SIGNS OF RA
USING NSAIDS FOR SYMPTOMATIC RELIEF
USING CORTICOSTEROIDS FOR SYMPTOMATIC RELIEF

SIGNS OF RA

RA IS A COMMON TYPE OF ARTHRITIS, AFFECTING OVER 1 MILLION PEOPLE IN THE UNITED STATES1

Signs and symptoms of RA include2:

  • Pain, stiffness, and swelling in multiple joints
  • The same symptoms on both sides of the body (such as both hands or both knees)

Inflammation causes the signs and symptoms of RA3

  • The release of inflammatory chemicals causes joint swelling, increased joint fluid and inflammation of the synovial membrane4

Treatment should aim to relieve both the inflammation and pain associated with RA

USING NSAIDS FOR SYMPTOMATIC RELIEF

SEVERAL TREATMENT OPTIONS ARE AVAILABLE FOR RA SYMPTOMS5,6

  • First-line recommendations for early and established RA are patient dependent and include traditional disease-modifying antirheumatic drugs (DMARDs) and biologics5
  • Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used for effective symptomatic relief in RA6

NSAIDS RELIEVE THE INFLAMMATION AND PAIN ASSOCIATED WITH RA6

  • NSAIDs inhibit the cyclooxygenase (COX-1 and COX-2) enzymes from producing prostaglandins which are mediators of inflammation and pain6-8
  • NSAIDs are also known to have an analgesic effect6
  • Without
    NSAIDs
  • With
    NSAIDs
  • COX-1 or COX-2 binds to arachidonic acid.
  • COX-1 and COX-2 are enzymes that convert arachidonic acid into prostaglandins.
  • This leads to the creation of prostaglandins, which mediate inflammation and pain.8
  • NSAIDs bind to COX-1 or COX-2 so it cannot bind to arachidonic acid.6,8
  • COX-1 or COX-2 cannot trigger prostaglandin creation. Prostaglandin-induced inflammation and pain is reduced.6,8

DRAG TO SEE HOW NSAIDs REDUCE INFLAMMATION & PAIN

For illustrative purposes only. The mechanism of action of NSAIDs is not completely understood.7

USING CORTICOSTEROIDS FOR SYMPTOMATIC RELIEF

For patients with moderate or high RA disease activity who are starting DMARDs

ACR RECOMMENDS CONSIDERING LOW-DOSE GLUCOCORTICOIDS5*†

Short-term (<3 months) glucocorticoids should also be considered for RA flares.5*†

ACR=American College of Rheumatology.

*Low-dose is defined as ≤10 mg/day of prednisone or equivalent.5

†Glucocorticoids should be used at the lowest possible dose and for the shortest period possible.5

American College of Rheumatology logo
ra gluco ra gluco

Glucocorticoids such as prednisone reduce a number of pro-inflammatory processes9

Prednisone has been shown to reduce production of lymphocytes, edema, fibrin deposition, capillary dilation, migration of leukocytes, and phagocytosis.9

RA DMARD RA DMARD

Low-dose glucocorticoids are often added to DMARD therapy to improve response10,12-14‡

Adding low-dose prednisone to stable DMARD therapy produced higher response rates as determined by ACR20 in RA.10,11‡

Multiple studies revealed that low-dose glucocorticoids slowed radiographic progression of RA.12-14

‡ACR20 was defined as a 20% improvement in tender or swollen joint count and a 20% improvement in 3 out of 5 of the following: patient’s global assessment, physician’s global assessment, patient’s assessment of pain, degree of disability, and level of acute-phase reactant.11

Choose the most appropriate treatment option for your RA patients

ra opioidsra opioidsra opioids

Things to keep in mind when considering opioids

GET THE FACTS
RA GastroprotectionRA GastroprotectionRA Gastroprotection

Consider the need for gastroprotection with NSAID therapy

SEE THE DATA

Things to keep in mind when considering low-dose glucocorticoids

GET THE DETAILS
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  • Arthritis Foundation. Rheumatoid arthritis. Arthritis Foundation website. https://www.arthritis.org/diseases/rheumatoid-arthritis. Accessed June 14, 2020.
  • Centers for Disease Control and Prevention. Rheumatoid arthritis (RA). Centers for Disease Control and Prevention website. https://www.cdc.gov/arthritis/basics/rheumatoid-arthritis.html. Accessed June 14, 2020.
  • Derksen VFAM, Huizinga TWJ, van der Woude D. The role of autoantibodies in the pathophysiology of rheumatoid arthritis. Semin Immunopathol. 2017;39(4):437-446.
  • Arthritis Foundation. Causes of inflammatory joint pain. Arthritis Foundation website. https://www.arthritis.org/health-wellness/healthy-living/managing-pain/understanding-pain/causes-of-inflammatory-joint-pain. Accessed June 14, 2020.
  • Singh JA, Saag KG, Bridges SL Jr, et al. 2015 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Care Res (Hoboken). 2016;68(1):1-25.
  • Crofford LJ. Use of NSAIDs in treating patients with arthritis. Arthritis Res Ther. 2013;15(suppl 3):S2.
  • DUEXIS (ibuprofen and famotidine) [prescribing information] Horizon.
  • Ricciotti E, FitzGerald GA. Prostaglandins and inflammation. Arterioscler Thromb Vasc Biol. 2011;31(5):986-1000.
  • RAYOS (prednisone) delayed-release tablets [prescribing information] Horizon.
  • Buttgereit F, Mehta D, Kirwan J, et al. Low dose prednisone chronotherapy for rheumatoid arthritis: a randomized clinical trial (CAPRA-2). Ann Rheum Dis. 2013;72(2):204-210.
  • American College of Rheumatology Subcommittee on Rheumatoid Arthritis Guidelines. Guidelines for the management of rheumatoid arthritis: 2002 update. Arthritis Rheum. 2002;46(2):328-346.
  • Kirwan JR. The effect of glucocorticoids on joint destruction in rheumatoid arthritis. N Engl J Med. 1995;333:142-146.
  • Wassenberg S, Rau R, Steinfeld P, Zeidler H; for the Low-Dose Prednisolone Therapy Study Group. Very low-dose prednisolone in early rheumatoid arthritis retards radiographic progression over two years. Arthritis Rheum. 2005;52:3371-3380.
  • van Everdingen AA, Jacobs JWG, van Reesema DRS, Bijlsma JWJ. Low-dose prednisone therapy for patients with early active rheumatoid arthritis: clinical efficacy, disease-modifying properties, and side effects. Ann Intern Med. 2002;136:1-12.