Title: BURDEN OF POLYMYALGIA RHEUMATICA
Authors:
Bhaskar Dasgupta
Hilal Maradit-Kremers
Eric Mattesson
Corresponding author:
Bhaskar Dasgupta, MD, FRCP
Department of Rheumatology
Southend University Hospital,
Prittlewell Chase
Westcliff, Essex SSO-ORY, UK
tel: 44 1702 221048
Fax: 44 1702 221990
Email: bhaskar.dasgupta@southend.nhs.uk
Hilal Maradit-Kremers, MD MSc
Department of Health Sciences Research
Mayo Clinic, 200 First St. SW
Rochester, MN 55905
tel: 1 507 266 3169
fax: 1 507 284 1516
e-mail: maradit@mayo.edu
Eric Mattesson, MD
Department of Internal Medicine, Division of Rheumatology
Mayo Clinic, 200 First St. SW
Rochester, MN 55905
tel: 1 507 284 3522
fax: 1 507 284 0564
e-mail: matteson.eric@mayo.edu
1
ABBREVIATIONS
APR
Acute phase reactants
CRP
C-reactive protein
CS
Corticosteroids
ESR
Erythrocyte sedimentation rate
GCA giant cell arteritis
HAQ Health Assessment Questionnaire
NICE National Institute for Clinical Excellence (UK)
OR
odds ratio
PMR Polymyalgia rheumatica
QOL quality of life
SF-36 Short Form Health Questionnaire 36
VAS
Visual analog scale
2
ABSTRACT
Polymyalgia rheumatica (PMR) is the most common inflammatory rheumatic disease occurring
principally in elderly Caucasians and a common indication for long-term glucocorticosteroid
therapy in community-based patients.
Although PMR has very characteristic symptoms, there are number of other autoimmune,
infectious, endocrine and malignant disorders which may present with polymyalgia like
symptoms. It is important to make the diagnosis in a safe step-wise manner based on ‘essential’
symptoms such as bilateral shoulder/hip pain and stiffness in people above 50 years age;
’essential’ exclusions such as active infection or cancer ; clinical evaluation and minimum
laboratory investigations to exclude other mimics and careful evaluation of clinical and
laboratory response to low-dose steroids.
The most commonly associated inflammatory condition is giant cell arteritis, which can occur in
a minority of patients. The course of disease is heterogeneous and unpredictable.
Glucocorticosteroid treatment results in a rapid improvement in disease symptoms in most
patients but may be associated with significant side effects. Quality of life of patients with PMR
is influenced early in the disease course by the initial pain, stiffness and functional limitations
caused by joint involvement and systemic symptoms, and later especially by treatment related
adverse effects. Life expectancy in patients with polymyalgia rheumatica is equivalent to that of
the general population.
In view of the uncertainty associated with diagnosis, flexibility of treatment required depending
on course and treatment side effects – we recommend that patients should be managed in a
‘seamless’ manner across primary and secondary care with early rheumatology evaluation
recommended in all atypical cases. There is a large unmet need for improvement in management
and research on PMR.
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INTRODUCTION
Polymyalgia rheumatica (PMR), a common inflammatory condition of the elderly, is
characterised by bilateral proximal pain and morning stiffness, an acute phase response involving
elevated erythrocyte sedimentation rate (ESR) and/or C-reactive protein (CRP), and a rapid
response to corticosteroids (CS). This widely prevalent condition is subject to variations of
practice in primary and secondary care and is a common indication for long-term steroid use in
the community1. Patients are therefore vulnerable to the manifold adverse events associated with
prolonged CS therapy. Accurate assessment of patient-based outcomes, disease activity and
course of disease are critical to balance the benefits of CS against increased risk of adverse
outcomes such as diabetic complications and fractures.
There is also considerable uncertainty regarding diagnosis and outcomes in PMR. Initial features
may be variable, e.g. PMR without an elevated ESR is reported in up to 22% of patients and
common mimicking conditions can present with the polymyalgic syndrome. There is no gold
standard test and several diagnostic criteria have been used. This may explain the lack of
agreement in PMR diagnoses between primary care physicians and rheumatologists and revision
of diagnoses in 5-23% of patients on long term follow up. An international initiative to address
this diagnostic conundrum is now underway to define classification criteria for the polymyalgic
syndrome.
Most clinicians consider a rapid resolution of symptoms with CS therapy a diagnostic hallmark
of PMR, though some studies report slower responses in many patients and lack of response may
indicate an incorrect diagnosis. However there is little evidence on what constitutes a typical
response and how it relates to longer term outcomes or revisions of the initial diagnosis. It is
accepted that around half of patients have relapses and median duration of CS treatment around
2-3 years. PMR appears to be a heterogeneous condition. The prognostic factors at presentation
that affect this heterogeneity of disease course, clinical outcomes and duration of treatment are ill
understood. ESR at presentation, but not at one month, has been reported as a prognostic factor
for treatment duration and relapses in PMR. A study of 27 patients proposed three categories of
disease course: a rapid response without significant relapse; a rapid response requiring extended
treatment; and incomplete resolution of symptoms requiring increased doses of steroids and
extended treatment2.
4
This chapter will discuss: (1) the epidemiology of PMR, (2) burden of disease including the
economic burden, (3) the impact of PMR, particularly the initial response to CS therapy, on
clinical and patient-based outcomes (early and long term) and examine the relationship between
laboratory measures and clinical outcomes, functional status and changes in QOL (4) potential
medical errors in the diagnosis and management of PMR and occurrence of preventable
complications, (5) guidelines and audit standards for diagnosis and management, (6) implications
of these guidelines for re-design to achieve an optimal service.
1. EPIDEMIOLOGY OF PMR
The epidemiology and population burden of PMR is documented in a limited number of studies.
The incidence of PMR varies markedly according to geographical region, with much higher rates
in countries in the northern latitudes. In Northern United States, the average annual age- and
sex-adjusted incidence of PMR per 100,000 population  50 years of age is estimated at 58.7
(95% CI: 52.8-64.7) with a significantly higher incidence in females (69.8; 95% CI: 61.2-78.4),
than in males (44.8; 95% CI: 37.0-52.6)3. The incidence in Northern United States is similar to
the incidence estimates from Denmark (68.3 per 100,000)4 and Norway (112 per 100,000)5, but
is substantially higher than those reported in Göteborg, Sweden (28.6/100,000)6, Reggio Emilia,
Italy (12.7/100,000)7 and Lugo, Spain (18.7/100,000)8. A recent large primary care database
study from the United Kingdom reported an incidence of 84 per 100,000 with a female to male
ratio of 2.09. This is the only study that also reported a marked increase in the incidence of PMR
throughout the 1990s, from 69 per 100,000 person-years in 1990 to 93 per 100,000 person-years
in 2001. However, a similar temporal increase in incidence was not observed in other studies. It
is unclear whether there is a true increase in incidence of PMR, over-diagnosis or increased
recognition of PMR over time. The prevalence of PMR among persons > 50 years of age in the
year 2000 is estimated at 739 per 100,000, with a higher prevalence in females than in males 10.
The prevalence increases dramatically with age from 21 per 100,000 for ages 50 - 54 years to
4,213 per 100,000 for ages 90 - 95 years. With these prevalence estimates, 711,000 Americans
are estimated to have PMR10. Survival was also examined in various studies and they all
indicate that survival in PMR patients is similar to those in the general population3, 4, 11. This has
been in part attributed to increased medical surveillance during the disease course.
5
2. HEALTH CARE UTILIZATION AND ECONOMIC BURDEN
Despite the relatively low incidence of PMR, in particular in countries in the southern latitudes,
the medical, economic and quality-of-life burden of PMR can be significant.
In a large
community-based study with an average 4 years of follow-up, 364 PMR patients utilized a total
of 5108 physician office visits and 2015 telephone calls12. More than two thirds of all physician
visits (70%) and 61% of rheumatologist visits occurred during the first year of the disease. Mean
number of generalist visits per person-years of follow-up was 7.0 during the 1st year, 3.8 during
the 2nd year and  3 visits after the 2nd year. The decline in the number of rheumatologist visits
was much more pronounced, from 2.2 visits per person-years during the 1st year to 0.8 visits
during the 2nd year and  0.6 thereafter12. In this population, generalists provided the large
majority of care and rheumatologist involvement was generally limited to diagnostic
confirmation and management of complications.
Interestingly, indicators of PMR disease
severity such as, occurrence of GCA, PMR relapses or CS complications, were not associated
with rheumatologist visits. However, the presence of these conditions was associated with an
increased number of rheumatologist visits. As addressed in the following sections, the health
care utilization patterns in this study is a consequence of diagnostic dilemmas in PMR and can
significantly increase the burden of the disease on the health care system. Indeed, a retrospective
chart review of 123 PMR patients referred to a tertiary care rheumatology clinic in Canada
demonstrated that the accuracy of PMR diagnosis by non-rheumatologists was very low (24%),
and that a large number of inappropriate tests were performed by non-rheumatologists in an
effort to reach diagnosis13.
High utilization of health care services and diagnostic tests in PMR may result in increased cost
of care, especially during the first year following diagnosis14. PMR patients have a substantially
higher number of outpatient services and laboratory tests compared to matched individuals of the
same age and sex. The total yearly direct medical cost of care appears to be highest during the
first year of the disease ($2,814) and then stayed relatively constant at about $1,500/year in
subsequent years. However, for non-PMR subjects, the total yearly cost of medical care was
relatively stable at about $1,000/year. PMR was associated with a significant incremental cost of
$2,233 at the 10th percentile of costs and $27,712 at the 90th percentile of costs and interestingly,
the increased incremental costs were mainly accounted for comorbid cardiovascular conditions,
hospital stays and imaging.
Indeed, previous analyses indicate that PMR patients are
significantly more likely to have a history of myocardial infarction (odds ratio [OR]: 1.78, 95%
6
CI: 1.13, 2.82), peripheral vascular diseases (OR: 2.21, 95% CI: 1.37, 3.60) and cerebrovascular
diseases (OR: 1.60, 95% CI: 1.08, 2.39) compared to the matched non-PMR subjects14.
These findings emphasize the importance of careful diagnostic investigations in diagnosis of
PMR as well as the economic burden associated with the management of comorbid
cardiovascular conditions in these elderly PMR patients.
3. QUALITY OF LIFE AND CLINICAL OUTCOMES IN PMR
Quality of life (QOL) and functional status in PMR have been the focus of a limited number of
studies15, 16. Kalke and colleagues reported on functional status in 18 newly diagnosed PMR
patients15. The Health Assessment Questionnaire (HAQ) correlated with measures of disease
activity and showed greater sensitivity to change than these other parameters. Sections of the
HAQ dependent on morning stiffness i.e. dressing, grooming, rising and also reaching were more
responsive to change and reflected disease activity better.
Short-term QOL was more
extensively addressed in a larger study from the UK16 and long-term QOL was examined in an
unpublished study in the USA.
The UK cohort study recruited 129 patients with new-onset PMR subsequently treated with
standard doses of oral prednisolone. QOL was assessed at baseline, 3 and 12 months using the
Modified Health Assessment Questionnaire (HAQ) and the UK version 2 of the Short Form
Health Questionnaire 36 (SF-36). Data on PMR symptoms, laboratory parameters (full blood
count, ESR, CRP) and adverse events were collected at all follow-up visits. The initial CS
response was assessed using proximal pain, morning stiffness, and acute phase response at the
week 3 visit. Complete response was defined as: no pain or at least 70% improvement in VAS
pain in the shoulders and pelvic girdle; morning stiffness of less than 30 minutes, ESR no higher
than 30mm/h and CRP no higher than 10mg/dl. A lack of response was a defined as a failure to
meet any of the three components, and a partial response was defined as patients meeting one or
two of the components. A relapse was defined as a return of PMR symptoms requiring an
increase in CS dose or maintenance of the CS dose beyond a scheduled reduction, either at or
between planned assessments.
Impact of PMR and the initial CS response on clinical outcomes and QOL: QOL at
presentation, as measured by mean SF-36 physical and mental scores (physical=31.4,
7
mental=39.3), was substantially lower than general population norms (physical=44.7,
mental=53.2). By 12 months of follow-up, physical and mental QOL scores improved, on
average, by 13.0 (95% confidence interval 11.2 to 14.8) and 11.8 (9.2 to 14.5) points,
respectively. The mean change in QOL, as measured by the HAQ, was -0.88 (-0.99 to -0.76) and
the percentage of patients with a score of less than 1 increased from 30% at baseline to 88% at
month 12.
The initial steroid response: Only 49 (38%) patients were categorised as having a complete
response to steroids at week 3 and 16 (12.4%) patients showed a lack of response, of whom one
was still categorised as non-responder at week 6. There was evidence for a difference in the PCS
at 3 months between complete responders and non-responders but there was little difference in
QOL at either 3 or 12 months between partial and complete responders.
Relapses: High incidence of relapses (46 relapses in 40 patients) and adverse events (81%) was
seen during the first year of follow up in the UK study. This observation is consistent with a US
study17 where up to 70% of patients relapsed if CS were tapered too quickly (Figure 2).
Compared to slow CS tapering (reference group), the risk of a relapse was 2.4 times higher when
tapering was medium and 5.3 times higher when tapering was fast17. A relapse as medical error
and complication of sub-optimal treatment is dealt with in the next section.
Impact of laboratory measures and clinical outcomes on changes in QOL: Higher levels of
disease activity in all markers were associated with lower physical and mental composite scores.
If all markers were considered separately for inclusion then only morning stiffness and proximal
pain were independently associated with physical composite score only; similar results were
found for the HAQ. Higher levels of ESR, CRP and morning stiffness were all independently
associated with lower mental composite score.
Long-term quality of life in PMR
The long-term quality of life in PMR patients was examined in 105 PMR patients in the USA,
after an average of almost 10 years (range: 1.6 - 27.3 years) following initial PMR diagnosis
(Gabriel et al., unpublished communication). In this study, the physical and mental scores were
standardized using the general population norms. The results indicated that, PMR patients were
functioning physically worse (physical composite score 48.45, SD:10.69) but mentally better
8
(mental composite score 52.85, SD:7.27) than their peers of the same age and sex. There was no
correlation between the 2 scores. The distributions of both physical and mental scores were
slightly skewed and the physical composite score seemed to have a bimodal distribution. These
findings are in line with the hypothesis that physical functioning declines with advancing age but
mental health remains stable regardless of advancing age.
The study also examined the
predictors of the physical and mental scores. Age, sex, ESR, marital status and time since
diagnosis (time from incidence date to survey date) were not associated with physical and mental
scores. Especially lack of any trend with time since diagnosis indicates that PMR, although
devastating during the course of the disease, has no long-term impact on physical and mental
functioning of patients shortly after full remission of symptoms.
In conclusion, there is considerable heterogeneity in PMR. Initial presentation and steroid
response does not predict the subsequent course. It is also a condition with major short term
impact on QOL, as well as high incidence of relapses and adverse events within the first twelve
months. These observations indicate an unmet need for improvement of therapy. Physical QOL
associates with inflammatory symptomatology such as pain and stiffness and functional status
indicating that the disease is best monitored based on symptoms. Similar to other rheumatic
diseases, such as RA, PMR too is perhaps best assessed through patient questionnaires18. The
association of mental QOL with acute phase markers is intriguing and needs further research.
There may not be a long term impact on QOL if there is full remission,especially if no serious
CS related side effects occur..
4. POTENTIAL MEDICAL ERRORS IN THE DIAGNOSIS AND MANAGEMENT OF
PMR
The foremost factor that has hampered development of rational therapeutic approaches to
management of PMR is the lack of standardized diagnostic criteria and reliable, valid and
sensitive outcome measures. These deficiencies have led to an inability to accurately distinguish
this clinical disease entity from other conditions presenting with the polymyalgic syndrome, and
difficulty with evaluation and comparison of the efficacy of different therapeutic approaches,
including novel drug therapies.
Because PMR is the most common inflammatory rheumatic disease of the elderly and the most
common indication for long-term CS therapy in the community, it is not surprising that it is the
9
rheumatic disease subject to the widest variations of clinical practice. Most patients are managed
in primary care settings by generalist physicians including family and general practitioners and
to a variable extent by rheumatologists19-21. Very often, specialist referral is made after a
prolonged disease course, for management of CS related complications12.
This heterogeneity in the clinical manifestations and the considerable heterogeneity in the
clinical course of PMR make the assessment and management of the disease particularly difficult
(figure 1). Treatment is with CS, but the variability of CS doses and duration required for
management of the condition are a source of clinical uncertainty and doubtless contribute to the
excess morbidity suffered by these patients. Better diagnostic strategies and identification of
predictors of treatment response, symptom relapse, and duration of therapy combined with better
treatments will shorten the disease course and reduce the need for CS therapy with its attendant
side effects.
There is a lack of recognition of PMR, particularly in primary care. The accuracy of PMR
diagnosis among family practitioners is low, while diagnostic investigations are generally overutilized19. Among the various rheumatologic diseases, the lowest agreement between primary
care physicians and rheumatologists is on the subject of diagnosis of PMR 22, 23. In another study
in the north-eastern USA, 128 physicians were presented with videos of patients presenting with
symptoms of PMR and depression24. The study was designed to assess whether patient or
physician attributes influenced clinical decision-making. Only 9 of the 128 physicians identified
PMR as the most likely diagnosis whereas 84 considered depression most likely24.
Many features of PMR predispose the unwary clinician to diagnostic error25. The proximal pain
and stiffness syndrome, which constitute the main symptoms of PMR, can occur in many other
illnesses. A third of the patients have systemic symptoms such as fever, anorexia and weight
loss.
Half the patients may have distal musculoskeletal manifestations such as peripheral
arthritis, distal hand swelling with pitting edema and carpal tunnel syndrome. Distal lower
extremity swelling is rarely due to the polymyalgic syndrome. PMR is also associated with giant
cell arteritis in 10% to 30% of cases26, 27.
The most treacherous error made in the diagnosis of PMR is the failure to consider that the
presenting symptoms are nonspecific and may reflect a number of other serious medical
conditions26-28. Clinicians should think of PMR as “polymyalgia syndrome” at first evaluation
and carefully assess whether another possible life threatening illness could be underlying the
10
symptom complex. These include bacterial endocarditis, systemic vasculitis or malignancy.
Many other medical conditions in the elderly may present with complaints of “stiffness”
including Parkinsonism, hypothyroidism or a flare of pre-existing fibromyalgia. Rheumatoid
arthritis or a late onset undifferentiated spondyloarthropathy may be the eventual diagnosis in
some cases of polymyalgia syndrome.
Laboratory tests, particularly acute phase reactants such as the ESR and CRP aid in the diagnosis
of PMR but are also a source of both diagnostic and therapeutic confusion (table 1). Although an
ESR of at least 40 mm/hour is considered an important finding for the diagnosis of PMR, an
acute phase response and elevated ESR values can occur in other settings such as neoplasia,
rheumatoid arthritis and infection. Furthermore, some studies have reported that a normal ESR
at diagnosis accounted for 7–20% of the patients with PMR29-31.
Treatment with a moderate dose of prednisone, 15-20 mg daily as a single AM dose helps to
confirm the diagnosis of PMR (Table 2)26, 27, 32, 33. Under no circumstances should patients be
given a larger dose of prednisone. Higher doses are unnecessary and will only contribute to
delays in diagnosis of another condition and lead to more CS morbidity. Frequently within 24 to
48 hours patients will spontaneously report dramatic improvement, even “a miracle”. At least a
70% patient reported global improvement with normalization of the ESR and CRP should be
expected within three to four weeks (table 3)32. If the initial response to treatment is not
dramatic, do not continue treatment without considering other possible diagnoses. The CS dose
should not be increased in an attempt to lower persistent elevation of acute phase reactants
without consideration of alternative diagnoses.
The high doses (often in excess of 40 mg/day of prednisone equivalent) often employed as initial
treatment for PMR are themselves a source of diagnostic confusion as well as a rocky disease
course33, 34. They may serve to obscure systemic manifestations of potentially life-threatening
diseases. Suppression of fever, malaise and weight loss in patients treated with high doses of CS
can delay the diagnosis for example of malignancies or subacute bacterial endocarditis, with
potentially life threatening or life limiting consequences.
The true outcome of standard CS therapy, which may only partially control disease and
symptoms, is not known.
Prednisone, 15 to 25 mg, usually suppresses inflammation
dramatically26, 27, 35. The median reported starting dose of prednisone was 20 mg/d, however, up
11
to 60% of patients experience disease relapse during CS8, 26, 32, 35, 36. Recent studies indicate that
oral CS should be administered for about 18 to 36 months26, 27, 33.
The uncertainty about the duration of treatment is a common cause of over-treatment. Reports
from the Mayo Clinic originally described a short duration of disease both for PMR (11 months
median duration of treatment with 75% of patients off CS at 2 years) and giant cell arteritis 37.
However, reports from Europe describe a more prolonged illness requiring several years of CS
therapy marked by frequent relapses32,
38-40
. The fact that the majority of patients with PMR
remain on long-term CS treatment suggests persistent symptoms, and indeed, only 24% of
patients may have discontinued CS completely 2 years after initiation of treatment32. There is a
high incidence of relapses, largely irrespective of original CS responsiveness and up to a third
complained of proximal pain at 12 months in the absence of raised inflammatory indices23, 26.
Complete, partial and non-responders to initial standard CS therapy with partial and nonresponders appear to have earlier relapses leading to greater cumulative dose of CS16.
Observational studies indicate that higher doses of CS about 15 mg of prednisone per day are not
more effective, in reducing the incidence of relapses, and are in fact associated with an increased
risk of relapse17.
The risks for side effects of this long-term treatment, particularly osteoporosis, hypertension,
hyperglycemia, and cataracts, support the need for improved therapeutic options, particularly in
patients at high risk for CS-related toxicity17, 41. Unfortunately there are to date no studies which
adequately support the role for other therapeutic agents or approaches. In one small clinical trial,
intramuscularly methylprednisolone acetate on a monthly basis was shown to have benefit in
reducing cumulative CS dose and toxicity while maintaining control of disease40. Nonsteroidal
anti-inflammatory agents are virtually of no value for management of polymyalgia rheumatica
and are associated with considerable drug related morbidity42.
A number of studies examined the efficacy of methotrexate with conflicting findings43-45. There
is some evidence to suggest that methotrexate use can reduce the duration of CS therapy and
disease flares. Other alternative and adjuvant CS sparing therapies which have been suggested
especially in refractory cases include anti-tumor necrosis factor-α agents are of uncertain benefit
in the management of PMR46, 47.
Fortunately, there are some clinical tools which have value in predicting the likelihood of relapse
in PMR. The frequently high dose of CS often employed at imitation of treatment for PMR,
12
faster tapering rate, and lack of specialist care are all factors related to a higher risk of relapse17.
Awareness of CS related side effects, which can be particularly problematic in elderly patients
include osteoporosis, insufficiency fractures and avascular necrosis, cataracts, CS induced
myopathy, diabetes and infections motivate a strong desire by physician and patient alike to
rapidly reduce the dose in the hope of a shortened disease course and less CS exposure.
Unfortunately, the opposite effect is often the reality: every 5mg/day increase in initial CS dose
is associated with a 7% increase in the risk of relapse at initial doses of >10 mg prednisone/day17.
The hazard of having a relapse has been found to be 4-fold higher when the CS tapering rate was
rapid (from 20 mg to 3 mg over 8 weeks), than when it is slow (from 20 mg to 13 mg over the
first 8 weeks of therapy)17. Management of comorbidities including prophylaxis for
cardiovascular disease and osteoporosis is imperative. Potentially avoidable CS related
complications due to over treatment with is frequently related to misinterpretation of underlying
degenerative symptoms as persistent PMR, or attributing a persistently elevated ESR to
underlying active disease.
5. GUIDELINES AND AUDIT STANDARDS FOR DIAGNOSIS AND MANAGEMENT
OF PMR
Guidelines and audit standards for diagnosis and management of PMR were recently published,
and will be briefly summarized here33. These guidelines incorporated evidence from the medical
literature and expert opinions solicited primarily through the International PMR Classification
Criteria Work Group and summary proposals of the British Society for Rheumatology48.
These guidelines emphasize (a) an approach to ensure more accurate diagnosis of patients
presenting with polymyalgic symptoms, (b) encourage timely specialist referral of appropriate
cases, (c) promote more cautious treatment, usually using lower doses of steroids and gradual
steroid taper, and (d) ensure early bone protection to reduce the common morbidity of
osteoporotic fractures.
Key Recommendations are the following:

Use core inclusion criteria as the first step in a staged process to diagnose PMR

Initiation of low-dose CS with gradual steroid taper
13

Introduce standardized evaluation of initial steroid response

Early referral to a specialist for atypical cases and treatment dilemmas

Vigilant monitoring of proximal pain, morning stiffness, disability, osteoporotic risk
factors and for any other symptoms that may suggest an alternative diagnosis

Prevention of osteoporotic complications
The guidelines are summarized in Tables 1-4 and the approach to the polymyalgic syndrome is
illustrated in the Figure. A step-wise diagnostic approach is advocated with essential inclusion
and exclusion criteria, careful evaluation of the steroid response and diagnostic confirmation on
follow up. Although PMR has been diagnosed with normal acute phase response, the general
consensus is that this requires further study and such patients should be referred for further
rheumatological evaluation. Clinical assessment should note presence/absence of co-existing
conditions (as a cause of persistent pain) such as osteoarthritis, degenerative and other periarticular conditions involving the shoulder, neck and hips.
Early referral to a specialist from a primary care provider is recommended for:
Patients with atypical features or features that increase likelihood of a non-PMR diagnosis
such as:

Younger patient < 60 years

Protracted (chronic) onset

Lack of shoulder involvement

Lack of inflammatory stiffness

Prominent systemic features, other ‘red flag’ features such as high grade fever, rashes,
lymphadenopathy

Peripheral arthritis or other features of connective tissue disease/ muscle disease

Normal acute phase reactants (APR) , or very markedly elevated APR
or treatment dilemmas such as:

Incomplete or non-response to corticosteroids

Ill-sustained response to corticosteroids

Unable to reduce corticosteroids
14

Contra-indications to corticosteroid therapy
Patients who do not have atypical features, have a complete sustained response to low dose CS
and have no adverse events can be managed by the primary care provider.
Measures of process and adherence to guidelines
The following constitute the minimum dataset recorded prior to CS therapy:

Clinical features e.g. symmetrical proximal pain and stiffness/ important exclusions

Investigations ; as specified in guidelines
Initial steroid dose and taper
Monitoring frequency
Bone protection:

Co-prescription of calcium and vitamin D

Bisphosphonates with additional risk factors

Bone mineral density measurements
7. RE-DESIGN REQUIRED TO ACHIEVE AN OPTIMAL SERVICE FOR PMR
Unlike the popular perception, it appears that the diagnosis and management of PMR often
presents a ‘challenge’. This is because of the lack of universally accepted and definitive criteria
for diagnosis and disease activity assessment, the large differential diagnoses for the polymyalgic
syndrome, heterogeneity of presentation, steroid responsiveness, clinical course and atypical
clinical features. All of these factors make it difficult to recommend a single approach and
therapeutic regimen for all cases of PMR. In many ways this is no different from our approach to
other inflammatory rheumatic diseases which have significant heterogeneity in clinical
presentation, severity and clinical course.
Currently PMR is mainly diagnosed and managed in primary care. It presents a considerable
workload for the primary care physician. There are wide variations in practice in its
management. It is often referred to the rheumatologist but this is usually late - for steroid
15
complications, inability to reduce dose or due to an alternate diagnosis. These errors of overdiagnosis and under-diagnosis, over and under-treatment may occur due to failure to appreciate
the complexities of PMR.
The ultimate objective of any clinical management strategy is to improve patient care. The
management of PMR lends itself ideally to a ‘building bridges' approach, by developing a
partnership between health care providers across the primary and secondary care divide49. Such
an approach is based on the implementation of common management guidelines with uniform
standards of clinical governance and audit. It needs to be underpinned by a consensus opinion on
the diagnostic and remission criteria of PMR and an international prospective study to validate
classification criteria for the polymyalgic syndrome is underway.
The general consensus is that most cases of PMR would merit early referral to the
rheumatologist for advice on diagnosis and management. Referrals should be especially
considered for treatment dilemmas, atypical features or features that increase likelihood of a nonPMR diagnosis. This will improve patient safety as well as reduce cost of investigations and
visits to the family practitioner.
An individualised care plan should be agreed which includes
the patient and emphasises education and self-assessment. Disease should be monitored through
appropriate patient questionnaires.
Formation of patient support groups which disseminate
factually correct and positive information giving advice on treatment guidelines, counselling,
exercises, steroid effects and prevention of complications would aid this care plan. Integrated
shared care guidelines should be promoted which implement seamless care pathways for disease
monitoring, dose adjustment and treatment of complications. Regulatory agencies (such as NICE
in the United Kingdom) for development and implementation of national guidelines need to be
approached to take interest in the correct management of this prevalent and long term condition
of the elderly which
exacts a large toll on the quality of life with its treatment and
complications.
16
TABLE 1 Polymyalgia Rheumatica: Diagnosis
Establish the diagnosis in a stepwise fashion in patients greater than 50 years, and almost
always greater than 60 of age and symptoms of greater than one to two weeks’ duration.
Symptoms:
Bilateral shoulder and/or pelvic girdle aching (essential)
Morning stiffness duration of greater than 45 minutes (essential)
Elevated inflammatory response parameters (erythrocyte sedimentation
rate and/or C-reactive protein) (essential)
Exclude active infections, active cancer (essential)
Exclude rheumatoid arthritis and other inflammatory conditions,
thyroid disorders, drugs including statins
Basic
Investigations:
Note coexisting relevant symptoms: osteoarthritis, soft tissue /periarticular lesions, fibromyalgia
Acute phase reactants (erythrocyte sedimentation rate and/or
C-reactive protein
Creatinine and urinalysis
Cholesterol
Triglycerides
Thyroid function test
Creatine phosphokinase
Alkaline phosphatase
Blood glucose
Complete blood cell count with differential
Bone mineral density study according to regional guidelines and
availability
Tuberculosis testing (purified protein derivative, PPD) and/or
QuanteFERON gold with or without chest x-ray) according to
regional guidelines and availability
Ultrasonography of the hip and shoulders, where available
(optional)
Legent to Table 1: This table outlines initial assessment of a potential PMR patient.
17
Table 2: Polymyalgia Rheumatica: Treatment
Treatment:
Initiate corticosteroids at 15 mg of prednisone per day.
The dose of prednisone can be increased up to 20 mg per day in patients
who have a response of less than 50 to 70 percent. In patients who have
less than 50 percent response, an alternative diagnosis should be
considered.
Steroid response:
Patients should be followed within the first week to establish the clinical
response (at least >70% patient global improvement) and laboratory
markers of inflammation should resolve in 3-4 weeks.
In the first three months of treatment, followup visits should be every two
to four weeks, and, thereafter, every three to six months, depending upon
the disease course.
A complete blood count and erythrocyte
sedimentation rate and/or C-reactive protein with periodic glucose should
be performed at patient visit. Bone mineral density should be performed
every one to two years according to regional/country guidelines.
Prevention
of Monitoring for diabetes
Corticosteroid
Prescription of calcium and vitamin D supplements
Related
Bisphosphonates, where appropriate
Complications:
Typical
Corticosteroid
Schedule:
Weeks 0-4: 15 mg per day
Weeks 5-6:
12.5 mg per day
Weeks 6-11:
10 mg per day
Weeks 12-15:
10 mg every-other-day, alternating with 7.5 mg everyother-day
Weeks 16-25:
7.5 mg per day
Weeks 26 and thereafter: 5 mg per day and according to treatment
response
Alternatively, initial prednisone dose may be 15 mg per day, and then the daily dose decreased
by 1 mg every 2 to 4 weeks, with a goal of 5 mg per day at week 26, and then according to
treatment response.
Intramuscular depot methylprednisolone which gives lower cumulative doses (initial dose 120
mg every 3 weeks for 4 injections, thereafter at monthly intervals at reducing doses) may also
be considered but is less well studied.
Legend to Table 2. This table describes basic principles of management of steroid therapy in
patients with polymyalgia rheumatica.
18
Table 3: Polymyalgia Rheumatica: Symptoms to Monitor

Morning stiffness

Proximal shoulder and hip girdle pain

Disability related to the polymyalgia rheumatica i.e. rising,
dressing, grooming, reaching

Fatigue

Adverse events including osteoporotic stress fractures

Symptoms and signs suggesting an alternative diagnosis

Laboratory monitoring (erythrocyte sedimentation rate and
CBC with periodic glucose)

Bone density every one to two years

It is important to treat the patient’s symptoms, not relying
exclusively on the acute-phase reactant to guide treatment.
Legend to Table 3. Continuous monitoring of response to treatment can be monitored with
symptoms and lab assessments listed in this table.
19
Table 4. Guidelines for PMR: QUICK REFERENCE GUIDE
1. Establish diagnosis of PMR in a step-wise manner
Include: Patients presenting age >50 years, duration >2 weeks, bilateral shoulder and/or
pelvic girdle aching, morning stiffness duration of >45 minutes, raised erythrocyte
sedimentation rate, C-reactive protein e.g. evidence of an acute phase response.
Exclude: active cancer, infection, RA & other inflammatory diseases, thyroid, local shoulder
& hip conditions, statins
2. Investigate: Full blood count, urea and electrolytes, liver function tests, C reactive protein,
erythrocyte sedimentation rate, rheumatoid factor (RF), creatinine kinase, thyroid stimulating
hormone, protein electrophoresis and urinalysis. May need CXR, ANA
3. Commence low dose steroids – 15mg prednisolone daily or I.M. depomedrone 120 mg
4. Evaluate steroid response
≥70% patient global response in 1 week: likely to be PMR
50- 70% response: consider increased dose up to 20 mg
< 50% response: reconsider diagnosis
5. Follow up evaluation – to ensure steroid response is complete and sustained with no other
features of alternative diagnosis
6. Early referral to a specialist for patients with atypical features or features that increase
likelihood of a non-PMR diagnosis or treatment dilemmas
7. Prevention of osteoporotic complications
Co-prescribe calcium and vitamin D supplements
8. On-going monitoring of:
Symptoms
Lab monitoring
Bone density
 Proximal pain
 Full blood count
 BMD every one to two
years
 Morning stiffness
 ESR/CRP
 Disability related to the PMR
 Urea
&electrolytes
 Adverse events
 Glucose
 Osteoporotic risk factors
 Other symptoms that may
suggest
an
alternative
diagnosis
9. Relapses
 Increase steroids to previous higher dosage 1st & 2nd relapse
 Single injection i.m. depomedrone 120 mg may also be considered
 Consider additional immunosuppression e.g. methotrexate at 3rd relapse
 GCA relapse: treat with high dose steroids 40- 60 mg prednisolone
 Consider alternative diagnosis with steroid non- or partial-response
Legend to Table 4. This is a quick reference guide when evaluating patients with polymyagia
rheumatica, including tests to be performed, examination of symptoms and management of
steroid treatment.
20
Figure 1. How should proximal pain and stiffness be evaluated?
Presenting complaint
Articular/periarticular/
nonarticular
Clinical features
Age >50 years,
predominant shoulder
and thigh symptoms
Symmetrical
Predominant peripheral
joint symptoms,
radiographs
Diagnosis
Polymyalgia rheumatica
RA, Other
inflammatory arthritis
INFLAMMATORY
Morning stiffness
Joint swelling
Peripheral hand/foot
oedema
Multisystem disease
autoantibodies
PROXIMAL
PAIN
OR
STIFFNESS
RS3PE syndrome
SLE
Vasculitis
Other Collagen vascular
diseases
Weakness of muscles,
high creatine kinase
Inflammatory
myopathy
ARTICULAR
Shoulder,
Acromioclavicular joints,
cervical spine, hips,
radiographs
Osteoarthritis
Septic arthritis
PERIARTICULAR
Capsular restriction etc.
Ultrasonography
Elevated sedimentation
rate, c-reactive protein,
relevant history and tests
e.g. urinalysis
Adhesive capsulitis
Rotator cuff lesions
Microscopic haematuria,
fever, murmur
NONINFLAMMATORY
Weight loss, associated
features
Tender spots, long
standing history
NONARTICULAR
TSH, Bone profile
(PTH, Vitamin D)
Rigidity, shuffle, stare,
gradual onset
Concomitant sepsis
e.g. Urinary infection
Occult and deep sepsis,
(hip, muscle and body
cavity abcesses,
osteomyelitis etc.),
Bacterial endocarditis
Neoplasia
e.g. myeloma
Fibromyalgia, Chronic
pain syndromes,
Depression
Endocrinopathy,
Metabolic bone disease
Parkinsonism
21
Legend to Figure 1. This figure outlines evaluation of a patient presenting with proximal pain
and stiffness
22
Figure 2. Risk of relapse by corticosteroid tapering rates (adopted with permission from17)
Legend to Figure 2. This figure illustrates time to disease relapse among subjects with
polymyalgia rheumatica. Patients have a higher risk of relapse if their steroid treatment is
tapered fast (i.e. dose reduced fast).
23
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26
DEFINITIONS, ACRONYMS, AND SYNONYMS OF KEYWORDS AND PHRASES
Polymyalgia rheumatica
A common inflammatory rheumatic condition of elderly people characterised by aching and
stiffness in shoulder and hip areas, elevation of markers of inflammation such as ESR and CRP
and a good response to steroids.
Giant cell arteritis
An inflammation of the blood vessels which is occasionally seen in association with polymyalgia
rheumatica; can cause strokes and acute loss of vision
Arthritis can be due to wear and tear or due to inflammation; inflammatory arthritis such as
rheumatoid arthritis in the older person can mimic and get misdiagnosed as polymyalgia
rheumatica
Steroid therapy
Anti-inflammatory treatment used in the treatment of many rheumatic and non-rheumatic
inflammatory diseases; they form the main line of treatment for both polymyalgia rheumatica
and giant cell arteritis
Osteoporosis
A process of thinning of the bones and deterioration of bone quality and strength; leading to
increased incidence of fractures (commonly of the wrist, spine and hip); long duration of steroid
intake frequently leads to osteoporosis
Outcomes
Measures by which the long term effects of treatment and course of a disease condition can be
judged; these can be either clinical measure such as remission, relapses, treatment side effects or
patient-reported such measures of disability and quality of life
Remission
The state where there are no clinical or patient perceived signs or symptoms of the disease
condition
Relapse
Recurrence of clinical or patient perceived signs or symptoms of the disease condition
Adverse events
Medical events that occur during or after the treatment of a disease condition; these may relate to
complications of the disease itself or its treatment
Health Assessment Questionnaire is a form that is used to assess the level of disability. It
documents the degree of difficulty a person may have in carrying out the common activities of
daily living
Acute phase reactant
A protein whose plasma concentration increases or decreases by 25% or more during
inflammatory diseases; C-reactive protein (CRP), is a commonly used acute phase reactant.
27
Erythrocyte sedimentation rate is also used as a marker of inflammatory disorders. It is the
rate at which red blood cells in a test tube separate from blood serum and become sediment over
time, most commonly reported after one hour.
Creatinine: a test that measures kidney function
Urinalysis: examination the urine for sugar, protein and signs of infection
Cholesterol, Triglycerides: Measure of fat content of the blood
Creatine phosphokinase: a test for muscle inflammation
Alkaline phosphatase : A test which can show abnormalities of the bone, liver or inflammation
Complete blood cell count with differential: A test of the formed elements of the blood –red
cells, haemoglobin, white cells and platelets
Bone mineral density: A measure of osteoporosis
Tuberculosis testing (purified protein derivative, PPD) and/or QuanteFERON gold: tests
for occult or hidden TB infection within the body
Ultrasonography : A technique that uses ultrasound (high frequency sound waves to study
inflammation within joints, ligaments, tendons and sacs of fluid called bursae
Bisphosphonates: Drugs used to treat osteoporosis; examples alendronate, risedronate etc
Immunosuppressives: Drugs which modulate the immune system; used to treat many
rheumatic inflammatory disorders including polymyalgia rheumatica and giant cell arteritis;
Methotrexate is one example
28