User login
LAS VEGAS – , Anne-Christine Bay-Jensen, PhD, said at the World Congress on Osteoarthritis.
That way, investigators maximize the likelihood of obtaining a positive outcome undiluted by giving the therapy to the wrong patients.
CRPM shows preliminary evidence of passing muster on both counts, according to Dr. Bay-Jensen, head of rheumatology at Nordic Bioscience in Herløv, Denmark.
The Danish researcher introduced herself to the Las Vegas audience by announcing, “My purpose in life is to develop biomarkers for identifying phenotypes in osteoarthritis.”
Indeed, she has been a pioneer in investigating the clinical utility of CRPM, a degradation fragment of C-reactive protein that is produced in the joint and thus reflects joint-specific tissue inflammation. Unlike C-reactive protein, which is an acute phase reactant, CRPM reflects chronic inflammation, she explained at the meeting sponsored by the Osteoarthritis Research Society International.
Her early work with CRPM explored its use as a biomarker in rheumatoid arthritis (RA) patients. She demonstrated, for example, in a secondary analysis of the phase III, double-blind, placebo-controlled LITHE trial that an 11% reduction in CRPM at week 4 of treatment with tocilizumab (Actemra) plus methotrexate was associated with a fourfold increased likelihood of a clinical response at week 16. That finding indicates that utilizing CRPM as an early predictor of tocilizumab efficacy promotes a more targeted, cost-effective, and personalized use of the biologic agent.
At OARSI 2017, Dr. Bay-Jensen presented evidence that even though the mean serum CRPM is significantly higher in patients with RA than in those with knee osteoarthritis (KOA), one-third or more of KOA patients have levels of joint tissue inflammation comparable to that seen in RA. That patient subset with a highly inflammatory KOA phenotype would be the logical focus of future clinical trials of agents having potent anti-inflammatory effects, rather than potential therapies with bone- or cartilage-modifying effects.
The data came from a biomarker study of 113 patients with early RA, as well as from two Nordic Bioscience–sponsored phase III randomized, multicenter, placebo-controlled clinical trials of oral salmon calcitonin in a total of 2,306 patients with knee osteoarthritis, both of which proved negative (Osteoarthritis Cartilage. 2015 Apr;23[4]:532-43). The mean baseline CRPM in the early RA patients was 17.1 ng/mL, compared with 8.5 ng/mL in the KOA patients. However, 31% of KOA patients in one phase III oral calcitonin trial and 41% in the other had a baseline serum CRPM greater than 9 ng/mL, a level that overlapped with 75% of the RA patients.
A related substudy of the oral calcitonin trials examined CRPM as a predictive biomarker. It included 153 knees without OA at baseline, 50 of which developed radiographic evidence of KOA, as evidenced by a Kellgren-Lawrence grade of 2 or 3 during 2 years of prospective follow-up. A serum CRPM of 9 ng/mL or more at baseline was associated with a 4.6-fold increased likelihood of incident KOA during follow-up.
Nordic Bioscience, Dr. Bay-Jensen’s employer, markets numerous proprietary biomarker assays, including one for CRPM.
LAS VEGAS – , Anne-Christine Bay-Jensen, PhD, said at the World Congress on Osteoarthritis.
That way, investigators maximize the likelihood of obtaining a positive outcome undiluted by giving the therapy to the wrong patients.
CRPM shows preliminary evidence of passing muster on both counts, according to Dr. Bay-Jensen, head of rheumatology at Nordic Bioscience in Herløv, Denmark.
The Danish researcher introduced herself to the Las Vegas audience by announcing, “My purpose in life is to develop biomarkers for identifying phenotypes in osteoarthritis.”
Indeed, she has been a pioneer in investigating the clinical utility of CRPM, a degradation fragment of C-reactive protein that is produced in the joint and thus reflects joint-specific tissue inflammation. Unlike C-reactive protein, which is an acute phase reactant, CRPM reflects chronic inflammation, she explained at the meeting sponsored by the Osteoarthritis Research Society International.
Her early work with CRPM explored its use as a biomarker in rheumatoid arthritis (RA) patients. She demonstrated, for example, in a secondary analysis of the phase III, double-blind, placebo-controlled LITHE trial that an 11% reduction in CRPM at week 4 of treatment with tocilizumab (Actemra) plus methotrexate was associated with a fourfold increased likelihood of a clinical response at week 16. That finding indicates that utilizing CRPM as an early predictor of tocilizumab efficacy promotes a more targeted, cost-effective, and personalized use of the biologic agent.
At OARSI 2017, Dr. Bay-Jensen presented evidence that even though the mean serum CRPM is significantly higher in patients with RA than in those with knee osteoarthritis (KOA), one-third or more of KOA patients have levels of joint tissue inflammation comparable to that seen in RA. That patient subset with a highly inflammatory KOA phenotype would be the logical focus of future clinical trials of agents having potent anti-inflammatory effects, rather than potential therapies with bone- or cartilage-modifying effects.
The data came from a biomarker study of 113 patients with early RA, as well as from two Nordic Bioscience–sponsored phase III randomized, multicenter, placebo-controlled clinical trials of oral salmon calcitonin in a total of 2,306 patients with knee osteoarthritis, both of which proved negative (Osteoarthritis Cartilage. 2015 Apr;23[4]:532-43). The mean baseline CRPM in the early RA patients was 17.1 ng/mL, compared with 8.5 ng/mL in the KOA patients. However, 31% of KOA patients in one phase III oral calcitonin trial and 41% in the other had a baseline serum CRPM greater than 9 ng/mL, a level that overlapped with 75% of the RA patients.
A related substudy of the oral calcitonin trials examined CRPM as a predictive biomarker. It included 153 knees without OA at baseline, 50 of which developed radiographic evidence of KOA, as evidenced by a Kellgren-Lawrence grade of 2 or 3 during 2 years of prospective follow-up. A serum CRPM of 9 ng/mL or more at baseline was associated with a 4.6-fold increased likelihood of incident KOA during follow-up.
Nordic Bioscience, Dr. Bay-Jensen’s employer, markets numerous proprietary biomarker assays, including one for CRPM.
LAS VEGAS – , Anne-Christine Bay-Jensen, PhD, said at the World Congress on Osteoarthritis.
That way, investigators maximize the likelihood of obtaining a positive outcome undiluted by giving the therapy to the wrong patients.
CRPM shows preliminary evidence of passing muster on both counts, according to Dr. Bay-Jensen, head of rheumatology at Nordic Bioscience in Herløv, Denmark.
The Danish researcher introduced herself to the Las Vegas audience by announcing, “My purpose in life is to develop biomarkers for identifying phenotypes in osteoarthritis.”
Indeed, she has been a pioneer in investigating the clinical utility of CRPM, a degradation fragment of C-reactive protein that is produced in the joint and thus reflects joint-specific tissue inflammation. Unlike C-reactive protein, which is an acute phase reactant, CRPM reflects chronic inflammation, she explained at the meeting sponsored by the Osteoarthritis Research Society International.
Her early work with CRPM explored its use as a biomarker in rheumatoid arthritis (RA) patients. She demonstrated, for example, in a secondary analysis of the phase III, double-blind, placebo-controlled LITHE trial that an 11% reduction in CRPM at week 4 of treatment with tocilizumab (Actemra) plus methotrexate was associated with a fourfold increased likelihood of a clinical response at week 16. That finding indicates that utilizing CRPM as an early predictor of tocilizumab efficacy promotes a more targeted, cost-effective, and personalized use of the biologic agent.
At OARSI 2017, Dr. Bay-Jensen presented evidence that even though the mean serum CRPM is significantly higher in patients with RA than in those with knee osteoarthritis (KOA), one-third or more of KOA patients have levels of joint tissue inflammation comparable to that seen in RA. That patient subset with a highly inflammatory KOA phenotype would be the logical focus of future clinical trials of agents having potent anti-inflammatory effects, rather than potential therapies with bone- or cartilage-modifying effects.
The data came from a biomarker study of 113 patients with early RA, as well as from two Nordic Bioscience–sponsored phase III randomized, multicenter, placebo-controlled clinical trials of oral salmon calcitonin in a total of 2,306 patients with knee osteoarthritis, both of which proved negative (Osteoarthritis Cartilage. 2015 Apr;23[4]:532-43). The mean baseline CRPM in the early RA patients was 17.1 ng/mL, compared with 8.5 ng/mL in the KOA patients. However, 31% of KOA patients in one phase III oral calcitonin trial and 41% in the other had a baseline serum CRPM greater than 9 ng/mL, a level that overlapped with 75% of the RA patients.
A related substudy of the oral calcitonin trials examined CRPM as a predictive biomarker. It included 153 knees without OA at baseline, 50 of which developed radiographic evidence of KOA, as evidenced by a Kellgren-Lawrence grade of 2 or 3 during 2 years of prospective follow-up. A serum CRPM of 9 ng/mL or more at baseline was associated with a 4.6-fold increased likelihood of incident KOA during follow-up.
Nordic Bioscience, Dr. Bay-Jensen’s employer, markets numerous proprietary biomarker assays, including one for CRPM.
EXPERT ANALYSIS FROM OARSI 2017