Rheumatoid Arthritis Treatment (Non-pharmacological options (Surgery,…
Rheumatoid Arthritis Treatment
Disease modifying antirheumatic drugs (DMARDs)
Ts-DMARDs ( target synthetic )
chimeric antibody binds to TNF and prevents its interaction with TNF receptors on inflammatory cells.
Methotrexate typically is given with it to suppress antibody production against the mouse derived portion of the molecule
Infusion-related reactions, may occur (rash, urticaria, flushing, headache, fever, chills, nausea, tachycardia, dyspnea).
human monoclonal antibody that binds to membrane-bound and soluble TNF
advantage of this agent over others in the class :once-monthly SC dosing or every-othermonth IV dosing.
fusion protein consisting of two p75-soluble TNF receptors linked to an Fc fragment of human IgG1.
MOA : The drug binds to TNF-α making it biologically inactive and preventing it from interacting with the cell surface TNF receptors that would lead to cell activation
Injection site reactions
headache, infections (including TB), lymphoma, And drug induced lupus.
a human IgG1 antibody to TNF
no foreign protein components, it is less antigenic than infliximab
The drug is provided as either premixed syringes or injection pens containing 40 mg, which is administered by subcutaneous injection every 14 days.
the same as etanercept
MOA : It contains PEGylated humanized anti-TNF Fab fragments leading to TNF-α inhibition
Side effect : same as etanercept
pegylation increase the duration of the drug inside the body
Conventional Synthetic (Cs-DMARDS)
not associated with renal, hepatic, or bone marrow suppression (unlike methotrxate )
but the results are delayed up to 6 weeks
a therapeutic failure only when 6 months of therapy without a response has elapsed.
**Ocular toxicity :
as benign corneal deposits
scotomas (small areas of decreased or absent vision in the visual field), and night blindness
so a baseline ophthalmologic examination within 1 year of initiation of tt and annual screening examinations after 5 years of therapy.
MOA : unknown
can be used for tt of malaria
drug drug interactions
Sulfasalazine’s absorption can be decreased when antibiotics are used that destroy the colonic bacteria.
Sulfasalazine also binds to iron supplements
potentiate warfarin’s effects by displacing it from protein-binding sites so Close monitoring of the patient’s international normalized ratio is indicated.
the effect should be seen within 2 months
antirheumatic MOA is unknown.
Gastrointestinal adverse effects could be minimized by :1):minimized by initiating therapy with low doses and titrating gradually to higher doses.
or 2)using enteric coated tablets
leukopenia, alopecia, stomatitis, and elevated hepatic enzymes.
It also may cause the patient’s urine and skin to turn a yellow-orange color
safe during pregnancy ( unlike methotrxate )
patients with sulfa allergy
NOA: inhibition of dihydrofolate reductase :red_cross: folic a req for replication of cells
Dose : 7.5 mg once weekly ( oral , subcutaneous , intramuscular )
DMARD of choice
a maximum dose of
while in cancer start from 50 mg/wk IV not IM or SC
onset of action : as early as 2 to 3 weeks after starting therapy.
Abdominal cramping, Anorexia, Bone marrow suppression, MTX-induced lung disease
Concomitant folic acid is given routinely to reduce the risk of folate-depleting reactions induced by methotrexate therapy.
:eg, stomatitis, diarrhea, nausea, alopecia, myelosuppression, and elevations in liver function tests).
patients with chronic liver disease
pregnant and nursing women ( HIGHLY TERATOGENIC)
lung diseases , pleural or peritoneal effusions
preexisting blood disorders ,leukopenia ,thrombocytopenia
Monitoring (should be done every 12 weeks.)
blood cell counts
liver transaminase levels
drug-drug interactions :
MTX and trimethoprim (2 antifolate agents) are an extremely serious and life-threatening combination that should be avoided.
bone marrow toxicity
so complete blood count with platelets is recommended monthly for 6 months and then every 6 to 8 weeks thereafter.
so alanine aminotransferase should be monitored monthly initially and periodically thereafter
preexisting liver disease
Onset of action :4 to 8 weeks
MOA : inhibits the T-lymphocyte response to various stimuli and halts the cell cycle.
it's teratogenic and has an exceptionally long half-life due to reabsorption via enterohepatic circulation .
therapy requires abrupt discontinuation (eg, due to toxicity or pregnancy), administering cholestyramine will accelerate leflunomide removal from the body ( bile acid binder )
women who have previously received leflunomide (even if therapy was years ago) should have blood levels drawn if they wish to become pregnant.
Bridge Therapy/Symptomatic Relief
they do not prevent joint damage
• Selecting an NSAID depends on multiple patient-specific factors, including
:check:cardiovascular risk, :red_cross: celecoxib :check:naproxin
:check:potential for GI-related adverse events, :red_cross:ketolac
:check: adherence to medication regimens & insurance coverage
analgesic and anti-inflammatory benefits for joint pain and swelling.
At equipotent doses, the analgesic and anti-inflammatory activity of all oral NSAIDs, including COX-2–selective inhibitors, are similar.
• Topical administration of NSAIDs minimizes systemic exposure while providing pain relief comparable to that of oral NSAIDs.
Low-dose glucocorticoid treatment (equivalent to prednisone 10 mg/day or less)
effectively reduces inflammation through :red_cross: of cytokines and inflammatory mediators and prevents disease progression.
Intraarticular glucocrticoid injection:
It can suppress joint inflammation fo
r several months
and can be a useful addition to DMARD therapy, especially when there is residual activity in large joints (eg, wrists, knees). لو فيه عندي جويبنت مش راضي يستجيب