This transcript has been edited for clarity.
Let's start with a patient whom we might see in primary care. Flora is a 65-year-old lady who presents with around a month's history of worsening pain and stiffness in both her shoulders and hips. She struggles with sitting to standing and is sore when lifting her arms to get dressed or washing her hair. Flora is generally not feeling herself. She also describes fatigue and loss of appetite, and she's lost around 2 kg in weight recently, unintentionally. There's no history of joint swelling or redness, fever, or focal neurological symptoms.
On examination, she was apyrexial. There were no signs of joint inflammation. However, there was evidence of proximal muscle tenderness in her shoulder and pelvic girdles, and she demonstrated notable difficulty rising from her chair. Muscle power was normal. Examination was otherwise unremarkable.
So, what is going on with Flora? Flora likely has developed polymyalgia rheumatica, or PMR, which is one of the more common inflammatory disorders we see in primary care, particularly in individuals over the age of 65 years. But we should suspect PMR in anyone over age 50 years with relevant presenting symptoms. PMR is rare in those under age 50 years. Additionally, women have a higher risk of developing polymyalgia than men.
What is PMR? PMR is an inflammatory rheumatological syndrome of unknown cause. Its underlying pathophysiology is still not fully understood, but increasingly, PMR is thought to be autoimmune in origin.
Now, importantly, there's considerable overlap between PMR and giant cell arteritis, or GCA. They are essentially two clinical syndromes that are part of the same clinical spectrum. It is estimated that 15% to 20% of individuals with PMR also have GCA, and up to 50% of individuals with GCA also have PMR. So, we should screen every individual with suspected PMR, like our patient Flora, for GCA and inquire about headache, jaw claudication, scalp tenderness, or any visual disturbance. GCA can occur weeks, months, or even years later in those with PMR. So, it is important to screen regularly for GCA. In a future podcast episode, I will be covering GCA in more detail from a primary care perspective.
Now, returning to PMR. PMR classically presents with bilateral shoulder and hip girdle pain with associated morning stiffness. There's often associated systemic upset with a mild fever, anorexia or loss of appetite, unintentional weight loss, and low mood or depression. Peripheral musculoskeletal symptoms can also occur, including carpal tunnel syndrome and pitting edema of the hands, wrist, and feet.
Bloods usually demonstrate elevated inflammatory markers, such as C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), or plasma viscosity. And remember, we only need to check a single inflammatory marker. My usual choice is CRP for suspected PMR due to its slightly superior diagnostic accuracy compared with ESR.
Differential diagnosis is extensive for PMR, and we also need to exclude other disorders that potentially mimic the symptoms of PMR. Degenerative disorders such as cervical or lumbar spondylosis, osteoarthritis, or, uncommonly, bilateral adhesive capsulitis or frozen shoulder can mimic PMR. Endocrine disorders such as thyroid or parathyroid disease can also masquerade as PMR.
We also need to exclude certain infections, chronic osteomyelitis, tuberculosis (of which we are seeing a reemergence in certain populations), and infective endocarditis. We need to exclude other inflammatory conditions such as rheumatoid arthritis, including seronegative rheumatoid arthritis, polymyositis, dermatomyositis, and systemic lupus erythematosus.
Malignancy and paraneoplastic syndromes can also often mimic PMR. So, consider underlying multiple myeloma, lymphoma, lung cancer, or other malignancies. Iatrogenic causes, such as statins, can also cause myalgia or, rarely, myositis. And finally, other underlying conditions to consider include osteomalacia secondary to vitamin D deficiency, fibromyalgia, and chronic fatigue syndrome.
Based on history and examination, we should consider further investigations to exclude these other conditions if suspected. Ideally, these investigations should be done before a trial of steroids. Investigations I consider on an individual basis for my patients with suspected PMR include bloods, full blood count, CRP, urea and electrolytes, liver blood tests, A1c to exclude diabetes, calcium and magnesium to exclude electrolyte disturbance, thyroid-stimulating hormone to exclude thyroid disease, anti-cyclic citrullinated peptide to screen for rheumatoid arthritis, vitamin D to exclude osteomalacia, creatine kinase to exclude myositis, antinuclear antibody as an initial autoimmune screen, and protein electrophoresis and urinary Bence-Jones proteins to exclude myeloma, a urinalysis, and chest X-ray. Of course, we don't need to do all of these investigations in everyone with suspected PMR, but do consider these on an individual basis.
If PMR is thought to be the likely diagnosis, a trial of prednisolone 15 mg is recommended, with follow-up at around 1 week to assess response. Patients typically describe a successful trial of steroids as life-changing. However, we can establish a diagnosis of PMR if there's an over 70% improvement in symptoms within 1 week and normalization of inflammatory markers within 4 weeks.
If individuals have a lesser response, we can consider increasing the dose of prednisolone to 20 mg. If they're still not responding, reconsider the diagnosis and perhaps consider referral to our rheumatology colleagues.
After 3 to 4 weeks of steroid treatment and with symptoms fully controlled, we should consider reducing the dose of prednisolone, guided by CRP or your inflammatory marker of choice. We need to reset expectations and inform patients that the average duration of steroid treatment for PMR is 1 to 2 years. Initially, we should reduce that dose of prednisolone from 15 mg to 12.5 mg for 3 weeks, then down to 10 mg for 4 to 6 weeks, and thereafter, we should reduce the dose of prednisolone by 1 mg every 4 to 8 weeks until treatment is stopped. A slower dose reduction may be beneficial at lower doses of prednisolone, particularly below 5 mg.
We should ensure that all individuals on long-term steroids have been issued a steroid card, and we should also discuss sick-day guidance, which I will also be covering in a future podcast.
Other key considerations include assessing and managing osteoporosis risk due to long-term steroid therapy. We should consider using a fracture risk assessment tool such as FRAX. The risk of fracture is dependent on the steroid dose and duration of treatment, and generally, the greatest rate of bone loss occurs during the first 6 to 12 months of treatment. Therefore, early bone protection therapy is often warranted. We should consider bone protection with a bisphosphonate for those at increased risk of fracture, which will be most individuals with polymyalgia on long-term steroids. Reassuringly, osteoporosis risk returns to baseline about 12 months after stopping steroids.
Additionally, we should consider gastric protection with omeprazole 10 mg or an equivalent proton pump inhibitor for those on long-term steroids, depending on age, comorbidities, and other prescribed medications such as nonsteroidals. When reviewing individuals with polymyalgia, we should ask about any relapsing symptoms, any symptoms of GCA, as previously discussed, and, importantly, any adverse effects of steroid therapy such as weight gain, dyspepsia, muscle weakness, skin thinning, easy bruising, adrenal insufficiency, and symptoms of diabetes, such as polyuria and polydipsia.
We should also check blood pressure regularly and consider checking bloods for A1c and a lipid profile to exclude diabetes and dyslipidemia.
Finally, how do we manage a flare-up of polymyalgia rheumatica when on a reducing schedule of steroids? First, we should consider an alternative diagnosis driving that flare, such as an infection. If any alternative diagnoses have been excluded, we should increase the dose of prednisolone to the dose that previously controlled symptoms. This might be as little as 1 mg. We should continue this dose for 1 month and then reduce the steroid dose as previously discussed or consider a slower reduction regimen. If individuals are unable to reduce their dose of prednisolone below 10 mg, we should refer to our rheumatology colleagues for consideration of steroid-sparing therapy such as methotrexate.
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Any views expressed above are the author's own and do not necessarily reflect the views of WebMD or Medscape.
Cite this: Polymyalgia Rheumatica: Key Symptoms and Treatment - Medscape - May 13, 2026.
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