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NSTRUCTION

Examine this patient's hands.

SALIENT FEATURES

History

Painful swollen joints, morning stiffness.

Examination

Ask the patient for permission to examine her hands and then ask whether the hands are sore.

Proceed as follows:

· Comment on deformities (Fig. 1) such as the following: - Subluxation at the metacarpophalangeal joint. -Swan-neck deformity.

-Boutonniere deformity (hyperextension at the terminal interphalangeal joint

and flexion at the proximal interphalangeal joint).

-Z deformity of the thumb.

- Dorsal subluxation of the ulna at the carpal joint.

· Comment on the following signs:

-Nail-fold infarcts and vasculitic skin lesions.

Palmar erythema.

-Wasting of the first dorsal interossei and other small muscles of the hand.

· Test grip and pincer movements. Quickly test for abductor pollicis brevis and mterossel, and pinprick sensation over index and

little fingers. The median nerve may be involved if there is associated carpal tunnel syndrome.

· Examine the elbow for rheumatoid nodules.

· Ask the patient to perform simple tasks involving hand function, such as unbuttoning her clothes, or writing.

· Tell the examiner that you would like to examine other joints.

· Highlight the following points:

-Whether terminal interphalangeal joints are spared or affected.

- Whether the arthritis is active (if the joints are inflamed) or inactive.

DIAGNOSIS

This patient has swan-neck deformity of the fingers (lesions) due to rheumatoid arthritis (aetiology) with marked active arthritis of the

interphalangeal joints, and is unable to button her clothes (functional status).

QUESTIONS

What is the significance of rheumatoid arthritis?

The presence of' nodules indicates seropositive and more aggressive arthritis.

Where else are nodules found?

Flexor and extensor tendons of the hand, sacrum, Achilles tendon, sclera, lungs and myocardium.

What are the skin lesions in rheumatoid arthritis?

Vasculitis, nail-lc)Id infarcts.

What are the causes of anaemia in rheumatoid arthritis?

· Anaemia of chronic disease.

· Megaloblastic anaemia due to folate deficiency or associated pernicious anaemia. · Felty's syndrome.

· Drugs: non-steroidal anti-inflammatory drugs (NSA1Ds) causing iron deficiency anaemia; bone marrow suppression caused by

gold.

What factors have been implicated in anaemia of chronic disease?

· Decreased production of red blood cells:

-Due to inadequate iron: impaired absorption and transport, failure to release

iron stores.

-Due to decreased concentration or marrow resistance to erythropoietin.

- Ineffective erythropoiesis.

-Abnormal development of erythroid progenitor cells.

· Increased destruction of red cells.

What is Felty's syndrome?

It is seen in some patients with severe rheumatoid arthritis and consists of spleno-megaly, anaemia, leukopenia and

thrombocytopenia (hypersplenism), and leg ulcers. Splenectomy ameliorates hypersplenism. Felty's syndrome is associated with

positive rheumatoid factor.

What are the pulmonary manifestations of rheumatoid arthritis?

· Pleural effusion or pleurisy (seen in 25%. of men with rheumatoid arthritis). · Rheumatoid nodules. · Fibrosing alveolitis.

· Caplan's syndrome (rheumatoid arthritis coexists with rounded fibrotic nodules 0.5-5 cm in diameter, mainly in the periphery of

lung fields in coal-worker's pneumoconiosis).

What are the eye manifestations of rheumatoid arthritis?

· Episcleritis.

· Scleritis.

· Scleromalacia, scleromalacia perforans.

· Keratoconjunctivitis sicca.

· SjOgren's syndrome (see above).

What precautions are necessary before upper gastrointestinal endoscopy or general anaesthesia ?

It is prudent to take a cervical spine radiograph to rule out atlanta-axial subluxation.

Which joints are commonly affected in rheumatoid arthritis?

Wrists, proximal interphalangeal joints and metacarpophalangeal joints of the hands, metatarsophalangeal joints and knees.

What is palindromic rheumatoid arthritis?

Palindromic onset is seen in some patients with recurrent episodes of joint stiffness and pain in individual joints lasting only a few

hours or days. Hydroxychloroquine may be of value in preventing recurrences.

ADVANCED-LEVEL QUESTIONS

How would you treat the arthritis?

Prescribe NSAIDs (ibuprofen is the safest at conventional doses) including aspirin. If, after I month of NSAIDs, the symptoms persist

with no sign of remission then a second-line drug should be added. Second-line drugs include hydroxy-chloroquine, sulfasalazine

and penicillamine. Low-dose methotrexate and gold salts are used to prevent disease progression. Treatment with monoclonal

antibody to tumour necrosis factor (etanercept, infiiximab) produces significant improvement in the severity of arthritis. Etanercept is

a fusion protein of the ligand binding region of the TNF receptor that is linked to the Fc portion of the human IgG, and infliximab is a

chimeric (mouse and human) monoclonal antibody against TNF. These TNF inhibitors have surprisingly few side effects. The most

common reactions are at the injection site (in the case of etanercept) and hypersensitivity reactions (in the case of infliximab).

TNF-alpha inhibitors suppress disease activity only during treatment and thus relapses are inevitable once the treatment is

discontinued (N Engl J Med 2000; 343: 1640-1).

If the patient is known to experience gastric distress with NSAIDs, what precautions would you take while prescribing them??

Prophylaxis for NSAlD-associated gastric distress may be attempted with con-current administration of an H2-receptor blocker (such

as ranitidine), omeprazole or misoprostol. The latter is a prostaglandin analogue which has been shown to protect the gastric

mucosa.

What are the neurological manifestations of rheumatoid arthritis?

* Peripheral neuropathy - glove-and-stocking sensory loss.

· Mononeuritis multiplex.

· Entrapment neuropathy, e.g. carpal tunnel syndrome.

· Cervical disease or atlanto-axial subluxation may cause cervical myelopathy.

What are the causes of proteinuria in patients with rheumatoid arthritis?

· Drug therapy: gold salts, penicillamine.

· Amyloidosis.

What is Sjogren's syndrome?

· The association of keratoconjunctivitis sicca (lack of lacrimal secretion) and xerostomia (dry mouth due to lack of salivary gland

secretion) in association with a connective tissue disorder, usually rheumatoid arthritis. This syndrome may be associated with

autoimmune thyroid disease, myasthenia gravis or autoimmune liver disease.

· The Schirmer filter paper test provides a crude measure of tear production. Filter paper is hooked over the lower eyelid; in

normal people at least 15 mm is wet after 5 minutes, whereas in patients with keratoconjunctivitis sicca it is less than 5 mm.

· Anti-Ro (SSA) and anti-SS-B antibodies may be seen in this syndrome.

· Treatment is symptomatic with artificial tears (hypromellose drops or 1% methyl-cellulose), artificial saliva and NSAIDs for the

arthritis.

What are the criteria for rheumatoid arthritis?

American Rheumatism Association criteria:

1. Morning stiffness for at least 1 hour for a duration of 6 weeks or more.

2. Swelling of at least three joints for 6 weeks or more.

3. Swelling of wrist, metacarpophalangeal or proximal interphalangeal joints for 6 weeks or more.

4. Symmetry of swollen joint areas for 6 weeks or more.

5. Subcutaneous nodules.

6. Positive rheumatoid factor.

7. Radiographic features typical of rheumatoid arthritis, i.e. erosions and periarticular osteopenia.

When four or more of the above criteria are met, there is 93% sensitivity and 90% specificity. It is important to note that the

diagnosis of rheumatoid arthritis should not be made on the basis of these criteria alone if another systemic disease associ-ated with

arthritis is definitely present.

What are the poor prognostic factors?

· Systemic features: weight loss, extra-articular manifestations.

· Insidious onset.

· Rheumatoid nodules.

· Presence of rheumatoid factor more than 1 in 512.

· Persistent activity of the disease for over 12 months.

· Early bone erosions.

What are the factors leading to ulnar deviation of the hands?

· In the normal grip the fingers move to ulnar deviation.

· Weakening of radial sides of the joint capsule and the radial insertion of the interossei ligaments.

· The volar supports of the flexor tendon sheath are weakened by inflammation, allowing the tendon to bow in the direction of the ulna during

gripping.

· Ulnar displacement of the extensor tendons in early deviation makes them slip, if the dorsal metacarpophalangeal joint is taut, and thereby

exacerbates the develop-ment of ulnar deviation by acting as a bowstring.

· The joint capsules of metacarpophalangeal joints are weaker on radial sides than on ulnar sides.

A.B. Garrod coined the term 'rheumatoid arthritis' in 1858.

H.S.C. Sjogren, a Swedish ophthalmologist, described this condition in 1933.

A. Caplan, a British physician, was an industrial officer in the Welsh coal mines.

In 1931, Philip S. Hench (1896-1965) of the Mayo Clinic observed that arthritic pain temporarily decreased in pregnant women. For the next 8 years he

studied the phenomenon that allergic conditions such as asthma, hay fever and food sensitivity were also lessened in the presence of jaundice or

pregnancy. He reasoned that a steroid hormone may be responsible, since hormone levels are high in the blood during pregnancy (Hench PS 1953 A

reminiscence of certain events before, during and after the discovery of cortisone. Minn Med 36: 705-10).

Edward Kendall (1886-1972), Chief of the Division of Biochemistry, suggested the name 'corsone' on a piece of paper but Hench amended this to

'cortisone', and thus the steroid hormone was 'baptized'. The 1950 Nobel Prize for Medicine was jointly awarded to Kendall, Hench and Tadeus

Reichstein (1897-) of Basel University, Switzerland, for their discoveries relating to the hormones of the adrenal cortex, their structure and biological

effects (Lancet 1999; 353: 1370).

Sir John Vane, showed that inhibition of prostaglandin synthesis was central to both

the actions and side effects of aspirin (Proc R Coil Physicians Edinb 2000; 30: 191-8).