Which is worse pmr or rheumatoid arthritis?

If you have this condition, you should have a treatment plan tailored to you, that includes:

You may be given a contact phone number or helpline number for access to your doctor or nurses, if you have concerns about any changes in your condition such as flares or side effects to drugs.

Steroid treatment is usually very effective to treat polymyalgia rheumatica.

Steroids work by reducing inflammation. They can’t cure your condition, but the symptoms will improve significantly within two weeks once steroid treatment is started. Normally, steroid treatment for polymyalgia rheumatica will be taken as tablets.

Your symptoms may almost disappear after four weeks of steroid treatment. However, treatment usually needs to continue for up to two years, or occasionally longer, to stop the symptoms returning.

The steroid tablet most often prescribed is called prednisolone.

Potential side effects can include weight gain and the condition osteoporosis, which can cause people’s bones to become thinner and more fragile, and therefore may fracture more easily.

There are groups of people who could be at an increased risk of side effects, including those who have:

If you’re in one of these groups, your doctor will talk to you about drugs that may be prescribed alongside steroids to reduce any risks.

After two to four weeks, your doctor will gradually reduce the dose of steroids.

The reduction will be made in stages depending mainly on your symptoms but helped by carrying out repeated blood tests to look for inflammation.

If symptoms return when the dose is reduced, your doctor may have to increase the dose for a short time, possibly several weeks, and then try to reduce it again.

You shouldn’t stop taking your steroid tablets suddenly or alter the dose unless advised by your doctor, even if your symptoms have completely cleared up. This is because your body stops producing its own steroids, called cortisol, while you’re taking steroid tablets. Your body will need some time to resume normal production of natural steroids when the medicine is reduced or stopped.

Even when you feel well, your doctor may wish to see you regularly so that you can be assessed for signs of the condition coming back, or side effects from the drugs. Your doctor may want to check your general health and check your blood pressure, blood sugar and cholesterol. You may also be asked to have a bone density (DEXA) scan to check the strength of your bones.

It’s recommended you carry a steroid card that shows what dose of tablets you’re on and how long you’ve been taking them.

This will help if you need to see another doctor, for example while you’re away from home, or another healthcare professional, for example a dentist. Please show them the card – depending on what additional treatment you need, the steroid dose may need to be adjusted.

Steroid cards are available from most pharmacies.

Like all medicines, steroids can have side effects. One of the side effects of steroids is osteoporosis, which can cause bones to become thinner and then fracture.

The nationally recommended treatment for this is medicine called bisphosphonates (biss-foss-fo-nates). These are a group of drugs that can slow down or prevent bone loss. You can ask your doctor about treatment with bisphosphonates. Examples include alendronate and risedronate.

Painkillers, such as paracetamol, or short courses of non-steroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen or naproxen, can help ease pain and stiffness. They can be taken at the same time as steroid tablets.

There may be some situations where your doctor will want to prescribe a type of drug called a disease-modifying anti-rheumatic drug (DMARD), alongside steroids.

These drugs work by reducing inflammation that is causing symptoms such as pain and stiffness.

DMARDs allow a lower dose of steroid to be used.

These drugs could be prescribed if:

Polymyalgia rheumatica (PMR) is considered the most frequent inflammatory rheumatic disease in the elderly.1,2 Its highest prevalence is between 70–80 years of age, with a slow increase until the age of 90 years.3 Classic symptoms are bilateral pain and aching and stiffness in the shoulders and pelvic girdle, associated with morning stiffness lasting >45 minutes. In some patients, an inflammatory pain in the neck is also present.4,5 Inflammatory markers (such as erythrocyte sedimentation rate [ESR] and C-reactive protein concentrations) are usually raised. However, normal ESR and C-reactive protein concentrations should not be a reason to exclude PMR.6-8

Elderly-onset rheumatoid arthritis (EORA) is, by definition, a rheumatoid arthritis (RA) developing in persons >60 years of age.9,10 Recent studies have confirmed that RA is among the most common inflammatory disease in older age groups, with a 2% prevalence.11 When rheumatoid factor (RF) and anticitrullinated peptide/protein antibodies (ACPA) are absent, seronegative EORA (SEORA) is diagnosed. In some patients, a clinical onset that mimics PMR is possible.12-14

SEORA can be considered the most frequent PMR mimicking-disease. In some studies, >20% of patients changed the first diagnosis of PMR to SEORA during follow-ups.15-17 In 1992, Healey18 suggested that PMR and SEORA might be the same entity. Recently, this point of view has been put forward again.19

In this review, the authors discuss the diagnostic and classification criteria of these two inflammatory rheumatic diseases. Furthermore, the authors highlight the main differences and similarities between seronegative and seropositive RA, EORA, and young-onset RA (YORA), and EORA and PMR-like EORA. Finally, the authors discuss therapeutic differences and similarities: both steroid and non-steroid therapeutic options are discussed.

The diagnosis of PMR is challenging, due to lack of any specific diagnostic test and the presence of other conditions mimicking PMR, mainly elderly onset seronegative RA.20-22 Due to uncertainty related to the diagnosis of PMR, a prompt response to glucocorticoid (GC) treatment has been commonly used to establish the diagnosis. However, only about half of patients respond completely to GC after 3 weeks of treatment with 15 mg oral prednisolone.23 Additionally, response to GC can be observed in other mimics of PMR.24

To date, several diagnostic and classification criteria sets for PMR have been defined in the literature; they have some features in common, such as an age cut off, elevated markers of inflammation, and pain and/or stiffness in the shoulder and/or hip girdles.1,25-28

To improve the criteria specificity for PMR, the 2012 provisional European League Against Rheumatism (EULAR)/American College of Rheumatology (ACR) classification criteria for PMR used, for the first time, findings of shoulder (subdeltoid bursitis, biceps tenosynovitis, and/or glenohumeral synovitis) and hip (synovitis and/or trochanteric bursitis) ultrasound (US) along with clinical presentations.28 In this regard, the absence of positive RA serology (RF and ACPA)and peripheral synovitis is in favour of diagnosis of PMR and aims to distinguish PMR from RA. Although autoantibodies such as RF and ACPA are mostly seen in RA, diagnostically insignificant low levels of RF can be detected in elderly people.29 It is worth noting that these classification criteria are designed to discriminate patients with PMR from other mimics of PMR and are not meant for diagnostic purposes.

In a single-centre study, Macchioni et al.30 compared the performance of 2012 EULAR/ACR classification criteria for PMR with prior criteria sets in new-onset, confirmed PMR patients using ultrasonography findings. They found that the EULAR/ACR classification criteria had the highest ability to discriminate PMR from RA and other inflammatory articular diseases.30 However, in a study by Ozen et al.31 comparing the performance of different criteria sets in patients >50 years of age, presenting with new-onset bilateral shoulder pain with elevated acute phase reactants who fulfilled the EULAR/ACR classification criteria, the sensitivity of the EULAR/ACR classification criteria for PMR was high but its ability to discriminate PMR from other inflammatory/noninflammatory shoulder conditions, especially from seronegative RA, was suboptimal.31

The 1987 ACR32 and, more recently, the 2010 ACR/EULAR33 classification criteria for RA provide criteria for the classification of patients as having RA as opposed to other joint diseases. The specificity and sensitivity of the old criteria was not adequate for the classification of patients with early inflammatory arthritis as having RA.34 To detect early RA, on the other hand, the new criteria give much weight to RA serologic biomarkers, which may result in failure to identify individuals with seronegative RA.35 Thus, the difference between proportions of patients fulfilling the new or old criteria sets highlights the importance of both criteria, especially in cases of seronegative RA.

Based on the status of RA serology (i.e., RF and ACPA), RA can be categorised into seronegative RA and seropositive RA. This classification is valuable for diagnosis, making the treatment decision, and predicting the prognosis of RA, where the presence of RF and ACPA have been regarded as poor prognostic factors.35-37 In comparison with seropositive RA, seronegative RA has been considered a less severe disease with less radiographic damage progression.38-42 Less intensive treatment has been suggested in previous literature, but the necessity of changing to another conventional synthetic disease modifying antirheumatic drugs (DMARD) was underlined by the 2016 update of the EULAR treatment recommendations, also applying to patients with seronegative RA when they do not achieve the treatment target.36

Findings in recent literature in respect to the influence of seronegative status on clinical course and treatment are controversial. In a recent study by Nordberg et al.,43 wherein 234 patients with RA (15.4% seronegative) who fulfilled the 2010 ACR/EULAR classification criteria were recruited between 2010 and 2013, the authors found that ultrasonography scores for joints and tendons, number of swollen joints, disease activity score, and Physician’s Global Assessment were significantly higher in seronegative patients compared with seropositive patients, representing a higher level of inflammation in seronegative RA patients.43 These findings may pinpoint the need for a high number of involved joints for seronegative patients to fulfil the 2010 ACR/EULAR classification criteria for RA.44,45 Furthermore, after a 2 year follow-up, the authors found similar disease activity measures, radiographic progression, and remission rates, but a slower treatment response in seronegative RA, despite higher levels of inflammation in seronegative RA at baseline.43 In contrast, seropositive RA has been suggested by other authors to represent a more aggressive subset of disease with significant radiological joint damage, which needs to be treated more intensively.46-49