Rheumatoid Arthritis: Understanding DMARDs and Biologics

Rheumatoid arthritis is an autoimmune disease in which the immune system attacks the lining of the joints. Untreated, it causes irreversible joint damage — and the damage happens early, which is why modern treatment moves quickly rather than waiting to see how things develop.

Treat to target

Current practice is built around a principle called treat to target: pick a goal — remission, or low disease activity where remission is not achievable — measure progress with a validated score, and escalate treatment every few months until the target is reached.

The alternative, adjusting only when a patient complains, allows silent joint erosion. The window in which damage can be prevented rather than managed is the first months after onset.

Conventional DMARDs

Disease-modifying antirheumatic drugs suppress the underlying process rather than just relieving symptoms. The conventional synthetic ones come first.

Methotrexate is the anchor. Taken weekly — never daily, and this is a genuinely dangerous error — with folic acid to reduce side effects. It works for a large proportion of patients, alone or as the base for combination therapy.

Others include leflunomide, sulfasalazine and hydroxychloroquine, used alone, in combination, or where methotrexate is not tolerated.

Monitoring is part of the treatment: regular blood counts and liver function tests, because these drugs are effective precisely because they are active.

Biologic DMARDs

Where conventional DMARDs do not reach the target, biologics are added. Each targets a specific part of the immune cascade:

• TNF inhibitors — adalimumab, etanercept, infliximab, golimumab, certolizumab
• IL-6 receptor blockers — tocilizumab, sarilumab
• T-cell co-stimulation blocker — abatacept
• B-cell depletion — rituximab

These are injected or infused. Biosimilar versions of several are now widely available, and have made this class considerably more accessible — see our guide to biosimilars versus generics.

Failing one biologic does not predict failing another, including another in the same class. Switching is normal practice, not a last resort.

JAK inhibitors

Targeted synthetic DMARDs — tofacitinib, baricitinib, upadacitinib, filgotinib — block Janus kinase signalling inside the cell. They are oral rather than injected, which many patients prefer, and act quickly.

Regulators in several regions have added restrictions following safety studies, particularly around cardiovascular events, blood clots and malignancy in older patients and those with risk factors. This makes them a considered choice rather than an automatic next step, and the discussion with a rheumatologist should cover it explicitly.

Infection risk is the shared trade-off

Every drug in this article works by damping an overactive immune system, which necessarily reduces some defence against infection.

Practical implications:

• Screening for latent tuberculosis and hepatitis B before starting biologics or JAK inhibitors
• Vaccinations brought up to date beforehand where possible; live vaccines are generally avoided during treatment
• Treatment usually paused during a significant infection, on medical advice
• Any fever or unusual infection reported promptly

What good control looks like

The goal is not merely fewer bad days. It is no swollen joints, normal inflammatory markers, no progression on imaging, and normal function. That is achievable for many patients now, and it is worth insisting on rather than settling early.

Browse our rheumatoid arthritis range or the full rheumatology and immunology catalogue.

This article is general information, not medical advice. Treatment decisions belong with a qualified clinician who knows your history. Every medicine mentioned is prescription-only and requires a valid prescription.