Polymyalgia Rheumatica: Biopsy Studies

Gordon, Ian; Rennie, A. M.; Branwood, A. W.

doi:10.1136/ard.23.6.447

Cited by 60 publications

(36 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The outflow:inflow ratio of 3 Thirty minutes after insertion of the microdialysis catheters, interstitial muscle concentrations of pyruvate and lactate peaked in the PMR patients and controls, after which the concentrations decreased and were stable (P Ͼ 0.05) from 60 minutes to 140 minutes ( Figure 1). Time courses were similar before and after prednisolone treatment and in the trapezius and vastus lateralis muscles (data not shown).…”

Section: Resultsmentioning

confidence: 99%

“…No labeled isotopes of any of the cytokines we studied were commercially available; therefore, 3 H-glucose was used as the common internal reference. Five microliters of dialysate from each sample was pipetted into a counting vial, 5 ml of scintillation fluid (Ultima Gold; PerkinElmer) was added, and the sample was counted in a beta counter.…”

Section: Patientsmentioning

confidence: 99%

“…Based on the paucity of laboratory evidence of muscle and vascular abnormalities, as well as on the histologic, MRI, computed tomography, ultrasound, and FDG-PET evidence from the shoulder and hip joints (3,10,(12)(13)(14) and the spinal column (2,12), the predominant view has, in recent years, been that the symptoms in patients with PMR reflect bursitis and synovitis (12,15,16). However, PMR symptoms may be seen in the absence of imaging evidence of inflammation, and conversely, such evidence may be present in the absence of symptoms of PMR or may remain after such symptoms have disappeared (13,14).…”

mentioning

confidence: 99%

See 2 more Smart Citations

Increased muscle interstitial levels of inflammatory cytokines in polymyalgia rheumatica

Kreiner¹,

Langberg²,

Galbo³

2010

Arthritis & Rheumatism

View full text Add to dashboard Cite

Objective. Polymyalgia rheumatica (PMR) is characterized by aching of the proximal muscles and increased blood levels of markers of inflammation. Despite the muscle complaints, the current view is that symptoms are caused by inflammation in synovial structures. The purpose of this study was to elucidate the disease mechanisms in symptomatic muscles by measuring interstitial levels of cytokines before and after prednisolone treatment.Methods. Twenty glucocorticoid-naive patients newly diagnosed as having PMR and 20 control subjects were studied before and after 14 days of prednisolone therapy (20 mg/day). Interstitial concentrations of interleukin-1␣/␤ (IL-1␣/␤), IL-1 receptor antagonist, IL-6, IL-8, tumor necrosis factor ␣ (TNF␣), and monocyte chemoattractant protein 1 were measured in symptomatic vastus lateralis and trapezius muscles using the microdialysis technique. Plasma levels were measured simultaneously.Results. Prednisolone abolished symptoms in all of the PMR patients within 1-2 days; the erythrocyte sedimentation rate and C-reactive protein levels were normalized on day 14. In both muscles, interstitial concentrations of all cytokines were markedly higher (P < 0.05) in the PMR patients than in the controls before treatment. In both patients and controls, interstitial levels of most cytokines were higher than plasma levels, with the exception of IL-1␣ and TNF␣, which were lower in both groups. In the PMR patients, interstitial concentrations were normalized after prednisolone treatment.Conclusion. This study introduces a novel view of PMR, indicating that increased interstitial levels of inflammatory cytokines in symptomatic muscles play a role in the pathophysiology of the disease and that cytokines may be released locally. To explore the disease specificity, similar studies in other primary inflammatory conditions are warranted.

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Patientsmentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Increased muscle interstitial levels of inflammatory cytokines in polymyalgia rheumatica

Kreiner¹,

Langberg²,

Galbo³

2010

Arthritis & Rheumatism

View full text Add to dashboard Cite

show abstract

“…Several developed polyarthritis despite their receiving doses of corticosteroids usually sufficient to control all manifestations of uncomplicated polymyalgia rheurnatica syndrome. While joint scans, synovial biopsy, and joint fluid findings support the contention of an active inflammatory syncivitis underlying the clinical features of polymyalgia rheumatica, such joint involvement does not tend to lead to chronic joint changes (5)(6)(7)(8)(9)(10)(11)(12). Moreover, in only 2 of the 9 patients whose polyarthritis preceded symptoms of giant cell arteritis were symptoms of polymyalgia rheurnatica recognized, because the affected joints were predominantly peripheral.…”

Section: Ginsburg Et Almentioning

confidence: 96%

“…This latter condition may be due to a mild synovitis of the axial joints, particularly affecting the synovial tissues of the shoulder joints, hip joints, sternoclavicular joints, and other proximal structures (5)(6)(7)(8)(9)(10). While erosions of such joints occasionally have been noted on long-term followup, the synovitis of polymyalgia rheumatica has not been considered a destructive arthropathy (5,11,12).…”

mentioning

confidence: 99%

Seronegative polyarthritis in giant cell arteritis

Ginsburg

Cohen

Hall

et al. 1985

Arthritis & Rheumatism

View full text Add to dashboard Cite

Nineteen of 520 patients with biopsy‐proven giant cell arteritis were found to have persistent seronegative, symmetric polyarthritis with a mean joint count of 20 (swollen plus tender). In 9 patients in the onset of polyarthritis occurred prior to the diagnosis of giant cell arteritis, 3 had simultaneous onset, and 7 developed polyarthritis within 3 years after the onset of giant cell arteritis. Ten of the 19 patients demonstrated radiographic features of joint space narrowing and/or erosions. In 1 patient in a synovial biopsy was performed, revealing marked multinucleated giant cell infiltration. A persistent seronegative polyarthritis, although uncommon in giant cell arteritis, may be its presenting symptom. Other symptoms of giant cell arteritis should be sought in patients who exhibit this feature, especially in those whose arthritis begins at age 50 or older.

show abstract

Diagnostic Dilemmas in Polymyalgia Rheumatica

Brooks

McGee²

1997

Arch Intern Med

View full text Add to dashboard Cite

Polymyalgia rheumatica is a clinical syndrome of proximal muscle pain in older patients that often presents a diagnostic challenge because of the large differential diagnosis, lack of definitive diagnostic criteria, and relatively frequent "atypical" clinical findings, such as peripheral synovitis, distal extremity pain, normal erythrocyte sedimentation rate, and mild weakness. Despite an extensive differential diagnosis that includes endocarditis and steroid-responsive malignant neoplasms, routine laboratory testing should be limited, and a low-dose corticosteroid trial is useful as the final step in the evaluation. The clinical overlap with seronegative rheumatoid arthritis is striking, suggesting that these diagnoses may represent different presentations of a similar disease process. While concurrent asymptomatic temporal arteritis is common, there are no data to support obtaining a temporal artery biopsy in patients with pure polymyalgia rheumatica symptoms.

show abstract

Polymyalgia Rheumatica: Biopsy Studies

Cited by 60 publications

References 11 publications

Increased muscle interstitial levels of inflammatory cytokines in polymyalgia rheumatica

Increased muscle interstitial levels of inflammatory cytokines in polymyalgia rheumatica

Seronegative polyarthritis in giant cell arteritis

Diagnostic Dilemmas in Polymyalgia Rheumatica

Contact Info

Product

Resources

About