I’ve got pain in my hands! Is it serious? Might it be rheumatoid arthritis?

Rheumatoid arthritis (RA) is the most common and serious chronic inflammatory arthritis. If left untreated, it results in progressive joint destruction, functional impairment, and increased mortality.

The outcome of the disease however, has improved considerably in recent years with early diagnosis, effective treatments, and early intensive treatment strategies. Drug-free remission has become a realistic outcome, and survival is comparable with that of the general population.

Inflammatory arthritis is defined as being when the painful joint is clinically tender and swollen with a limited range of motion; redness and warmth might also occur. The typical joints involved in RA inflammation are the small joints of the hands and feet (metacarpophalageal (MCP), proximal interphalangeal (PIP) and metatarsophalangeal (MTP) joints). Distal interphalangeal joints, the carpo-metacarpophalangeal joint of the thumb and metatarsophalangeal joint of the big toe are exceptions, they are sites of degenerative joint diseases. Large joint involvement is characteristic of severe RA.

Rheumatoid inflammation results in structural joint damage early, within the first weeks or months. Already within 3 months of disease onset, 25% of patients have erosions evident on X-ray examination. More sensitive imaging techniques such as magnetic resonance imaging (MRI) and musculoskeletal ultrasound (US) confirm evidence of damage within weeks of the onset of symptoms.

The crucial role of RA treatment is to delay and prevent joint damage, to recognize patients with inflammatory arthritis, to define and treat potential RA patients as early as possible. Clinicians must differentiate signs and symptoms of early RA from those arthritides that will remit spontaneously (1/3) and from diseases that may present with similar clinical features of arthritis (1/3) e.g. SLE, Sjögren’s syndrome.

Development of RA (phases)

Rheumatoid arthritis

No pathognostic sign exists, therefore diagnosis of RA is based on internationally accepted and validated criteria. The old 1987 classification defined RA when already established; diagnosis was certain when joint erosion on X-ray could be detected. With our expanding knowledge, early diagnosis of RA was needed, the old criteria were revised and the new 2010 (EULAR/ACR) classification criteria were developed. Early diagnosis was mainly founded on clinical signs and symptoms. It consisted of 4 categories: the number of joints involved, the presence of characteristic autoantibodies (rheumatoid factor/anti-CCP antibody), the level of systemic inflammation (ESR/CRP values) and disease duration of longer than 6 weeks. If the score of criteria was above or equal to 6, definite RA could be diagnosed.

Undifferentiated arthritis

If the inflammatory arthritis does not fulfil the 2010 RA criteria, undifferentiated arthritis is diagnosed, which might later either recover spontaneously or progress to definite RA.Nevertheless, inflammatory arthritis seems to begin much earlier than the clinically evident phases of undifferentiated arthritis and definite RA. Clinically suspect arthralgia and asymptomatic pre-clinical period might precede.

Pre-arthritis (arthralgia)

Nowadays, clinicians aim to recognise RA very early. Clinically suspect arthralgia must be differentiated, as 20% of cases will progress to RA. In 2016, criteria of the clinically suspect arthralgia were defined by European and American international rheumatology leagues. The more criteria are fulfilled, the greater the chance is for RA development. The 2016 criteria are: involvement of the metacarpophalangeal joints, positive MCP squeeze test, restricted fist formation of the hands, predominate morning signs, with pronounced morning stiffness (> 6o mins), positive family history of RA and less than 1-year disease duration.

Pre-clinical phase (autoimmunity)

In the earliest phase, asymptomatic autoimmunity appears long before RA development as a result of genetic susceptibility and environmental risk factors; appr. 10 years before the onset of clinical arthritis, characteristic autoantibodies (anti-CCP antibody!) can be detected in sera of RA patients. Autoantigens are triggered by innate, environmental and lifestyle stimuli (smoking!), which can lead to formation of non-matured autoantibodies. In a genetically susceptible person response matures as reflected by increasing titers, extensive isotypes and affinity spreading. It is supposed that persons in this phase might already experience arthralgia.

As a consequence, the best practical advice to anyone with pain in their hands and perhaps swelling, with a positive family history of RA, is to go to their rheumatologist as soon as possible. Early diagnosis of RA and early effective treatment will prevent functional and structural damage and result in a symptom-free favourable outcome.