Joint pain can be a manifestation of disorders confined to the joint and also of a number of systemic disorders. Identifying the cause of joint pain, therefore, can be difficult because of extensive differential diagnosis. In some cases the diagnosis may be hindered by atypical presentation (as in the elderly or immunocompromised), or masked in those with multiple comorbidities and / or symptoms. Consequently it’s prudent to keep the diagnosis open in patients who present with pain in multiple joints. For instance, what may begin as a monoarthritis may in course of time become polyarthritis, thereby necessitating a review of alternative diagnostic possibilities. Similarly, an elderly woman, diagnosed initially as RA, might later develop a molar rash and oral ulcer which would change the diagnosis to SLE.

A careful history and physical examination are essential which will help guide appropriate investigations and management. The most relevant aspects to decide are threefold:

1.       1 - Whether the underlying disorder is inflammatory or not.

2.     2 -Establish the type of onset (acute or otherwise), and its subsequent evolution (i.e. self-limiting, monoarticular, polyarticular symmetrical, polyarticular non-symmetrica. and

3.     3 - The presence of associated extra-articular and systemic manifestations (e.g. fever, rash, eye involvement, bowel symptoms, Raynaud’s, etc.)

The majority of conditions are benign and self-limiting, but a minority (trauma, sepsis, gout) may require an urgent assessment and treatment. 

Presently, in many rheumatologic disorders, applying information from various imaging modalities, such as conventional radiography, CT, MRI, arthrography, bone scintigraphy, and ultrasound within the context of the patient’s history and clinical presentation can help select the best test and lead to a reliable diagnosis, appropriate therapy, and overall better patient care with lower costs and risks.

It’s a common knowledge that ESR,CRP are nonspecific indicators of inflammation, not useful as screening tests for rheumatic diseases, and cannot differentiate one disease from another. Repeated studies of workup for polyarticular complaints and rheumatoid disease demonstrate many variable factors (e.g. age, gender, pregnancy, comorbid diseases, etc.) associated with CRP/ESR discordance. In many studies ESR and CRP values were modestly correlated with each other and they were weakly correlated with disease activity measures. These data suggest that another look at the role of ESR and CRP as markers of inflammation in RA patients seen in routine care may be in order.

Some studies state that it is not necessary to obtain both ESR and CRP measures for clinical disease activity assessment in clinical trials of RA. Neither test adds significantly to clinical measures of disease activity including joint counts and global assessments. Where available, the CRP alone may be preferred for disease activity assessment as a simple, validated, reproducible, non age-dependent test.

In office practice, test selection is generally guided by whether the clinical assessment suggests inflammatory or noninflammatory disease. One inquires into the characteristic hallmarks of inflammation: redness, warmth, soft-tissue swelling, and tenderness. If such symptoms are localized to and encompass an entire joint, one has excellent presumptive evidence for synovitis and an inflammatory process. A good history and clues on physical examination increase the “pretest probability” by asking questions that support the diagnosis of inflammatory arthropathy or systemic rheumatic disease.

In general, although ESR / CRP can be helpful to monitor certain patients, laboratory measures cannot serve as a gold standard for diagnosis and management in all individual patients with RA or any rheumatic disease. I suppose, we (and our patients’ as well) would benefit from an improved understanding of the limitations of laboratory tests in diagnosis and management of patients with rheumatologic disorders.