Revmatoid Polymyalgi

Polymyalgia rheumatica (PMR) is an inflammatory rheumatic disease of unknown cause¹. It leads to inflammation in large muscle groups, particularly in the shoulders and hips, and may be accompanied by systemic symptoms such as malaise, fatigue, fever, and weight loss². In patients with PMR, the synovial membranes and bursae around major joints become inflamed, resulting in pain and stiffness. Unlike other inflammatory joint diseases, PMR does not cause structural damage to either muscles or joints². The condition is also referred to as muscular rheumatism³ and has a significant negative impact on quality of life⁴.

Clinically Relevant Anatomy

The name polymyalgia rheumatica translates directly to “many (poly) painful muscles (myalgia)”⁵. In PMR, inflammation mainly affects the bursae and synovial structures of the shoulder and hip regions. Patients often experience bilateral pain and stiffness, and the condition is usually accompanied by elevated acute-phase markers⁶.

Prevalence and Etiology

PMR occurs worldwide, but the incidence is highest in Scandinavia and among people of Northern European descent¹⁶. In the United States, the estimated lifetime risk of PMR is 2.43% in women and 1.66% in men⁷. Lower prevalence has been reported in Southern European countries such as Italy and Spain⁷.

The disease primarily affects individuals over 50 years of age. Prevalence is about 7% in people aged 50+ and around 4 per 10,000 among those over 60 years³. There is a clear gender difference, with the condition being twice as common in women as in men⁸.

Several observations suggest that infection may be a triggering factor. Onset is often abrupt, and new cases occur in waves – indicating a possible infectious component. Viruses such as parvovirus B19, parainfluenza virus, Mycoplasma pneumoniae, and Chlamydia pneumoniae have been considered potential triggers⁹.

A genetic predisposition has also been suggested, based on family clustering and some genetic findings⁹. Associations with HLA-DRB104 and HLA-DRB101 have been reported, but results are not conclusive¹⁰. In addition, there appears to be an immunological imbalance between inflammatory Th17 cells and regulatory Treg cells. PMR patients have reduced numbers of Treg cells and increased levels of Th17 cells, which may contribute to a sustained inflammatory response⁹.

Symptoms and Clinical Presentation

A Characteristic Onset

A hallmark of PMR is the sudden onset of symptoms – many patients recall precisely when it began. Typically, they wake up one morning with pronounced stiffness and pain in the shoulders and hips without warning. The pain is mainly due to synovitis and bursitis in these areas and is usually bilateral¹⁰.

In addition, 40–50% of patients experience systemic symptoms such as:

• Morning stiffness lasting more than 30 minutes

• General weakness

• Fatigue and exhaustion

• Fever and night sweats

• Headache

• Unexplained weight loss

• Low mood

• Visual disturbances

The symptom profile is characteristic but may overlap with many other conditions. It is therefore essential to rule out alternative diagnoses.

Differential Diagnosis

PMR may mimic or be mistaken for several other diseases, especially inflammatory joint disorders. With swelling or pain in distal joints such as fingers, wrists, or feet, rheumatoid arthritis should be considered. Some patients may also present with swelling and pitting edema of the hands or feet, typical of remitting seronegative symmetrical synovitis with pitting edema (RS3PE)¹⁰.

PMR must be differentiated from the following conditions:

Rheumatic diseases:

• Rheumatoid arthritis

• Spondyloarthropathies

• Crystal arthropathies (calcium pyrophosphate and hydroxyapatite)

• RS3PE

• Connective tissue diseases

• Vasculitis (including temporal arteritis and ANCA-associated vasculitis)

• Inflammatory myopathies (dermatomyositis, polymyositis)

Non-inflammatory conditions:

• Rotator cuff disorders (ruptures, tendinopathy)

• Adhesive capsulitis

• Osteoarthritis and degenerative disc disease

• Fibromyalgia

Endocrine and metabolic conditions:

• Hypothyroidism

• Parathyroid disease

• Vitamin D deficiency

• Drug-induced myopathy (e.g., statins)

Infections and malignancies:

• Viral infections and bacterial sepsis

• Endocarditis

• Septic arthritis

• Tuberculosis

• Cancer (including myeloproliferative disorders)

Neurological and psychiatric differentials:

• Parkinsonism

• Depression

Diagnosis and Workup of Polymyalgia Rheumatica

Clinical Evaluation is Key

PMR is primarily a clinical diagnosis requiring detailed history and examination. The main goal of workup is to rule out differential diagnoses such as seronegative rheumatoid arthritis and paraneoplastic syndromes. Laboratory tests often show nonspecific signs of systemic inflammation, but there is no single diagnostic test for PMR¹¹.

Common laboratory findings include normochromic normocytic anemia, leukocytosis, and elevated inflammatory markers such as ESR and CRP. Some patients also have elevated liver enzymes, particularly transaminases and alkaline phosphatase. Some clinicians use an ESR above 30–40 mm/h as a diagnostic indicator, but 6–20% of PMR patients may have normal ESR¹¹. Rheumatoid factor and anti-CCP antibodies are usually negative – if positive, rheumatoid arthritis should be considered.

Pain in PMR is often bilateral and symmetrical, affecting shoulders, hips, upper arms, and neck. Tenderness on palpation is common, but objective muscle strength is usually preserved. Muscle wasting appears only in advanced disease, secondary to inactivity¹². Active range of motion is generally reduced due to pain, with patients describing marked morning stiffness that improves during the day and after rest. Mild synovitis of wrists and knees may occur. Systemic symptoms include fatigue, fever, and weight loss.

Imaging and Ultrasound

X-rays of affected areas are mainly used to exclude other conditions, as there are no typical radiographic findings in PMR. Ultrasound can be helpful, showing findings such as subdeltoid bursitis and biceps tenosynovitis, which are more common in PMR patients but not diagnostic on their own¹³. EULAR/ACR has reported high specificity for ultrasound in differentiating PMR from other shoulder disorders (89%), but lower when differentiating from rheumatoid arthritis (70%)¹³.

Diagnostic Criteria

Several criteria-based systems support the diagnosis of PMR, though none are sufficient on their own. The two most well-known are Bird/Wood criteria and Hunder criteria¹⁵:

Bird/Wood criteria (diagnosis likely if ≥3 criteria are met):

• Bilateral shoulder stiffness

• Onset < 2 weeks

• ESR > 40 mm/h

• Stiffness > 60 minutes

• Age > 65 years

• Low mood and/or weight loss

• Bilateral upper arm tenderness

With at least one criterion combined with tenderness of the temporal artery, diagnosis is also likely. A positive response to glucocorticoids further supports the diagnosis.

Hunder criteria (all points must be present):

• Age > 50 years

• Bilateral aching in neck, shoulders, upper arms, hips, or thighs > 1 month

• ESR > 40 mm/h

• Exclusion of other diagnoses

Both systems have sensitivity >90%.

EULAR/ACR Classification Criteria

In 2012, the European League Against Rheumatism (EULAR) and the American College of Rheumatology (ACR) proposed a classification system for PMR¹⁶–¹⁷. These are provisional criteria, applied only in patients >50 years with bilateral shoulder pain and elevated CRP/ESR where other causes have been excluded.

Clinical criteria (point system):

• Morning stiffness > 45 minutes – 2 points

• Hip pain/reduced range of motion – 1 point

• Negative rheumatoid factor and anti-CCP – 2 points

• No involvement of other joints – 1 point

Ultrasound criteria:

• At least one shoulder with bursitis, biceps tenosynovitis, or glenohumeral synovitis AND one hip with synovitis or trochanteric bursitis – 1 point

• Both shoulders with the above findings – 1 point

Interpretation:

• Clinical score > 4 → sensitivity 68%, specificity 78%

• Combined score (clinical + ultrasound) > 5 → sensitivity 66%, specificity 81%

Treatment and Follow-Up

Long-Term Glucocorticoid Therapy as the Mainstay

PMR is primarily treated with prednisolone. There is no universal consensus on the starting dose, but many guidelines suggest 15–20 mg per day with gradual tapering over several months¹⁸. Symptoms often improve within a few days after initiation. The treatment course may last for several years, and relapse is common if tapering is too rapid. Clinical remission may take up to five years¹⁹.

Long-Term Side Effects Require Close Monitoring

Prolonged use of glucocorticoids carries risks of:

• Osteoporosis

• Diabetes

• Hypertension

• Cataracts

• Muscle weakness

• Increased infection risk

Prevention should begin simultaneously with steroid therapy: calcium and vitamin D are routinely recommended. In addition, blood pressure, blood sugar, and body weight should be closely monitored.

Physiotherapy and Multidisciplinary Approach

No Documented Effect of Physiotherapy – But Still Relevant

At present, there are no studies showing that physiotherapy directly alters the disease course of PMR. Nevertheless, physiotherapy plays an important role in preventing secondary complications and functional decline in this patient group²⁰. This is especially relevant for:

• Movement training and mobilization

• Prevention of inactivity and muscle atrophy

• Adaptation of physical activity

• Patient education and coping strategies

Multidisciplinary Collaboration Improves Care Quality

PMR patients may benefit from a comprehensive care model. In some countries, multidisciplinary teams are used, involving contributions from rheumatologists, general practitioners, physiotherapists, occupational therapists, nurses, nutritionists, psychologists, and orthopedic specialists²¹. The effect of such teams on health outcomes is not yet well documented but offers opportunities for better coordination and holistic patient care.

References

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15. Dasgupta B et al. 2012 provisional classification criteria for polymyalgia rheumatica: a EULAR/ACR collaborative initiative. Arthritis Rheum. 2012;64:943–54.

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