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Tratamento Da Polimialgia Reumática
Tratamento Da Polimialgia Reumática
Author: William P Docken, MD; Section Editor: Eric L Matteson, MD, MPH; Deputy Editor: Monica Ramirez Curtis, MD,
MPH
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jul 2020. | This topic last updated: Sep 07, 2018.
INTRODUCTION
The treatment of PMR will be reviewed here. The clinical manifestations of PMR, as well as the
clinical manifestations, diagnosis, and treatment of GCA, are discussed separately. (See "Clinical
manifestations and diagnosis of polymyalgia rheumatica" and "Clinical manifestations of giant cell
arteritis" and "Diagnosis of giant cell arteritis" and "Treatment of giant cell arteritis".)
INITIAL MANAGEMENT
Overall approach — Initial treatment with low-dose glucocorticoids is recommended for all patients
diagnosed with polymyalgia rheumatica (PMR). The primary goal of treatment is the relief of
symptoms. The initial dose of prednisone needed to alleviate musculoskeletal symptoms in PMR is
lower than that used to control the vascular inflammation associated with giant cell arteritis (GCA)
(see "Treatment of giant cell arteritis"). Treatment has not been shown to improve prognosis or
prevent progression to GCA.
Initial dose — In most patients, an initial prednisone dose of 15 mg/day (or equivalent) given orally is
suggested. The starting dose can be modified depending on the patient's weight, severity of
symptoms, and comorbidities such as diabetes mellitus, severe hypertension, or heart failure. Lower
doses of 7.5 to 10 mg/day may suffice in smaller patients with mild symptoms or brittle diabetes. By
comparison, an initial dose of 20 or occasionally 25 mg/day may be appropriate in an otherwise
healthy patient with severe aching and stiffness and constitutional symptoms. Patients typically
respond quickly. Occasional patients report dramatic symptomatic relief after only a single
glucocorticoid dose, and the majority of patients experience substantial improvement within days of
starting treatment, even in the context of longstanding symptoms.
If symptoms are not significantly improved within one week of initiating therapy, the prednisone dose
can be escalated to 20 mg/day. A divided dose of prednisone (twice daily) can be useful for securing
symptomatic relief if a single morning dose is not fully effective. A salient feature of PMR is the
intensity of the gel phenomenon, which refers to a worsening of pain and stiffness with inactivity. In
consequence, some patients find that a single morning dose of prednisone will not prevent a
significant recrudescence of aching and stiffness at night and the following morning; in such patients,
split-dose glucocorticoid treatment can be an effective therapeutic maneuver. The administration of
prednisone in divided doses for PMR has not been formally studied.
There are limited data regarding the optimal starting dose of glucocorticoids, and practice is largely
based on experience by experts and conclusions drawn from systematic reviews. A systematic review
of evidence comparing different starting doses of glucocorticoids identified one randomized trial and
seven observational studies [1]. The randomized trial of 39 patients with PMR found that patients
treated with starting doses of 20 mg daily were less likely to flare within two months compared with
those who were started on prednisone 10 mg (11 versus 65 percent of patients, respectively) [2]. The
observational studies included in the analysis, however, showed inconsistent results in terms of the
effect of higher versus lower starting doses of prednisone on rates of relapse and remission [3-9].
Nonetheless, all patients experienced some degree of symptom improvement with glucocorticoids.
Another study suggested that the optimal initial dose may depend on body weight [10].
Although the response to prednisone is typically described as brisk, two prospective studies have
described slower responses to treatment with low-dose glucocorticoids. In one study, 26 percent of
129 patients reported continued proximal myalgias after three weeks of 15 mg/day
of prednisolone [11], and in another study, 29 percent of 125 patients did not achieve a definition for a
complete response to low-dose glucocorticoids at four weeks [12]. Nevertheless, the usually prompt
and impressive therapeutic response to low-dose glucocorticoids remains a widely appreciated
feature of PMR.
Alternate routes of administration of glucocorticoids have been studied but are generally not used in
clinical practice. A double-blind randomized trial of intramuscular methylprednisolone, 120 mg every
three weeks, versus oral prednisone showed comparable remission rates and lower cumulative
glucocorticoid doses in the methylprednisolone-treated group [13].
Practically all patients with PMR alone will respond to 12.5 to 20 mg/day of prednisone or, at the
most, 25 mg/day. Persistent aching and stiffness mandate pursuit of an alternative diagnosis. If
musculoskeletal symptoms subside but fevers and other constitutional symptoms continue,
underlying GCA or another illness should be considered. (See "Diagnosis of giant cell arteritis",
section on 'Differential diagnosis'.)
This approach is generally consistent with published guidelines [14-16] and expert reviews [1,17-20].
Guidelines proposed by a collaboration of the American College of Rheumatology (ACR) and the
European League Against Rheumatism (EULAR) suggested the use of the lowest effective dose
within a range of 12.5 to 25 mg of prednisone equivalent, administered once daily [14,15].
Clinical assessment — The initial clinical response to therapy should be closely monitored. After
one to two weeks, it is reasonable to seek some form of communication with the patient, either by
phone or e-mail, for the purpose of determining whether there has been the prompt symptomatic
response to treatment characteristic of PMR, or whether adjustments in glucocorticoid dosing are
needed. A formal return visit at four to eight weeks should be arranged in order to confirm resolution
of symptoms and to outline a plan for glucocorticoid tapering, or, if symptoms persist, to initiate the
workup for an alternative diagnosis. Subsequent follow-up visits can be scheduled at intervals
between three to six months, depending on the clinical course of the individual patient. At each visit,
patients should be questioned as to symptoms referable to PMR and GCA and should be assessed
for glucocorticoid side effects (see 'Minimizing risks of glucocorticoid therapy' below). Patients must
also be educated about the diagnosis of GCA once the initial diagnosis of PMR is confirmed and
instructed to promptly report symptoms suggestive of this diagnosis. (See 'Assessment for
GCA' below and "Clinical manifestations of giant cell arteritis".)
Laboratory testing — Elevations in the acute phase reactants (erythrocyte sedimentation rate [ESR]
and serum C-reactive protein [CRP]) generally revert to normal with low doses of prednisone in
association with symptomatic improvement. Some data [21] and clinical experience indicate that the
CRP appears to be a more sensitive and reliable index of disease activity compared with the ESR,
though controlled studies in this regard are lacking.
The acute phase reactants should be checked at the time of the patient's first return visit following the
diagnosis of PMR; if they have normalized, it is generally not necessary to monitor these values
regularly in a patient whose clinical course is stable. Repeat determinations are indicated for the
assessment of recurring symptoms, but minor fluctuations in the ESR or CRP, in the absence of
symptoms directly attributable to PMR, are not of themselves sufficient reason for increasing the
glucocorticoid dose.
Continued or recurrent high levels of the acute phase reactants in the asymptomatic patient should
raise concern about concurrent GCA (see 'Assessment for GCA' below). Other explanations for such
elevations, such as coincidental malignancy or infection, should not be overlooked. (See "Clinical
manifestations and diagnosis of polymyalgia rheumatica", section on 'Differential diagnosis'.)
Interleukin (IL)-6 has also been shown to correlate with disease activity [22,23]. As assays are not
available in most laboratories, however, a role for IL-6 measurement in routine clinical care has not
been established. Fibrinogen levels have also been reported to track with disease activity in patients
with PMR but, in most settings, are not used routinely for assessment of the disease course [24].
Glucocorticoid tapering — As is the case with the starting dose of glucocorticoids, there is no
consensus regarding an optimal tapering regimen. In general, the glucocorticoid dose that controls
symptoms is maintained for two to four weeks after aching and stiffness have resolved. The dose is
then reduced by small decrements every two to four weeks thereafter as tolerated to the minimum
amount needed to maintain suppression of symptoms. For example, in patients receiving over 10 mg
of prednisone/day, the dose can be lowered by 2.5 mg/day decrements every two to four weeks.
Below 10 mg/day, the use of 1 mg decrements is advised because of the characteristic and distinctive
sensitivity of the symptoms of PMR to even minor changes in the glucocorticoid dose. Dose
reductions by 1 mg per month are reasonable, provided there are no flares. With this regimen,
patients without a relapse in symptoms will have been treated for approximately one year.
(See 'Duration of therapy' below.)
Duration of therapy — In most patients, PMR runs a self-limited course, and glucocorticoids can
eventually be discontinued. In about one-half of patients, treatment can be stopped after one to two
years [25]. Other patients require continuation of prednisone for longer periods of time, commonly at
stable doses of 5 mg/day or less. At one center, the median duration of some glucocorticoid therapy
was 37 months [26]. Another study found that one-third of patients required management with
glucocorticoids for more than six years [27]. Clinical inertia likely accounts for a protracted course of
low-dose glucocorticoid treatment in some patients.
Practically, there appear to be two broad subgroups of PMR. In one, glucocorticoids can be rather
uneventfully tapered off over a year or two, while in another, a relapsing course requires longer
treatment.
Assessment for GCA — GCA can occur before, concurrent with, or after the diagnosis of PMR. All
patients with PMR should be carefully assessed for symptoms and signs referable to GCA at initial
diagnosis and then routinely screened for underlying GCA at subsequent visits. (See "Clinical
manifestations of giant cell arteritis".)
Estimates of the overall occurrence of GCA in PMR patients vary; clinical practice suggests that
about 10 percent of patients with PMR are at some point diagnosed with GCA. PMR can appear for
the first time during the treatment of GCA as glucocorticoids are tapered to low doses. In about one-
half of cases of GCA, the initial clinical presentation includes PMR. Late GCA, developing after an
initial diagnosis of PMR, occurs in 7 to 10 percent of patients [28,29]; the duration between initial
diagnosis of PMR and subsequent diagnosis of GCA ranges from months to years. GCA can occur
despite prior or ongoing low-dose glucocorticoid treatment.
As risk factors for the occurrence of GCA have not been defined in patients with PMR, sustained and
regular clinical vigilance for GCA is essential. In an otherwise asymptomatic PMR patient with
unexplained elevations of the acute phase reactants, patients should be evaluated for the possibility
of GCA, with regard to either cranial arteritis or large vessel vasculitis.
In an inception cohort of 359 patients with PMR compared with population-based controls, however,
only cataracts were found to be more common in PMR than comparators [32]. The rates of
glucocorticoid-related diabetes mellitus, hypertension, hyperlipidemia, and fragility fractures were not
significantly different between the two groups. It should be observed that this and other studies on
adverse events from glucocorticoid treatment for PMR have not tracked side effects that are
frequently more problematic in practice, such as facial hirsutism, Cushingoid facies, weight gain, and
capillary fragility. Capillary fragility can result in widespread ecchymoses and slowly healing
lacerations, especially in patients on concurrent treatment with aspirin or anticoagulants.
As most patients with PMR require glucocorticoid treatment for more than several months, standard
guidelines for prevention of glucocorticoid-induced osteoporosis should be followed, including an
assessment of bone mineral density at or near the time prednisone is begun, treatment with calcium
and vitamin D supplementation, and, when indicated by treatment guidelines, prophylactic use of
bisphosphonates. These issues are discussed in detail elsewhere. (See "Prevention and treatment of
glucocorticoid-induced osteoporosis".)
Blood pressures should be monitored regularly, and, when indicated, glycosylated hemoglobin
(hemoglobin A1c) levels should be obtained to monitor for the development of diabetes mellitus.
(See "Screening for type 2 diabetes mellitus".)
Indications for referral to a rheumatologist — PMR is common and, depending on prevailing
clinical practices, can often fall under the purview of a generalist. Referral to a rheumatologist should
be considered if there are atypical features (eg, younger patients, presenting fever), prominent
peripheral arthritis, an inadequate response to initial glucocorticoid treatment, or difficulties with
glucocorticoid tapering.
Patients with recurrent symptoms — Relapses of aching and morning stiffness are frequent during
the course of the glucocorticoid taper and have been reported in over 50 percent of patients [3,33,34].
In clinical practice, relapses during tapering are more the rule than the exception. Relapses are most
common in the first one to two years of treatment and at prednisonedoses under 10 mg/day [34]. As
would be expected, a relapsing course is associated with a longer duration of glucocorticoid treatment
[33]. Recurrences of polymyalgia rheumatica (PMR) after complete discontinuation of glucocorticoid
treatment, months or even years later, also occur [35]. Why PMR is monophasic in some patients and
polyphasic in others is unclear. (See 'Prognosis' below.)
Reports on prognostic factors for relapses in PMR are marred by inconsistencies [1]. Relapse has
been variably associated with female sex, longer duration of morning stiffness, peripheral arthritis,
higher erythrocyte sedimentation rate (ESR) at diagnosis, and persisting elevations of C-reactive
protein (CRP), interleukin (IL)-6 levels, and soluble IL-6 receptor levels [4,33,34,36-38]. Increased
relapses have also been described with larger initial doses of prednisone [3] and a faster rate of
tapering [3,34]. In the absence of defined risk factors for relapses, treatment centers on finding the
lowest glucocorticoid dose that controls stiffness and preserves function for the individual patient.
Asymptomatic patients with abnormal testing — Elevations in the ESR and/or CRP can occur in
the asymptomatic patient. In the absence of symptoms, minor increases do not warrant any change in
the glucocorticoid dose. Asymptomatic patients with more significant elevations in the acute phase
reactants should be carefully evaluated for symptoms and signs of giant cell arteritis (GCA).
Limited role for glucocorticoid-sparing therapies — The routine use of adjunctive therapy is not
recommended because definitive symptomatic control of PMR can usually be achieved with low
doses of glucocorticoids and the adverse effects from treatment are often mild. Symptomatic relapses
during the course of the glucocorticoid taper are common, and, if managed with only a minor change
in the glucocorticoid dose, need not be construed as a failure of treatment.
Indications for considering the addition of an adjunctive medication to glucocorticoid therapy include
preexisting comorbidities (eg, osteoporosis or insulin-requiring or decompensated diabetes mellitus),
the development of serious glucocorticoid-related side effects, or multiple relapses of symptoms. In
these situations, methotrexate (MTX) can be used, with the caveat that the use of this drug in
contemporary doses used for management of rheumatoid arthritis (up to 25 mg/week) has not been
formally studied in PMR. Results from preliminary studies on the use of IL-6 receptor blockade are
encouraging, but controlled studies are needed to assess the efficacy, toxicity, and economic viability
of this approach. There are insufficient data to support the use of tumor necrosis factor (TNF)
inhibitors. Generally similar recommendations are included in the European League Against
Rheumatism (EULAR)/American College of Rheumatology (ACR) guidelines [14,15] and in a
systemic review [39].
OTHER THERAPIES
●Physical therapy – Physical therapy has no role in the initial management of a patient
with untreated polymyalgia rheumatica (PMR), as the extent of associated stiffness usually
precludes meaningful participation in a program of therapeutic exercise. In an older adult
who has become deconditioned, physical therapy can assist with the restoration of fitness
once effective treatment for PMR has been implemented.
●Nonsteroidal antiinflammatory drugs – Nonsteroidal antiinflammatory drugs (NSAIDs)
have no role in the initial management of PMR. Patients typically report no or minimal
symptomatic improvement if these medications have been tried prior to initiation of
glucocorticoid therapy.
rheumatica (PMR) [52]. PMR is not erosive and does not cause structural damage. Pain and
functional limitations are eliminated with low doses of glucocorticoids. Morbidity in PMR most often
relates to the longer-term impact of its treatment. Relapses of symptoms commonly respond to minor
adjustments in the glucocorticoid dose, and treatment to prevent relapses must be weighed against
the risks of drug-related toxicities.
The heterogeneity of the clinical course commits the clinician to the care of an older adult patient on
glucocorticoids for what can be an extended period of time. Guidelines for initial management with
glucocorticoids and for subsequent tapering can be outlined, but ultimately, treatment must be flexible
and individualized.
from selected countries and regions around the world are provided separately. (See "Society
guideline links: Giant cell arteritis and polymyalgia rheumatica".)
INFORMATION FOR PATIENTS UpToDate offers two types of patient education
materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in
plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a
patient might have about a given condition. These articles are best for patients who want a general
overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces
are longer, more sophisticated, and more detailed. These articles are written at the 10 th to 12th grade
reading level and are best for patients who want in-depth information and are comfortable with some
medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-
mail these topics to your patients. (You can also locate patient education articles on a variety of
subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topics (see "Patient education: Polymyalgia rheumatica and giant cell arteritis (The
Basics)")
●Beyond the Basics topics (see "Patient education: Polymyalgia rheumatica and giant cell
arteritis (Beyond the Basics)")
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