr. Pincus said. “Both the OA and RA patients improved, but considerably greater improvement in RA versus OA resulted in significantly poorer status for OA versus RA at 6 months.”

However, that’s not to say that OA is a worse disease than RA in every patient, Dr. Pincus was keen to point out. “Some patients with each disease have mild, moderate, or severe disease,” he stated. RA is used as benchmark for a severe disease, so these data highlight that “OA is a severe disease as well.”

This sentiment was the focus of a 2016 white paper produced by OARSI and submitted to the Food and Drug Administration, which states the case for the need to take OA more seriously and for regulatory restrictions to be removed to enable new treatments to be developed.

The prevalence of OA is at least 10-20 times higher than RA, and it’s likely that a large percentage of OA patients never get to see a rheumatologist, Dr. Pincus said. Yet the resources that go into managing RA are far greater if one excludes joint replacement.

Dr. Pincus noted that RA was not always regarded as a severe disease: 30 years ago the textbooks were stating that it had a good prognosis in the majority of cases and that patients could, by and large, use conservative regimens to manage their disease. However, real-world evidence showed that RA was associated with severe declines in function, high levels of work disability, and increased mortality, Dr. Pincus observed.

“Is osteoarthritis in 2018 where rheumatoid arthritis was in 1988, 30 years ago?” he asked rhetorically.

“The risk of long-term mortality in RA, OA, and most rheumatic disease is similar to, or greater than, hypertension, diabetes, as well as many cardiovascular and neoplastic diseases,” Dr. Pincus continued. Whereas mechanisms exist to try to log all cancer cases and compile data on the number of deaths, a rheumatic disease often is not listed anywhere on the death certificate, even as contributing to mortality, as rheumatic diseases generally are not the acute cause of death.

Functional disability and socioeconomic status are more important predictors of work disability and mortality than “any biomarker or imaging data, except x-ray.” Perhaps, Dr. Pincus said, these could also be important indicators of poor prognosis in OA and all chronic diseases?

“Physical function is a big deal,” he said. Data from a study looking at adults over the age of 50 years in the general Finnish population showed 5-year survival was significantly reduced by poorer functional capacity and less frequent physical exercise, at levels higher than smoking. Perhaps, the musculoskeletal system is more important than the other organs of the body for maintaining health, Dr. Pincus suggested.

Assessing functional status with tools such as the MDHAQ/RAPID3 is “really useful” in daily practice, Dr. Pincus said. He concluded with the words of Rudolph Virchow, who observed more than 100 years ago, that “the improvement of medicine would eventually prolong human life, but improvement of social conditions could achieve this result now and more rapidly and successfully.”

Dr. Pincus is the president of Medical History Services, which receives royalties and license fees from copyright and trademark of MDHAQ, RAPID3, or both, all of which are used to support further development of quantitative clinical measurement by both patients and physicians. He holds stock in the company and has received research funding from the company. Dr. Pincus also disclosed having a consulting agreement with Lilly.

SOURCE: Pincus T et al. Osteoarthritis Cartilage. 2018:26(1):S4. Abstract I-11.

*This story was updated 5/24/2018.

LIVERPOOL, ENGLAND – Osteoarthritis is associated with a “considerably higher disease burden” than rheumatoid arthritis 6 months after initial presentation, according to one expert’s analysis at the World Congress on Osteoarthritis.

This may partly be because of the improved treatments now available for rheumatoid arthritis, whereas there remain few treatments, and no disease-modifying therapy as yet, for osteoarthritis, Theodore Pincus, MD, suggested at the congress sponsored by the Osteoarthritis Research Society International.

The MDHAQ/RAPID3 is a simple assessment tool that consists of two pages and asks patients to rate items such as their physical function in activities of daily living and levels of pain in the past week. It also asks about levels of anxiety, depression, and quality of sleep, and it includes a self-reported joint count and a patient global assessment. Scores on RAPID3 range from 0 to 30, and comprise three 0-10 scores for physical function, pain, and patient global assessment subscales in which higher scores indicate greater disease burden.

“Using this tool, we’ve been able to obtain data on patients with OA and RA for at least 30 years,” Dr. Pincus said.

One of the issues with comparing the burden of the two diseases, he noted, is that there are few places that have used the same assessment tool.

Dr. Pincus and his associates at Rush University have also shown that the disease burden in OA remains high 6 months after first visit, while greater improvement is seen in RA over this period (Osteoarthritis Cartilage. 2018;26[1]:S260. Abstract 491).

In a study of 151 patients with OA and 202 with RA, they found the composite RAPID3 scores were equally high in patients with OA and RA at their first visit (16.0 vs. 15.5, respectively) but higher in OA patients at the 6-month reassessment (14.3 vs. 11.9; P less than .004).

“We can now say that at presentation, OA and RA are similar in MDHAQ/RAPID3 scores, which were adjusted for age and BMI,” Dr. Pincus said. “Both the OA and RA patients improved, but considerably greater improvement in RA versus OA resulted in significantly poorer status for OA versus RA at 6 months.”

However, that’s not to say that OA is a worse disease than RA in every patient, Dr. Pincus was keen to point out. “Some patients with each disease have mild, moderate, or severe disease,” he stated. RA is used as benchmark for a severe disease, so these data highlight that “OA is a severe disease as well.”

This sentiment was the focus of a 2016 white paper produced by OARSI and submitted to the Food and Drug Administration, which states the case for the need to take OA more seriously and for regulatory restrictions to be removed to enable new treatments to be developed.

The prevalence of OA is at least 10-20 times higher than RA, and it’s likely that a large percentage of OA patients never get to see a rheumatologist, Dr. Pincus said. Yet the resources that go into managing RA are far greater if one excludes joint replacement.

Dr. Pincus noted that RA was not always regarded as a severe disease: 30 years ago the textbooks were stating that it had a good prognosis in the majority of cases and that patients could, by and large, use conservative regimens to manage their disease. However, real-world evidence showed that RA was associated with severe declines in function, high levels of work disability, and increased mortality, Dr. Pincus observed.

“Is osteoarthritis in 2018 where rheumatoid arthritis was in 1988, 30 years ago?” he asked rhetorically.

“The risk of long-term mortality in RA, OA, and most rheumatic disease is similar to, or greater than, hypertension, diabetes, as well as many cardiovascular and neoplastic diseases,” Dr. Pincus continued. Whereas mechanisms exist to try to log all cancer cases and compile data on the number of deaths, a rheumatic disease often is not listed anywhere on the death certificate, even as contributing to mortality, as rheumatic diseases generally are not the acute cause of death.

Functional disability and socioeconomic status are more important predictors of work disability and mortality than “any biomarker or imaging data, except x-ray.” Perhaps, Dr. Pincus said, these could also be important indicators of poor prognosis in OA and all chronic diseases?

“Physical function is a big deal,” he said. Data from a study looking at adults over the age of 50 years in the general Finnish population showed 5-year survival was significantly reduced by poorer functional capacity and less frequent physical exercise, at levels higher than smoking. Perhaps, the musculoskeletal system is more important than the other organs of the body for maintaining health, Dr. Pincus suggested.

Assessing functional status with tools such as the MDHAQ/RAPID3 is “really useful” in daily practice, Dr. Pincus said. He concluded with the words of Rudolph Virchow, who observed more than 100 years ago, that “the improvement of medicine would eventually prolong human life, but improvement of social conditions could achieve this result now and more rapidly and successfully.”

Dr. Pincus is the president of Medical History Services, which receives royalties and license fees from copyright and trademark of MDHAQ, RAPID3, or both, all of which are used to support further development of quantitative clinical measurement by both patients and physicians. He holds stock in the company and has received research funding from the company. Dr. Pincus also disclosed having a consulting agreement with Lilly.

SOURCE: Pincus T et al. Osteoarthritis Cartilage. 2018:26(1):S4. Abstract I-11.

*This story was updated 5/24/2018.

LIVERPOOL, ENGLAND – Osteoarthritis is associated with a “considerably higher disease burden” than rheumatoid arthritis 6 months after initial presentation, according to one expert’s analysis at the World Congress on Osteoarthritis.

This may partly be because of the improved treatments now available for rheumatoid arthritis, whereas there remain few treatments, and no disease-modifying therapy as yet, for osteoarthritis, Theodore Pincus, MD, suggested at the congress sponsored by the Osteoarthritis Research Society International.

The MDHAQ/RAPID3 is a simple assessment tool that consists of two pages and asks patients to rate items such as their physical function in activities of daily living and levels of pain in the past week. It also asks about levels of anxiety, depression, and quality of sleep, and it includes a self-reported joint count and a patient global assessment. Scores on RAPID3 range from 0 to 30, and comprise three 0-10 scores for physical function, pain, and patient global assessment subscales in which higher scores indicate greater disease burden.

“Using this tool, we’ve been able to obtain data on patients with OA and RA for at least 30 years,” Dr. Pincus said.

One of the issues with comparing the burden of the two diseases, he noted, is that there are few places that have used the same assessment tool.

Dr. Pincus and his associates at Rush University have also shown that the disease burden in OA remains high 6 months after first visit, while greater improvement is seen in RA over this period (Osteoarthritis Cartilage. 2018;26[1]:S260. Abstract 491).

In a study of 151 patients with OA and 202 with RA, they found the composite RAPID3 scores were equally high in patients with OA and RA at their first visit (16.0 vs. 15.5, respectively) but higher in OA patients at the 6-month reassessment (14.3 vs. 11.9; P less than .004).

“We can now say that at presentation, OA and RA are similar in MDHAQ/RAPID3 scores, which were adjusted for age and BMI,” Dr. Pincus said. “Both the OA and RA patients improved, but considerably greater improvement in RA versus OA resulted in significantly poorer status for OA versus RA at 6 months.”

However, that’s not to say that OA is a worse disease than RA in every patient, Dr. Pincus was keen to point out. “Some patients with each disease have mild, moderate, or severe disease,” he stated. RA is used as benchmark for a severe disease, so these data highlight that “OA is a severe disease as well.”

This sentiment was the focus of a 2016 white paper produced by OARSI and submitted to the Food and Drug Administration, which states the case for the need to take OA more seriously and for regulatory restrictions to be removed to enable new treatments to be developed.

The prevalence of OA is at least 10-20 times higher than RA, and it’s likely that a large percentage of OA patients never get to see a rheumatologist, Dr. Pincus said. Yet the resources that go into managing RA are far greater if one excludes joint replacement.

Dr. Pincus noted that RA was not always regarded as a severe disease: 30 years ago the textbooks were stating that it had a good prognosis in the majority of cases and that patients could, by and large, use conservative regimens to manage their disease. However, real-world evidence showed that RA was associated with severe declines in function, high levels of work disability, and increased mortality, Dr. Pincus observed.

“Is osteoarthritis in 2018 where rheumatoid arthritis was in 1988, 30 years ago?” he asked rhetorically.

“The risk of long-term mortality in RA, OA, and most rheumatic disease is similar to, or greater than, hypertension, diabetes, as well as many cardiovascular and neoplastic diseases,” Dr. Pincus continued. Whereas mechanisms exist to try to log all cancer cases and compile data on the number of deaths, a rheumatic disease often is not listed anywhere on the death certificate, even as contributing to mortality, as rheumatic diseases generally are not the acute cause of death.

Functional disability and socioeconomic status are more important predictors of work disability and mortality than “any biomarker or imaging data, except x-ray.” Perhaps, Dr. Pincus said, these could also be important indicators of poor prognosis in OA and all chronic diseases?

“Physical function is a big deal,” he said. Data from a study looking at adults over the age of 50 years in the general Finnish population showed 5-year survival was significantly reduced by poorer functional capacity and less frequent physical exercise, at levels higher than smoking. Perhaps, the musculoskeletal system is more important than the other organs of the body for maintaining health, Dr. Pincus suggested.

Assessing functional status with tools such as the MDHAQ/RAPID3 is “really useful” in daily practice, Dr. Pincus said. He concluded with the words of Rudolph Virchow, who observed more than 100 years ago, that “the improvement of medicine would eventually prolong human life, but improvement of social conditions could achieve this result now and more rapidly and successfully.”

Dr. Pincus is the president of Medical History Services, which receives royalties and license fees from copyright and trademark of MDHAQ, RAPID3, or both, all of which are used to support further development of quantitative clinical measurement by both patients and physicians. He holds stock in the company and has received research funding from the company. Dr. Pincus also disclosed having a consulting agreement with Lilly.

SOURCE: Pincus T et al. Osteoarthritis Cartilage. 2018:26(1):S4. Abstract I-11.

*This story was updated 5/24/2018.