Reducing Prenazone and Feeling Stifness Again

Polymyalgia rheumatica is an inflammatory status that causes a particular pattern of joint pain and stiffness, most ordinarily in older people. Information technology is a rheumatic disorder closely associated, and often co-existing, with giant cell arteritis. Diagnosis is based on the patient's clinical features, supported past laboratory investigations.

Polymyalgia rheumatica is an inflammatory condition that causes a detail pattern of joint pain and stiffness, virtually commonly in older people. It is a rheumatic disorder closely associated, and frequently co-existing, with behemothic cell arteritis. Diagnosis is based on the patient's clinical features, supported past laboratory investigations. Before making a diagnosis, other conditions which can mimic polymyalgia rheumatica should exist ruled out, and most importantly, the patient should be assessed for co-existing behemothic cell arteritis. Treatment of polymyalgia rheumatica, with long-term oral prednisone, can usually exist managed in master care, but referral to a Rheumatologist may be necessary if the diagnosis is unclear, the response to treatment is poor or multiple relapses of symptoms occur during tapering.

What is polymyalgia rheumatica?

Polymyalgia rheumatica is an inflammatory rheumatological syndrome that causes pain and stiffness, most commonly in the neck, shoulders and pelvic girdle. The pain and stiffness is worse in the morn, usually lasts for one hr or more and may be accompanied by systemic features, such as fever, fatigue and anorexia.ⁱ The onset of symptoms is typically between 2 weeks and 2 months.ⁱⁱ

The incidence of polymyalgia rheumatica increases with age, with an average historic period of onset of approximately lxx years, and it rarely occurs in people aged under 50 years.³ The incidence of polymyalgia rheumatica is highest in people of Scandinavian or Northern-European descent, although it does occur in people of other ethnicities.³ Polymyalgia rheumatica is twice as common in females.³ In total, the yearly incidence is approximately fifty per 100 000 people aged over 50 years.^iv

It is not known what causes polymyalgia rheumatica. Information technology is closely associated with giant prison cell arteritis, although it is two to three times more common.^two Like giant prison cell arteritis, both genetic and external factors, east.g. infection, are thought to be involved in the development of the condition.ⁱⁱⁱ

Polymyalgia rheumatica is managed with corticosteroids and meaning remission of symptoms can exist expected within one week of starting handling.^five The prognosis is normally skilful and complications, such as recurrent relapse of symptoms, are limited.³

Never trust a diagnosis of polymyalgia rheumatica

As polymyalgia rheumatica has a non-specific clinical presentation and few pregnant sequelae, information technology should exist diagnosed with caution. Ruling out other illnesses, such as cancers or insidious-onset rheumatoid arthritis, is more than of import than immediately treating polymyalgia rheumatica, if information technology is present. Unlike giant jail cell arteritis, a delay in handling volition not significantly endanger a patient. Conversely, long-term corticosteroid handling can accept meaning adverse effects and a daily handling course of up to iii years will be a burden for many people. In improver, an initial or partial response to corticosteroids may be seen in people with other conditions who present with similar features to polymyalgia rheumatica, such every bit rheumatoid arthritis, and this may provide false reassurance that the right diagnosis has been identified. Therefore, even if a patient presents with clinical features typical of polymyalgia rheumatica, and a working diagnosis is made, they should be regularly reviewed and other possible causes ever considered, particularly if the patient does non respond to treatment.

For further information, see: "Giant jail cell arteritis".

Making a diagnosis

The British Order for Rheumatology has developed a gear up of inclusion and exclusion criteria for diagnosing polymyalgia rheumatica.^six These criteria were derived by consensus and stand for a clinically typical patient with polymyalgia rheumatica. They are most useful for "ruling in", i.e. a patient who meets the criteria is likely to have polymyalgia rheumatica, rather than "ruling out", equally people with polymyalgia rheumatica can present atypically, such as with a shorter duration of symptoms or found to have a normal acute phase response.

The cadre inclusion criteria are:⁶

Age > 50 years
Symptom duration > two weeks
Bilateral shoulder or pelvic girdle agonized, or both
Morn stiffness duration of > 45 minutes
Evidence of an acute-phase response, e.g. raised CRP

The core exclusion diagnoses are:⁶

Infection
Malignancy
Giant prison cell arteritis

Patient presentation, history and exam

Shoulder, neck, hip and pelvic pain

Shoulder pain occurs in 70 – 95% of people with polymyalgia rheumatica.^two Between 50 – 70% of people report hip and neck pain.² Upper arm pain is also mutual. Pain is commonly bilateral and symmetrical, although it may be worse on one side early in the course of the condition.^three Pain will commonly worsen with movement of the affected area. Pain may radiate to the elbows and knees.^three There may be tenderness on examination, most normally in the upper arms, cervix and shoulders, usually related to synovial or bursal inflammation. Muscle weakness is non a feature of polymyalgia rheumatica, although this may exist difficult to appraise due to muscle pain.⁵

Stiffness

Marked morning time stiffness that persists for at least 45 minutes is typical for people with polymyalgia rheumatica.^half-dozen The patient may depict difficulties with daily activities, such every bit brushing their hair or getting out of bed. In some patients the stiffness will be so severe that rising from a chair or turning over in bed are difficult. Asking the patient about the severity of stiffness in the morning compared to the evening may be helpful. Stiffness and hurting that lessens over the course of the twenty-four hours can exist important in differentiating polymyalgia rheumatica from other forms of degenerative arthritis, which ordinarily cause pain or stiffness that is worse with activity and worse afterwards in the day.¹

Systemic symptoms and signs

Systemic features may be present in approximately one-3rd of patients and include low grade fever, malaise, anorexia and weight loss.ⁱⁱ A brief general exam, including assessment of temperature, pulse and blood pressure, is recommended.

Peripheral symptoms

Symptoms, such as pain or stiffness in the joints of the easily and anxiety, are present in approximately half of people with polymyalgia rheumatica, nonetheless, peripheral symptoms are also common in other, similar conditions, such every bit rheumatoid arthritis and other inflammatory arthritides.ⁱⁱ A predominance of peripheral symptoms may suggest an alternative diagnosis, such as rheumatoid arthritis.³ It is of import to besides examine the hands, feet, knees and elbows for signs of articulation inflammation.

Giant cell arteritis symptoms

E'er specifically enquire about symptoms that may suggest giant cell arteritis, such as unilateral temporal headaches, scalp tenderness, jaw claudication or visual symptoms.³

For further information, see: "Giant cell arteritis".

Differential diagnosis

The differential diagnosis of polymyalgia rheumatica is critically important, particularly for atypical cases, or where inflammatory markers are normal. Incorrectly diagnosing polymyalgia rheumatica and missing a diagnosis such as cancer or an occult infection tin accept significant consequences. Conversely, a patient with polymyalgia rheumatica who remains untreated in the short term is unlikely to take any significant adverse effects. The aim should be to rigorously exclude all other possibilities rather than quickly diagnosing polymyalgia rheumatica. Atypical clinical features such as historic period < threescore years, chronic onset (longer than 2 months), lack of shoulder involvement, muscle weakness, peripheral joint affliction, predominance of hurting with trivial or no stiffness, prominent systemic features, a very high or normal CRP (run into "Laboratory investigations") or lack of response to a trial dose of prednisone (see "Treatment of polymyalgia rheumatica") should lead to consideration of alternative diagnoses and consultation with a Rheumatologist where necessary.

Conditions that should be considered include:^{3, half dozen}

Behemothic cell arteritis
Malignancy
Rheumatoid arthritis and other arthritides
Endocrine and iatrogenic causes of proximal myopathy, due east.g. hypothyroidism, Cushing'southward affliction, statin-induced myopathy/myalgia
Osteoarthritis and other degenerative musculoskeletal conditions, eastward.thousand. rotator cuff tendinopathy
Systemic lupus erythematosus or polymyositis
Fibromyalgia and localised causes of pain
Occult infection, e.1000. sub-acute bacterial endocarditis

Laboratory investigations

If the patient's presentation suggests polymyalgia rheumatica is likely, the following tests should be requested:^iv-6

C-reactive protein (CRP)
Full blood count (FBC)
Liver function tests (LFTs)
Creatinine and electrolytes – equally a baseline prior to initiation of corticosteroid treatment

An elevated CRP level in a patient with symptoms of polymyalgia rheumatica should increase suspicion of the condition.⁶ However, a normal acute phase response does not dominion out polymyalgia rheumatica. ESR is sometimes recommended in the literature, however, CRP alone is likely to be sufficient to aid the diagnosis of polymyalgia rheumatica in most people. In add-on, some laboratories volition no longer accept requests for ESR outside of a express range of weather. If the initial CRP is normal, and the patient'south symptoms strongly suggest polymyalgia rheumatica, it may exist appropriate to then request an ESR at follow-up.

Most patients with polymyalgia rheumatica take mild-to-moderate anaemia, and may have elevated white blood cell and platelet levels.² Approximately i-3rd of patients will take mildly aberrant liver function tests, particularly alkaline phosphatase.²

Depending on the patients symptoms and signs, boosted tests may need to be added to rule out other potential diagnoses, including:^{half dozen}

Thyroid stimulating hormone (TSH)
Rheumatoid factor and, potentially, anticyclic citrullinated peptide (anti-CCP) antibodies
Serum protein electrophoresis (consider serum free light chain analysis if electrophoresis is negative)
Creatine kinase
Antinuclear antibodies

Imaging is not essential for diagnosis

If ultrasound is accessible, assessment of the shoulder and hip joints can exist considered.⁶ Bursitis and synovitis are common manifestations of polymyalgia rheumatica.^two Plain 10-rays of affected joints will unremarkably be normal and therefore are non required for investigating polymyalgia rheumatica.

Additional investigations such equally CT scanning, and MRI imaging may be used in a secondary care setting to help identify bursitis, synovitis or tenosynovitis in the shoulders and hips in singular cases, and for ruling out other potential diagnoses.

Distinguishing polymyalgia rheumatica from rheumatoid arthritis

Rheumatoid arthritis tin be a challenging condition to differentiate from polymyalgia rheumatica, especially in patients who are after found to have seronegative or late-onset rheumatoid arthritis.³ Although the initial clinical presentation tin be very similar with many overlapping symptoms and signs, the following features may help distinguish between the two conditions:

Polymyalgia rheumatica is rare in people aged < l years, therefore rheumatoid arthritis is a much more probable diagnosis in this age group⁵
The onset of symptoms tends to exist more gradual in people with rheumatoid arthritis
Typically, symptoms of pain and swelling in the smaller distal joints are more mutual in people with rheumatoid arthritis, however, approximately half of people with polymyalgia rheumatica volition besides have involvement of the peripheral jointsⁱⁱⁱ
Characteristically the wrist and metacarpophalangeal (MCP) joints are affected in people with rheumatoid arthritis, therefore a patient presenting with myalgia and clinical evidence of symmetric synovitis in the wrists or MCP joints is more likely to accept a diagnosis of rheumatoid arthritis than polymyalgia rheumatica³
A family history may increase the individual risk of rheumatoid arthritis, and should be considered⁷

If the clinical diagnosis remains uncertain:

Rheumatoid factor should be requested, however, a negative test does not rule out the condition as some patients will have seronegative rheumatoid arthritis. If there is still incertitude about the diagnosis, anti-CCP antibodies may be useful.²
X-rays of afflicted joints may bear witness erosive changes consequent with rheumatoid arthritis

A trial of treatment with corticosteroids can be considered in patients who are seronegative for rheumatoid gene and have symptoms and signs that could exist indicative of either condition. In a patient with polymyalgia rheumatica there is likely to be a rapid, potent clinical response to low dose prednisone (xv mg). If the patient has rheumatoid arthritis, the response to low dose prednisone is likely to be less pronounced.^three,8 In some patients, clinical features more characteristic of rheumatoid arthritis may evolve during the trial of corticosteroid.

Handling of polymyalgia rheumatica

Corticosteroids are the starting time-line treatment for polymyalgia rheumatica. Corticosteroid treatment is predominantly for symptom control, and there is no clear prove that information technology will alter the natural history of the status, which is largely self-limiting.

Once all other differential diagnoses have been considered, the patient should be assessed for response to an initial dose of prednisone, xv mg, daily.⁶ The dose should be taken in the forenoon, with nutrient.

If the patient reports a significant improvement in their symptoms within i week, this is consequent with polymyalgia rheumatica, and treatment can continue.^six Alternative diagnoses should exist considered if there is a minimal response to corticosteroid treatment.

The patient'southward acute stage response, measured with CRP, should normalise within four weeks.⁶

The British Gild for Rheumatology guidelines suggests the following method for titrating the dose of prednisone in people with polymyalgia rheumatica:^{half dozen}

Initial dose – fifteen mg, one time daily, for three weeks, followed by;
12.5 mg, once daily, for three weeks, followed by;
10 mg, once daily, for four to half dozen weeks, followed past;
A reduction of ane mg from the daily dose, every four to eight weeks

In practice, Rheumatologists may use a faster tapering regimen to lessen exposure to prednisone, such as reducing the dose every 2 weeks, downward to 10 mg, followed by reductions of 1 mg per month, depending on the patient'southward symptoms. If the patient is at higher take a chance of adverse effects from long-term steroid apply, e.k. is elderly or has co-morbidities, discuss an appropriate dosing regimen with a Rheumatologist.

If symptoms of polymyalgia rheumatica reoccur during the dose tapering period, return the patient to their previous steroid dose and and then re-start the taper once again from that point. The low dose "tail" of the taper will need to be very gradual in some people to prevent symptom recurrence. Some patients will require treatment with low-dose corticosteroids for two to 3 years due to recurrent relapses.

Vitamin D supplements should be prescribed alongside long-term corticosteroid treatment for all people with polymyalgia rheumatica. Adequate dietary calcium, or supplementation if this is not possible, is also necessary.

Bisphosphonates should be considered in patients with a previous history of fragility fractures or reduced bone-mineral density.⁶

A proton pump inhibitor (PPI), such equally omeprazole may be considered for people who feel adverse gastrointestinal affects when taking prednisone.⁶

For further data, see "Practical consideration when prescribing long-term corticosteroids".

Follow-up of people with polymyalgia rheumatica

Early follow-up to assess the response to handling is recommended. A follow-up consultation should be scheduled inside a few days later starting corticosteroid treatment, and then further follow up appointments scheduled i, 2, three and half-dozen weeks later, where possible. Follow-up should and then occur once every three months for the duration of corticosteroid handling.

A history and clinical examination including an cess for symptoms and signs of giant jail cell arteritis, such as scalp tenderness, temporal artery tenderness and new-onset or new type of headache, should be included in each follow-up. If symptoms of giant cell arteritis arise, the patient should be presumed to have the status, and referred to secondary intendance for temporal artery biopsy.⁶ As well appraise for symptoms and signs of corticosteroid adverse furnishings (see: "Applied considerations when prescribing long-term corticosteroids" for further information).

Clinical signs and symptoms are the primary marking for relapse, with laboratory tests providing supporting data just.¹ CRP, FBC, creatinine, electrolytes and HbA_1ctests* (due to the increased gamble of diabetes in people taking long-term steroids) are recommended at each follow-up consultation,^{half dozen} however, in practice, not all tests would exist necessary in each follow up appointment and this is based on clinical sentence.

Relapses of polymyalgia rheumatica symptoms should be treated with a return to the higher, previous dose of prednisone.^{half dozen} After two relapses, consideration should be given to a trial of disease-modifying anti-rheumatic drugs (DMARDs), usually methotrexate.⁶ This will require consultation with a Rheumatologist, and if a DMARD is prescribed, regular monitoring is necessary. The dosing and monitoring regimen should exist decided upon in consultation with the Rheumatologist. Methotrexate is usually continued until the corticosteroids can be tapered without the recurrence of polymyalgia rheumatica symptoms.^iv In one case the steroids take been successfully tapered, methotrexate can usually be tapered over approximately 3 months.⁴

* A fasting glucose test should be used for monitoring in the starting time two months of steroid handling, as serum glucose will rise too rapidly to be accurately captured by HbA_1c. Afterwards two months, an HbA_1c test tin be used.

Applied considerations when prescribing long-term corticosteroids

Corticosteroids are associated with pregnant adverse effects and they must exist slowly tapered rather than stopped abruptly. The everyman constructive dose should be used, then tapered and stopped every bit soon as possible.

The following practice points should be considered whenever a patient is prescribed corticosteroids long-term:⁹

The patient's co-morbidities and take chances factors for adverse effects should exist evaluated and managed where indicated, these include; hypertension, diabetes, peptic ulcer, contempo fractures, cataract/glaucoma, chronic infection, dyslipidaemia and concurrent NSAID use
During the grade of treatment, monitor body weight and claret pressure, assess for peripheral oedema and heart failure and test serum lipids, HbA_1c (or fasting glucose in the first two months) depending on the individual patient'due south risk of agin effects, dose and duration
If the patient's dose is ≥7.5 mg, daily, for more than than iii months, vitamin D supplementation is necessary, along with acceptable dietary calcium
Bisphosphonates should be prescribed to patients with risk-factors for osteoporosis
Patients treated with corticosteroids and NSAIDS should be given appropriate gastro-protective medicines, normally a proton pump inhibitor
Patients taking corticosteroid handling for longer than one month, who need to undergo surgery, will require perioperative management with adequate glucocorticoid replacement to overcome potential adrenal insufficiency

Tapering the dose

Tapering must exist done carefully to avert relapses of the condition and potential adrenal deficiency resulting from hypothalamic-pituitary-adrenal axis (HPA) suppression. Higher doses of corticosteroid, e.g. 20 mg daily, for more than than three weeks, or bedtime dosing increase the likelihood of HPA axis suppression. Higher doses also increase the likelihood of adverse affects. The taper is normally started as soon as symptoms are under control. The dose is reduced by x% every two to iv weeks depending on the severity of symptoms, response to prednisone and the starting dose. The individual condition being treated will alter the length of the taper, east.thousand. in a person with polymyalgia rheumatica, the course of treatment is usually 2 to three years, with a gradual taper flow. The dose of prednisone should be titrated against the patient'due south symptoms, not their acute phase response, i.eastward. the dose may not need to be increased when the CRP rises if the patient remains asymptomatic.

The agin effects of corticosteroid handling

Adverse furnishings of corticosteroids include:^x

Pare changes and disorders, e.g. thinning and bruising, striae, acne, baldness and hirsuitism
Torso composition changes, eastward.g. weight gain, Cushingoid features
Ocular disorders, eastward.g. glaucoma and cataracts
Cardiovascular disease
Gastrointestinal disorders, e.thousand. dyspepsia, oesophagitis, gastritis, ulcers, bleeding
Osteoporosis
Primal nervous system changes, e.k. mood changes, restlessness, depression, psychosis
Diabetes
Renal changes, e.g. hypertension and fluid retentivity

Older age, higher cumulative doses of corticosteroids and female sex increase the hazard of adverse effects occurring.¹¹

Preventing the agin effects of corticosteroids

Vitamin D supplements should be prescribed aslope long-term corticosteroid treatment, in patients taking doses of ≥7.v mg, daily, for more than three months.^ix Colecalciferol* ane.25 mg, once monthly, is recommended for vitamin D supplementation.¹⁰ Patients do not need their vitamin D levels to be tested, but if they take been, and severe deficiency has been detected, a loading dose of one i.25 mg tablet, daily for ten days is recommended.^ten Calcitriol, 500 – 750 nanograms, daily, tin be used instead of colecalciferol for patients with severe renal damage.¹⁰

* Recommended International Not-proprietary Names (RINN or INN) spelling

Calcium supplementation is besides recommended, but in that location accept been concerns that calcium supplementation may increment cardiovascular risk, especially in older people.^{12, thirteen} General dietary advice may exist more advisable for most people, and supplementation reserved for people in whom dietary calcium intake alone is insufficient. If calcium supplementation is required, oral calcium carbonate ane.5 1000, daily, tin be considered.¹⁰

Ideally a os-mineral density (BMD) scan of the lumbar spine and hip should be requested for patients when starting long-term corticosteroids, however, this depends on the availability and funding of the local service, e.one thousand. some services require that patients have been taking corticosteroid treatment for 3 months before a scan is prioritised.²

Bisphosphonates should be considered in patients with a previous history of fragility fractures or reduced bone-mineral density.⁶ Alendronate or zoledronic acid are recommended for nigh people who require a bisphosphonate for corticosteroid-related osteoporosis prevention, based on patient preference and the expected length of corticosteroid handling.

Alendronate, 70 mg, once weekly, should be taken start matter in the morning, on an empty stomach, with a total glass of water to ensure acceptable absorption.¹⁰ The patient should then refrain from eating or taking other medicines and remain upright (i.e. sitting or standing) for thirty minutes to minimise the hazard of oesophageal irritation or erosion.

Zoledronic acid, v mg 4 infusion over xv minutes, once per year is an alternative.¹⁰ The patient should be well hydrated prior to starting the infusion. The patient should have their renal function assessed prior to starting, and exist informed that dizziness and influenza-similar symptoms are common after infusion.

The Special Authority requirements for the initial application for either alendronate or zoledronic acid require that:

The patient is receiving systemic glucocorticosteroid treatment (≥v mg per mean solar day prednisone equivalent) and has already received or is expected to receive treatment for at least three months, and;
- The patient has documented BMD ≥1.5 standard deviations beneath the mean normal values in young adults (i.due east. T-Score ≤i.v), or;
- The patient has a history of one significant osteoporotic fracture demonstrated radiologically, or;
- The patient has had a Special Authorization approval for alendronic or zoledronic acid* (underlying cause – glucocorticosteroid therapy) or raloxifene

* If either alendronate or zoledronic acid has been approved, and the other bisphosphonate is to exist trialled, so the patient is considered to take already meet the requirements for the new medicine.

If a funded bisphosphonate is required, but the patient does non see the Special Authority requirements of alendronate or zoledronic acrid, etidronate disodium may be used, however, etidronate is significantly weaker than either alendronate or zoledronic acid.

Etidronate disodium is prescribed at 400 mg, daily on and empty tummy, for 14 days, repeated every iii months.

Risedronate, an alternative to alendronate, is to exist listed on the Pharmaceutical Schedule, without restrictions, from i September, 2013.

Acknowledgement

Give thanks you to Associate Professor Andrew Harrison, Rheumatologist, Clinical Head of Department, Wellington Regional Rheumatology Unit and Wellington School of Medicine, University of Otago, Wellington for expert review of this commodity.

References

Mackie Due south, Pease C. Diagnosis and direction of giant cell arteritis and polymyalgia rheumatica: Challenges, controversies and practical tips. Postgrad Med J. 2013;89:284–92.
Salvarani C, Cantini F, Hunder One thousand. Polymyalgia rheumatica and behemothic-cell arteritis. Lancet. 2008;9634:234–45.
Kermani T, Warrington K. Polymyalgia rheumatica. Lancet. 2013;381(9860):v–eleven.
BMJ Best Practice. Polymyalgia rheumatica. BMJ; 2012. Available from: http://bestpractice.bmj.com/all-time-exercise/monograph/153.html (Accessed May, 2013).
Mitchet C, Matteson E. Polymyalgia rheumatica. BMJ. 2008;336:765.
Dasgupta B, Borg F, Hassan N, et al. BSR and BHPR guidelines for the management of polymyalgia rheumatica. Rheumatology. 2010;49(1):186–90.
Larkin J. Family history of rheumatoid arthritis - a not-predictor of inflammatory disease? Rheumatology. 2010;49(iii):608–9.
Pease C, Haugeberg Thousand, Montague B, et al. Polymyalgia rheumatica can be distinguished from late onset rheumatoid arthritis at baseline: results of a 50yr prospective report. Rheumatology. 2009;48(2):123–seven.
Hoes J, Jacobs J, Boers One thousand, et al. EULAR evidence-based recommendations on the direction of systemic glucocorticoid therapy in rheumatic diseases. Ann Rheum Dis. 2007;66(12):1560–7.
New Zealand Formulary (NZF). NZF v12. NZF; 2013. Available from: www.nzf.org.nz (Accessed Jun, 2013).
Fardet L, Flahault A, Kettaheh A, et al. Corticosteroid-induced clinical adverse events: frequency, risk factors and patient's stance. Brit J Dermatol. 2007;157(1):142–8.
Bolland MJ, Avenell A, Baron JA, et al. Effect of calcium supplements on risk of myocardial infarction and cardiovascular events: meta-assay. BMJ. 2010;341:c3691.
Bolland MJ, Avenell A, Gamble M, Reid I. Calcium supplements with or without vitamin D and run a risk of cardiovascular events: reanalysis of the Women's Health Initiative express access dataset and meta-analysis. BMJ. 2011;342:D2040.

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