With many treatment options now available for rheumatoid arthritis, choosing the best option is often a case-by-case scenario depending on comorbidities.
Faculty in How I Treat Difficult RA: Panel Session presented difficult-to-treat cases for RA patients with interstitial lung disease (ILD), patients with treatment refractory RA, and RA in patients with liver disease. ACR Convergence 2020 registered attendees have on-demand access to watch a replay of the session through Wednesday, March 11.
Joan M. Bathon, MD, professor of medicine at Columbia University Irving Medical Center, kicked off the session by presenting a 65-year-old man with type 2 diabetes who had seropositive RA and coronary artery disease, and was admitted to her facility with dyspnea. He was treated with methotrexate (MTX) and leflunomide in 2015 when diagnosed with RA. On admission, he had crackles on his exam and required oxygen, and his chest CT showed bilateral ground-glass opacities and bilateral pleural fusions. The diagnostic dilemma: Was this decompensated heart failure or RA-ILD? He was treated for both with diuresis, oxygen, and IV steroids and saw a rapid improvement, but was not able to be discharged. Dr. Bathon said pulmonary function tests prior to hospitalization showed moderately severe restrictive physiology, and so they were able to conclude he had “RA-ILD and probably new mild heart failure as well.”
“We chose abatacept,” Dr. Bathon said. “And we put him on nintedanib for his ILD. His RA responded nicely to abatacept. We don’t know whether his ILD stabilized, worsened, or approved at all because we don’t have follow up-studies yet.”
Dr. Bathon laid out several common questions in this case. Did methotrexate or leflunomide cause or worsen his ILD? She outlined a few studies that looked at this, including Kiely P. et al, an early RA inception cohort story that showed methotrexate exposure in newly diagnosed RA patients was not associated with increased risk of ILD.
“It seems unlikely at least based on that early onset cohort study, but I don’t know that we’ll ever really get to the root of this problem with the design of studies because RA itself causes ILD, and sorting that from the treatment is always difficult,” she said.
Another question she aimed to answer was: Would nintedanib or pirfenidone be more efficacious than disease-modifying antirheumatic drugs (DMARDs) for managing RA-ILD?
“We don’t know,” she said. “There’s no direct comparison data; moreover, there’s no study, yet, on pirfenidone at all in RA, though there is a clinical trial in progress.”
Adding to the difficult-to-treat RA cases, Josef S. Smolen, MD, in the Division of Rheumatology, Department of Medicine 3, Medical University of Vienna, Austria, addressed treatment of refractory RA—the inability to reach the treat-to-target goals of remission or at least low disease activity with treatment. The case he presented was a 65-year-old female living with rheumatoid arthritis for 11 years. Her x-ray showed several erosions, and she failed many therapies, including bDMARDs, MTX, two anti-TNFs, RTX, and abatacept. She also had 14 tender joints and 10 swollen joints. She received a JAK-inhibitor, and the number of tender and swollen joints went down at six weeks, and then was further reduced another six weeks later to three tender joints and two swollen joints.
“In light of the many available therapeutic options, continuing an insufficiently effective drug is just not appropriate,” he said.
Dr. Smolen said the goal is to aim at best care for refractory RA, and part of that is making a shared decision with the patient. The primary target for treatment of RA should be remission or low disease activity, treatment should also be goal-oriented and governed by a strategic treatment approach, and patients should be closely monitored using composite disease activity measures.
“Finally, treatment should be adapted if the treatment aim is not reached within three to six months,” he said.
Stanley Cohen, MD, clinical professor of internal medicine, UT Southwestern Medical School, medical director, Metroplex Clinical Research Center, and rheumatology program director, THR Presbyterian Hospital, addressed RA and liver disease, noting that liver damage is not an extra-articular manifestation of RA. He discussed a 64-year-old female who presented with symmetrical polyarthritis, and her exam revealed 14 tender joints and six swollen joints. The patient was placed on low-dose prednisone (5 mg/d) with meloxicam, with a hepatitis panel ordered. The patient returned after two weeks and modestly improved with nine tender and four swollen joints, and the hepatologist report showed the patient was a hepatitis B carrier. The patient continued with active disease on sulfasalazine/prednisone and hydroxychloroquine and refused to take antiviral therapies despite multiple discussions on benefit/risk and need for more aggressive treatment. Hepatitis B viral DNA load remained low. The patient returned and again modestly improved but was referred to a hepatologist.
Dr. Cohen reviewed the AASLD HBV Testing and Treatment Algorithm in addition to the ACR recommendations for the use of DMARDs and biologics in the treatment of RA for hepatitis B infection:
- For patients initiating rituximab therapy who are hepatitis B core antibody positive (regardless of hep B surface antigen status), prophylactic anti-viral therapy is strongly recommended over frequent monitoring of viral load and liver enzymes alone.
- For patients initiating any bDMARD or tsDMARD who are hep B core antibody positive and hep B surface antigen positive, prophylactic anti-viral therapy is strongly recommended over frequent monitoring alone.
- For patients initiating a non-rituximab or bDMARD or a tsDMARD who are hep B core antibody positive and hep B surface antigen negative, frequent monitoring alone of viral load and liver enzymes is conditionally recommended over prophylactic anti-viral therapy.