Rheumatology and bone disease

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10 Rheumatology and bone disease

Questions

How can gabapentin and carbamazepine act with a cervical disc prolapse?

Do patients with cervical spondylosis, experiencing neck pain and stiffness, benefit from putting on a neck collar? If so, for how long should the collar be worn?

What is indicated by a straightening of the lumbar spine with a loss of normal lordosis, and is there any relation to ankylosing spondylitis?

Can cervical spondylosis cause hypertonia in one upper limb?

Should a female patient, with mild congestive cardiac failure, microalbuminuria and cervical spondylosis receive IV vitamin D/ analogues? Would this not increase the risk of calcium stones owing to the mild renal impairment? Would oral vitamin D be preferable?

What is the recommended treatment for spinal canal stenosis? Do carbamazepine or vasodilators have a role to play in its treatment?

What technique is used for injecting steroids locally in the case of carpal tunnel syndrome?

In a patient who has sustained an anterior cruciate ligament (ACL) knee injury and whose pain and swelling have subsided on conservative treatment, what are the chances of complications (e.g. osteoarthritis, fibrosis) from the torn ligament. Will the patient be able to lead a normal life?

Is either gapapentin or carbamazepine effective in the treatment of meralgia paraesthetica?

What is the clinical differentiation between Dupuytren’s contracture and ulnar nerve palsy? Is it the absence of sensory deficit in the former? Are there any other differentiating factors?

1. Is a local corticosteroid injection in the palm effective in the case of Dupuytren’s contracture?

2. Can Dupuytren’s contracture occur in early or well-controlled diabetes, or is it more likely to occur in uncontrolled diabetes?

Besides cirrhosis of the liver and diabetes mellitus (DM), what other causes of Dupuytren’s contracture are there? What is the pathophysiology behind it?

According to one of my lecturers, who is a very well-qualified doctor and orthopaedic specialist, there is an indirect connection between osteoarthritis and subclinical local infections (such as periodontal abscesses), changing the pH of bodily fluids. Can you explain this mechanism?

What do you mean by saying that in nodal osteoarthritis each joint is affected one at a time? Is it that each proximal interphalangeal (PIP) or distal interphalangeal (DIP) joint is affected alone, or that at any one time PIP or DIP joints are affected together in one or both hands?

What are the criteria for diagnosing osteoarthritis (OA) of the knee joint radiologically? Are changes to be expected with advancing age? To what extent would I consider it significant in those below 50 years of age? Would you give me some X-ray examples if possible?

1. In a young patient with osteoarthritis, does long-term treatment with paracetamol (acetaminophen) 500mg/day, rather than ibuprofen 600mg/day, lower the incidence of renal toxicity?

2. How great is the risk of renal toxicity with both these treatments?

In India, total knee replacements are being recommended for every case of severe osteoarthritis, without considering factors such as age, weight or medical condition. What are the correct indications for surgery?

Methotrexate therapy is usually begun in rheumatoid arthritis that doesn’t respond to NSAIDs plus 40–120mg methylprednisolone depot. If a remission is then induced, how long should methotrexate therapy be continued? Will the patient (now in remission) be given maintenance therapy?

What is the dose and regimen for folinic acid rescue after methotrexate in rheumatoid arthritis?

1. What are the indicators of remission in rheumatoid arthritis? Is it normalization of erythrocyte sedimentation rate (ESR) or clinical improvement?

2. Does the rheumatoid factor disappear during a remission of rheumatoid arthritis?

What is the relationship between rheumatoid arthritis and weight loss? Can treatment aid the weight loss at the same time as controlling the disease?

Can oral folic acid (1mg/day) be used for high-dose methotrexate therapy with subsequent leucovorin rescue in the treatment of rheumatoid arthritis?

How often should a patient, on 8 mg/day methylprednisolone for the treatment of rheumatoid arthritis and on osteoporosis prophylaxis in the form of 1000mg calcium and 400 IU vitamin D daily, have a dual energy X-ray absorptiometry (DXA) scan to detect the development of osteoporosis?

In what percentage of patients with psoriatic arthritis does the arthritis precede the onset of skin or scalp lesions?

1. Is reactive arthritis a synonym for Reiter’s syndrome?

2. It is said that Reiter’s disease has been related to Chlamydia trachomatis infection. Is this correct?

1. Is the response of an acutely inflamed joint to colchicine pathognomonic of gouty arthritis?

2. We are told that, other than clinical tests, joint fluid microscopy is the specific diagnostic test for gout. What does joint fluid microscopy reveal? Is it the same as a polarized light study revealing needle-shaped urate deposits?

In the prevention of gout, should allopurinol be used for life in a patient who is hypertensive, alcoholic and overweight?

Does a serum uric acid level of 5.7mmol/L need treatment? Can it be significant with cholesterol levels of 213mg/dL (5.5mmol/L)? What is the treatment?

In the diet of patients suffering from gout, should tea, coffee or other compounds containing methylxanthine products be restricted?

1. When do joints that appear slightly swollen, but not warm, need to be tapped?

2. In what circumstances might an immunologically suppressed patient not mount a fever or not have heat around a septic joint?

What is the cause of Pott’s disease?

One thing that often baffles me is that patients with systemic lupus erythematosus often suffer recurrent thrombosis due to lupus anticoagulants (antiphospholipid syndrome). How can an anticoagulant cause thrombosis?

Are elevated homocysteine levels an independent risk factor for progression of systemic lupus erythematosus (SLE)/scleroderma? Kindly suggest some references if possible.

1. What are the indicators of remission in systemic lupus erythematosus (SLE)? Is it the normalization of erythrocyte sedimentation rate (ESR) and the disappearance of antinuclear antibodies (ANA) and other antibodies, or is it clinical improvement?

2. During remission of SLE, do ANA and other antibodies disappear?

When should the use of cyclophosphamide in systemic lupus erythematosus (SLE) be commenced? What is the correct and safe dosage of cyclophosphamide?

1. Given the benefits of dexamethasone, which lacks any mineralocorticoid activity, why is this not prescribed in your book for diseases that require long-term steroid therapy, such as systemic lupus erythematosus or giant cell arteritis?

2. Does dexamethasone have more serious adverse effects than prednisolone? Why is it not generally preferred?

Would an elevated C-reactive protein (CRP) level, in association with a high erythrocyte sedimentation rate (ESR) and in the absence of infection and serositis, exclude the diagnosis of systemic lupus erythematosus?

How do steroids precipitate a crisis in patients with systemic sclerosis?

Are neck and face muscles commonly affected in poly- and dermatomyositis? Does this differ from the muscles that are affected with myasthenia gravis?

1. In dermatomyositis, what is the shawl sign?

2. How frequently is dermatomyositis associated with Gottron’s papules?

How can cranial arteritis be diagnosed in the absence of any physical symptom or feature of the disease other than headache?

Do pulmonary manifestations in Behçet’s syndrome present with pulmonary infiltrates in the upper zone of the lung?

1. Is Behçet’s disease accompanied by an elevated erythrocyte sedimentation rate (ESR)? If so, how often?

2. Can Behçet’s disease be diagnosed in a young adult with an ischaemic stroke and a history of almost weekly mouth ulcers that heal quickly, but with no other symptoms of Behçet’s disease?

Mouth ulcers are too common to be a cardinal feature in the diagnosis of Behçet’s disease. Are there any distinguishing features other than mouth ulcers that would confirm diagnosis?

Please explain how to diagnose familial Mediterranean fever. Is a diagnosis of exclusion still used or are there now more up-to-date tools for the diagnosis?

Is a leucocytoclastic reaction in a tissue biopsy specific for Henoch-Schönlein purpura or is it also associated with other problems?

What are the anatomical, histological and radiological differences between:

3. epiphyseal disc

4. epiphyseal line?

Why does the serum alkaline phosphatase increase in bone disorders and in some other disorders?

What is the normal amount of calcium excreted in the urine in a 24-hour period?

Does hydrochlorothiazide have a prophylactic effect against osteoporosis?

How effective is parathyroid hormone in the management of osteoporosis? Please explain the mechanism.

1. What is the recommended treatment for severe osteogenesis imperfecta?

2. Where two siblings have already been born with severe osteogenesis imperfecta, what is the risk of subsequent children of the same parents being born with this condition?

Why does achondroplasia not affect the mandible (when all other bones are affected)?

If an elderly patient with rheumatoid arthritis who has been taking myocrisin (injectable gold) for several years presents with pancytopenia, should the gold treatment be stopped? If so, what treatment should replace it?

In a patient with dermatomyositis, what laboratory tests should be ordered to exclude systemic lupus erythematosus (SLE)?

What treatment is recommended for tarsal tunnel syndrome?

In a patient with documented antiphospholipid syndrome, should lupus anticoagulant be investigated for? If it is found to be present, will this necessitate the use of anticoagulants?

What are the findings to be looked for during routine fundus examination in patients on long-term chloroquine or any other antimalarial therapy for the treatment of systemic lupus erythematosus (SLE)?

What is the sensitivity of plain X-ray in detecting ankylosing spondylitis-related spine lesions in both early and late disease, and is there a specific diagnostic test for this?

It is reported by the Oxford Handbook of Clinical Medicine that glucosamine and chondroitin sulphate have failed an NEJM trial for the treatment of osteoarthritis? Is there still a valid use for these compounds?

Can high serum titres of C-reactive protein (CRP) with normal erythrocyte sedimentation rate (ESR) indicate relapse of rheumatoid arthritis in established rheumatoid arthritis which is in remission?

What is the positive predictive value of hyperuricaemia in the diagnosis of gout?

What is Scheuermann’s disease? And is this a specific clinical or radiological or haematological disease? What is the treatment for this disease?

Both of these drugs are useful in neuropathic pain. Gabapentin has fewer side-effects and is becoming a first-line drug for nerve injury pain.

A collar might be needed in the first 1–2 days. Fortunately, most patients are sensible enough not to wear them for any longer! They do not help in the long term.

This does occur in ankylosing spondylitis. The lumbar spine can become straighter with the loss of the normal curvature (lordosis).

Cervical spondylosis can lead to upper motor neurone signs. A spastic parapesis is the most common finding. There is often, in addition, evidence of a lateral disc protrusion with cervical root symptoms and signs.

Yes. Oral vitamin D is always preferable, except sometimes in chronic kidney disease. There seems, however, no reason for this particular patient to be given vitamin D at all.

Spinal canal stenosis is diagnosed by the clinical history with confirmation of spinal cord compression on magnetic resonance imaging (MRI). The best treatment in these confirmed cases is surgery. Many patients with back pain are misdiagnosed because of slight but insignificant narrowing of the cord on MRI. Carbamazepine can be helpful in chronic back pain of undetermined cause. Vasodilators are of no help.

This procedure should only be carried out by an experienced person who has been trained in the procedure. Nerve atrophy or necrosis can occur if steroids enter the median nerve directly.

The injection site is on the radial side of palmaris longus tendon; a mixture of lidocaine and steroid is used. The patient should be asked if he or she feels any distal sensation, which suggests that the needle is in the median nerve. Some operators use ultrasound to help to get the steroid into the tendon sheath.

With good physiotherapy, patients can lead a normal life but in young athletes ACL repair is a better option. Osteoarthritis can occur in later life.

Both drugs have been used with varying success. This self-limiting condition usually improves without medication.

Dupuytren’s causes flexion contracture of the fingers with thickening of the palmar fascia. Ulnar nerve palsy causes fixed flexion of the fingers, mainly the ring and little finger. Sensation can be lost.

1. Triamcinolone is used in early and painful contractions with some benefit.

2. It occurs in 40% of diabetics; the incidence increases with age and duration of diabetes.

It is also associated with alcohol abuse, DM, chronic obstructive pulmonary disease (COPD) and epilepsy. The pathophysiology is not understood.

The pathogenesis of osteoarthritis is unclear and might well be different in different locations in the body. One explanation has been that it could be the result of occult infections. There is no good evidence to support this and most workers in this field think it unlikely.

Further reading

Poole AR, Howell DS (2001) Etiopathogenesis of OA. In: Moskowitz RW, Howell DS, Goldberg VM, Hankin HJ (eds) Osteoarthritis: Diagnosis and Management, 3rd edn. Philadelphia, Saunders, pp. 29–47.

In osteoarthritis there is stuttering onset of inflammation affecting one joint at a time.

Plain X-ray and skyline views of the patella are necessary. Joint space narrowing, osteophytes, subchondral radiolucencies and sclerosis are the classic signs of OA (Fig. 10.1). Osteophytes are the best predictor of knee pain. Some of these changes will be seen in a patient of advanced age and the significance must be correlated with the symptoms and signs. MRI is commonly used for more precise identification of the damage in osteoarthritis.

Fig.10.1 The early signs of osteoarthritis. Medial compartment narrowing results from cartilage thinning with subarticular sclerosis and marginal osteophyte formation.

1. Acetaminophen is called paracetamol in many countries. It has no renal toxicity in therapeutic dosage. Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID).

2. The prevalence of renal toxicity is relatively low but because of intensive usage, many persons are at risk.

These are evolving and now many patients with stiff painful knees are being offered arthroplasty. There are, however, risks to these procedures and medical therapy should be provided first.

Methotrexate therapy is often continued for many years (at least 10 years) if the patient remains well. Remember to check the liver biochemistry carefully and make sure that the prescription is for a once weekly dose.

Give as calcium folinate 24 hours after the methotrexate, 15 mg orally every 6 hours for 2–8 doses.

1. Both; clinical improvement is the most important but normalization of the ESR is also helpful.

2. Reduction in the rheumatoid factor titres occurs with disease-modifying anti-rheumatic drug (DMARD) therapy.

‘Active’ rheumatoid arthritis makes people feel unwell so that they don’t eat, and hence lose weight. Control of the disease will allow them to regain appetite. Be careful not to let the patient get overweight.

Further reading

Firestein GS (2006) Inhibiting inflammation in rheumatoid arthritis. New England Journal of Medicine354: 80–82.

Methotrexate 7.5mg weekly is used in rheumatoid arthritis. Folic acid 5mg weekly can be given to reduce the side-effects. Calcium folinate (Leucovorin) is given after high-dose methotrexate to counteract the folate antagonist action of the drug.

Six per cent of patients have arthritis preceding the skin lesions.

1. Reiter’s describes a form of reactive arthritis where there is arthritis with urethritis, conjunctivitis, keratoderma blenorrhagica and circinate balanitis (see K&C 7e, p. 536).

2. In this context, joint fluid microscopy refers to polarized light. In gout, crystals are needle shaped and negatively birefringent.

In such a patient the hypertension should be treated. Drug therapy may well be needed but both reduction in weight and reduction in alcohol consumption are helpful in reducing blood pressure. Reduction in alcohol consumption (especially beer) will also reduce the number of attacks of gout.

The above measures are not always successful in preventing further attacks of gout, and in such a patient allopurinol will be required for life. However, a new drug, febuxostat, has become available.

Further reading

Becker MA et al. (2005) Febuxostat compared with allopurinol in patients with hyperuricaemia and gout. New England Journal of Medicine353: 2450–2461.

Do not treat uric acid levels unless they are very high. You treat the symptoms produced by a raised uric acid; that is, gout. Cholesterol levels should be taken in isolation and not related to the uric acid level. The level of 213mg/dL of cholesterol will require treatment in patients who have evidence of cardiovascular disease, usually with a statin.

Yes, a diet that reduces total calories as well as cholesterol intake (avoiding offal, fish, shellfish, spinach and beer – all rich sources of purines) is advised. This can reduce the serum urate by 15%.

Aspiration of a joint should always be undertaken if septic arthritis is a possibility (even if unlikely!). Aspiration is also useful in crystal arthritis. Constitutional symptoms are common but might not be present in severely debilitated patients and in patients on steroids or immunosuppressive agents.

Tuberculosis of the spine.

This paradoxical association between a prothrombotic state and the anticoagulant effect of antibodies is not fully understood.

Further reading

Lockshin MD, Erkan D (2003) Treatment of the antiphospholipid syndrome. New England Journal of Medicine349: 1177–1179.

Yes; homocysteine levels are an independent risk factor for the progression of cardiovascular disease in SLE/scleroderma.

Further reading

Loscalzo J (2006) Homocysteine trials – clear outcomes for complex reasons. New England Journal of Medicine354: 1629–1632.

Svenungsson E et al. (2001) Risk factors for cardiovascular disease in systemic lupus erythematosus. Circulation104: 1887.

High serum levels of ANA and anti-dsDNA with low complement do reflect disease activity. Clinical improvement is still the best indicator but a fall in antibody levels is helpful. They do not disappear. The ESR is raised in proportion to the disease activity.

Many patients with SLE do well with little treatment. Cyclophosphamide is mainly used for lupus nephritis and vasculitis. For lupus nephritis, 0.75g/m² has been used IV over 60 minutes.

Dexamethasone is a highly potent glucocorticoid. Its main use is topically on the skin and by inhaler in asthma. Its high potency means that steroid side-effects occur very easily and dose can not be adjusted quickly; prednisolone is therefore usually preferred for chronic conditions.

No. The ESR is raised; the CRP is usually normal but this is not reliable enough to be diagnostic.

There is evidence to suggest that steroids precipitate a renal crisis in scleroderma. The mechanism is unclear but might be related to hypertension.

Symmetric proximal muscle weakness is the most common presentation of polymyositis. Myasthenia gravis initially affects the eyes and other muscles controlled by cranial nerves. There can, however, be overlap.

1. Involvement of the skin of the back of the neck, upper torso and shoulders in a shawl-like distribution.

2. 70–80% and is pathognomonic.

Headache in an elderly person with a high erythrocyte sedimentation rate (ESR) is often all that is required. Without a rise in ESR the diagnosis is unlikely. Biopsy of the temporal artery is usually performed to confirm diagnosis; but remember, the inflammation is segmental and therefore might be negative.

The findings are variable but nodular and reticular shadowing in the upper zone have been noted.

Further reading

Erkan F, Gul A, Tasali E (2001) Pulmonary manifestations of Behçet’s disease. Thorax56: 572–578.

1. Yes, in over 50% of cases. The C-reactive protein is also raised.

2. No; you need recurrent aphthous ulcers occurring more than three times per year, plus two of the following: genital ulcers, eye lesions, skin lesions, positive pathergy test.

The international criteria for diagnosis of Behçet’s state that the oral ulcers must recur more than three times per year. In addition to this, the ulcers are usually more extensive – genital ulcers, defined skin or eye lesions with a positive pathergy test (papule or pustular formation after a skin injury for e.g. by a needle) also occur.

The diagnosis is still made on clinical grounds because identifying mutations in the FMF gene (MEFV on chromosome 16) is not always possible. The criteria used are:

• Intermittent episodes of fever.

• Serositis with abdominal pain and tenderness; pleuritis.

• The presence of amyloidosis.

• The therapeutic response to colchicine.

• Being of Mediterranean descent with sometimes a possible family history.

Further reading

Hatem El-Shanti et al (2006) Familial Mediterranean fever in Arabs. Lancet367: 1016–1024.

A leucocytoclastic reaction also occurs in the condition known as leucocytoclastic vasculitis.

• Physis: used for the growing part of a bone.

• Metaphysis: the site of advancing ossification adjacent to the epiphyseal cartilage.

• Diaphysis: shaft of bone.

• Epiphysis: extremity of bone with separate ossification centre. The ‘line’ is the junction of the epiphysis and diaphysis. The ‘disc’ is the band of cartilage between the epiphysis and diaphysis which is replaced by bone in later life.

Osteoblasts are rich in alkaline phosphatase, so that in any bone condition with increased activity of osteoblasts, e.g. in the growing child or in Paget’s disease, there will be an increase in the serum alkaline phosphatase.

Alkaline phosphatase is also found in the placenta so that the serum level is raised in pregnancy.

6.25mmol (250mg) in females to 7.5mmol (300mg) in men in 24 hours.

Further reading

Ray WA et al (1989) Long-term use of thiazide diuretics and risk of hip fracture. Lancet1: 687–690.

Recombinant human parathyroid hormone peptide 1–34 (teriparatide) and the whole protein 1–84 stimulate bone formation. Teriparatide has been shown to reduce vertebral and non-vertebral fractures in postmenopausal women with established osteoporosis.

Further reading

Sambrook P, Cooper C (2006) Osteoporosis Lancet367: 2010–2018.

1. Bisphosphonates are used for moderate and severe disease (see reference).

2. The risk is 1:2 but may be less with decreased penetrance.

Further reading

Rauch F, Glorieux FH (2004) Osteogenesis imperfecta. Lancet363: 1427.

This is not known.

The gold treatment should be stopped. If there is ‘active’ disease then referral to a rheumatologist for possible consideration of infliximab is recommended.

The differentiation is usually not a problem. The proximal muscle weakness is unusual in SLE. The creatine kinase is usually raised in dermatomyositis. Double-stranded DNA is specific for SLE but is present in only 50% of cases. Remember the overlap syndrome (see K&C, 7e, p. 548) in which features of both diseases can be present.

Arch supports and wider shoes often help, and NSAIDs are useful for pain and inflammation. Steroid injection into the tendon is also effective; surgery is the last resort.

The lupus anticoagulant is usually looked for but treatment of the syndrome does not depend entirely on this. Treatment is given if the patient has had a thrombotic episode or, occasionally, if there are high levels of antibody and lupus anticoagulant present.

All patients should have near visual acuity of each eye performed before treatment and annually on treatment. Patients who have any visual symptoms should be seen immediately. Fundoscopy will show round, pigmented lesions near the macula but it is the visual acuity and visual field examination that will give the first clue.

In early disease the sensitivity is low. In one series of 199 patients diagnosed clinically, 76 had a normal plain X-ray. It is very sensitive for late disease, >95%. In patients suspected clinically to have AS (ankylosing spondylitis) an MRI scan should be performed if the plain X-ray is normal.

A recent trial showed no benefit but some doctors believe a subset of patients (unidentified) may benefit.

Yes, the CRP is more sensitive and usually rises before the ESR in many chronic inflammatory conditions such as rheumatoid arthritis.

Hyperuricaemia is not useful in gout. Gout is a clinical diagnosis supported by finding needle-shaped crystals in the joint fluid. The serum uric acid is usually raised but the level falls after an acute attack so a normal level is not helpful. Gout never occurs with the serum uric acid level in the lower half of the range.

Scheuermann’s disease is a juvenile kyphosis with anterior wedging of 5° or greater in at least three adjacent vertebral borders as seen on lateral spine X-ray. Treatment is with strengthening and stretching exercises.

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