In the first two differential diagnoses there are often other features. In SLE photosensitive rashes, hair loss, serositis and oral ulceration are seen. Erythrovirus B₁₉ nearly always presents with flu-like symptoms and a widespread rash.

Post-streptococcal arthritis may be preceded by a sore throat but is rare. Psoriatic arthritis is usually asymmetrical but can occasionally present with a symmetrical pattern. Psoriatic nail changes and other evidence of psoriasis are usually present, although these might develop after the onset of arthritis.

Sjögren’s syndrome can be associated with intermittent parotid swelling and sicca symptoms: dry eyes (keratoconjuctivitis sicca) and dry mouth (xerostomia).

How would you manage this patient?

Remember

Rheumatoid arthritis is a multisystem disease so look carefully for pulmonary, cardiac or neurological involvement, although these are less common at presentation.

A full history and general medical examination is essential. Specific points:

• Look for nodules or vasculitis: uncommon at first presentation.

• A full musculoskeletal examination noting the symmetry of the joint involvement.

• Look for persistent inflammatory symmetrical arthritis (PISA). The most common cause of this is rheumatoid arthritis.

The most commonly involved joints at onset in rheumatoid arthritis are: wrists, MCPs, PIPs and MTP joints.

Admission is necessary if the patient is very unwell systemically and to exclude other pathology.

Investigations

• FBC/ESR, biochemistry including globulin level, CRP (the finding of a high ESR but normal CRP is characteristic of SLE)

• ANA/rheumatoid factor

• Anti CCP is positive early in the disease

• X-ray hands and feet for erosions, periarticular osteopenia (Fig. 8.4) (MRI if necessary)

• ASO titre if sore throat

• Blood cultures if febrile

• Erythrovirus B₁₉ titres if the ANA/RhF are negative

Figure 8.4 X-ray of early RA showing typical erosions at the thumb and middle MCP joints and at the ulnar styloid (arrows).

Initial management

• A short period of bed rest, ice packs if only a few joints involved.

• NSAIDS: ibuprofen is the safest; other NSAIDs have a higher risk of GI toxicity, although this patient is young.

• Disease-modifying anti-rheumatic drugs (DMARDs): these should be given at the earliest opportunity because RA is a systemic disease that leads rapidly to joint damage and disability. It is no longer acceptable to treat RA with NSAIDs alone. There is accumulating evidence to show that early DMARD use delays joint damage and functional disability.

Initial DMARDs commonly used include sulfasalazine, methotrexate or azathioprine. Others, such as IM gold and D-penicillamine, are less commonly used but still effective. Hydroxychloroquine and auranofin are the least effective but can be used in combination regimens. Combination therapies are showing good results.

Anti-TNFα agents, e.g. infliximab and etanercept, are effective when initial DMARD therapy has failed. Infectious complications such as tuberculosis are a concern with these agents.

Late manifestations of RA

Changes in the hand are shown in Figure 8.5. Other joints such as knees and hips become involved later in the disease course.

Figure 8.5 Rheumatoid arthritis (RA) – late manifestations.

All drugs need careful explanation to the patient and close monitoring for toxicity.

Prednisolone is not used in young patients but intramuscular methyl prednisolone 40–120 mg gives excellent short-term benefit.

The addition of prednisolone 7.5 mg to existing DMARD therapy might retard the progression of erosions, but studies in this area remain controversial and this is not recommended for general use at present.

Diagnosis.

This patient had a high ESR of 60 mm/h and a CRP of 90 mg/L, suggesting active disease. Her anti-CCP antibodies and rheumatoid factor were positive in the serum, typical of rheumatoid arthritis. The X-rays of her hands showed only soft tissue swelling. An MRI was therefore performed and showed early erosions, confirming the diagnosis.

Progress.

This patient was admitted and symptomatically treated with analgesics. She was started on prednisolone and methotrexate. The pain and swelling improved and she was discharged with still some remaining residual problems. She was given a follow-up in clinic for 2 weeks.

SLE and vasculitis

Case history

A 28-year-old woman is referred to you by her doctor. Six weeks ago she delivered her first baby and the pregnancy and delivery were uneventful. Two weeks after delivery she developed a widespread polyarthritis affecting her hands, feet and knees and a photosensitive rash on her face. In the last week or two she has become extremely unwell with weight loss and painful lesions on her hands and feet.

On examination she is clearly unwell with a facial rash and severe oral ulceration. Examination of her hands and feet shows extensive digital infarcts with necrotic ulceration on the palms, finger pulps and soles of the feet. There are splinter haemorrhages and nail-fold infarcts.

Discuss the differential diagnosis, investigation and management

The differential diagnosis includes an inflammatory autoimmune rheumatic disease such as systemic lupus erythematosus (SLE), which has developed after delivery of her baby. The lesions on her hands (Fig. 8.6) and feet are strongly suggestive of vasculitis, which is a serious prognostic factor that requires immediate therapy.

Figure 8.6 Vasculitic lesions seen in the fingers.

Investigations (Table 8.1) are performed to look for the possibility of major organ involvement, which might be vasculitic. Her urine must be tested immediately for blood and protein and sent for urine cytology looking for fragmented red cells and/or casts. The presence of an ‘active’ urine sediment with fragmented or dysmorphic red cells and granular casts has a > 90% specificity for glomerulonephritis.

Table 8.1 Investigations for SLE and vasculitis

Investigation	Typical finding
FBC	Immune cytopenias, especially neutropenia and thrombocytopenia, are common in SLE
	There may be anaemia of chronic disease or haemolytic anaemia – check Coombs’ test.
ESR and CRP	The pattern of a high ESR but normal CRP is characteristic of SLE
Renal function	U&E, 24-h urine protein/eGFR
Liver biochemistry	Hypoalbuminaemia is common
Lupus serology
ANA	Present in 95% of SLE patients
dsDNA	Specific marker for SLE. A negative dsDNA, however, does not exclude SLE
ENA	Ro/La photosensitivity/Sjogren’s RNP/Sm often seen in severe SLE
Complement	Low values indicate activation of complement or rarely congenital deficiency
ANCA	A marker of vasculitis: a systemic vasculitis is an alternative to SLE