Related Experiment Videos

Polymyalgia rheumatica

Carlo Salvarani1, Fabrizio Cantini, Luigi Boiardi

  • 1Rheumatology Service, Arcispedale S. Maria Nuova, V. le Risorgimento N80, 42100 Reggio Emilia, Italy. salvarani.carlo@asmn.re.it

Best Practice & Research. Clinical Rheumatology
|September 30, 2004
PubMed

Insights

Polymyalgia rheumatica (PMR) causes aching and stiffness in the shoulders and hips. While corticosteroids are the primary treatment, further research is needed to explore corticosteroid-sparing options for managing this inflammatory condition.

Area of Science:

  • Rheumatology
  • Immunology

Background:

  • Polymyalgia rheumatica (PMR) is an inflammatory condition causing pain and stiffness in the shoulders, hips, and neck.
  • Historically, PMR was linked to giant cell arteritis (GCA) or elderly-onset rheumatoid arthritis (EORA).
  • Current diagnostic criteria are empirically based on expert consensus.

Purpose of the Study:

  • To review the understanding of PMR, including its pathophysiology, diagnosis, and management.
  • To highlight the role of synovitis in PMR symptoms.
  • To discuss the limitations of current diagnostic markers and treatment strategies.

Main Methods:

  • Literature review and synthesis of existing research on Polymyalgia Rheumatica.
  • Analysis of diagnostic criteria and imaging studies (arthroscopy, radioisotopic, MRI).
  • Evaluation of laboratory markers (ESR, CRP, IL-6) and treatment outcomes.

Main Results:

  • Imaging studies confirm synovitis in proximal joints and periarticular structures, likely causing PMR symptoms.
  • Distal musculoskeletal manifestations occur in about half of PMR patients.
  • Normal erythrocyte sedimentation rate (ESR) does not rule out PMR; C-reactive protein (CRP) and interleukin-6 (IL-6) are more sensitive indicators of disease activity.

Conclusions:

  • Corticosteroids are the mainstay treatment for PMR, often requiring 1-2 years of therapy, with some patients needing long-term low-dose treatment.
  • Further large-scale studies are essential to establish the efficacy of methotrexate and anti-TNF-alpha agents as corticosteroid-sparing therapies in PMR management.

Related Concept Videos

Rheumatic Heart Disease II: Clinical Manifestations and Diagnostic Studies01:22

Rheumatic Heart Disease II: Clinical Manifestations and Diagnostic Studies

The key clinical manifestations of Rheumatic heart disease (RHD) include several distinct cardiac symptoms.Carditis, a hallmark of acute rheumatic fever, involves inflammation of the heart's endocardium, myocardium, and pericardium. Chronic RHD often results from recurrent episodes of carditis. Its symptoms include the following:Murmurs are caused by valvular damage, especially to the mitral and aortic valves. Mitral stenosis or regurgitation is common, with characteristic heart murmurs...
Rheumatic Heart Disease I: Introduction01:23

Rheumatic Heart Disease I: Introduction

Rheumatic heart disease or RHD is a chronic condition that results from rheumatic fever, causing permanent damage to the heart valves.Etiology and Risk FactorsIt primarily arises from rheumatic fever, an inflammatory disease that can develop after untreated or inadequately treated group A streptococcal (GAS) pharyngitis. Streptococcus spreads through direct contact with oral or respiratory secretions. While the bacteria are the causative agents, factors like malnutrition, overcrowding, poor...
Cardiomyopathy IV: Restrictive Cardiomyopathy01:29

Cardiomyopathy IV: Restrictive Cardiomyopathy

Restrictive cardiomyopathy (RCM) is a rare heart muscle disease characterized by impaired ventricular filling due to stiffened ventricular walls, leading to significant diastolic dysfunction.EtiologyRestrictive cardiomyopathy can arise from both inherited and acquired diseases, many of which are systemic. It is categorized into four main types: infiltrative, storage, non-infiltrative, and endomyocardial diseases.Infiltrative diseases, such as amyloidosis, lead to RCM by depositing amyloid...
Myasthenia Gravis ll: Pathophysiology01:22

Myasthenia Gravis ll: Pathophysiology

The disease process of myasthenia gravis begins at the neuromuscular junction, where antibodies attack key proteins needed for muscle activation. This immune reaction weakens signal transmission, leading to the characteristic muscle fatigue and weakness that define the condition.Immune-Mediated DamageIn most individuals, antibodies target acetylcholine receptors (AChRs) on the postsynaptic membrane of muscle cells. By blocking acetylcholine binding, these antibodies prevent the nerve signal...
Rheumatic Heart Disease III: Medical Management01:21

Rheumatic Heart Disease III: Medical Management

Rheumatic heart disease (RHD) management can be divided into two main strategies: prevention and long-term management.Primary PreventionPrimary prevention focuses on timely diagnosis and management of group A streptococcal pharyngitis to prevent acute rheumatic fever. The most widely used antibiotic for treating this condition is intramuscular benzathine penicillin G.Acute Rheumatic Fever TreatmentThe primary treatment goal for a patient diagnosed with acute rheumatic fever is to suppress the...
Myasthenia Gravis: Overview and Treatment01:20

Myasthenia Gravis: Overview and Treatment

Myasthenia gravis is a neuromuscular transmission disorder characterized by weakness and increased fatigability of skeletal muscles. It is an autoimmune disease affecting approximately one in 2000 people, where antibodies against the α1 subunit of nicotinic acetylcholine receptors are produced.
These antibodies interfere with the function of the nicotinic receptors in three ways: by binding to the receptor and disrupting acetylcholine binding; by causing cross-linking of receptors which leads...