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Early diagnosis of polymyalgia rheumatica is often difficult. A missed diagnosis and inadequate treatment can result in severe and prolonged disability and expose the patient to the hazards of temporal arteritis. Treatment is effective and relatively straightforward provided that good doctor-patient communication is maintained.
Presenting symptoms in polymyalgia rheumatica (PMR) may be atypical. We report herein two old females who developed a bilateral carpal tunnel syndrome several months before the typical symptoms of PMR appeared. In both patients the diagnosis of PMR was overlooked and a surgical release of the median nerve was performed. PMR should be considered in elderly people who develop an acute or subacute carpal tunnel syndrome.
Polymyalgia rheumatica (PMR) is a periarticular rheumatic condition characterized by pain and stiffness, primarily in the neck, shoulders, hips, and pelvic girdle. Temporal arteritis (TA) or giant cell arteritis, the most common primary vasculitis in older adults, is found in approximately 10% to 30% of people who have PMR. Left untreated, TA can result in sudden, irreversible blindness. Geriatric nurses need to familiarize themselves with these disorders to accurately assess and manage people with them.
Most physicians regard polymyalgia rheumatica (PMR) as a disease that affects only the elderly. This case report of a 24-year-old man with proximal limb girdle muscle pain, stiffness, tenderness, weakness, and an elevated erythrocyte sedimentation rate, who had a dramatic response to steroids, supports the premise that PMR may affect a wider range of our population. Increased physician awareness that this illness does occur in patients younger than 50 may prevent delays in diagnosis, and decrease the needless suffering and incapacitation of younger patients with this disorder.
A case of polymyalgia rheumatica (PMR) with biopsy-proven giant cell arteritis (GCA) is described in which there were marked abnormalities noted on electromyography (EMG). Spike potentials, positive waves, and fibrillation potentials were seen in the proximal musculature of the upper and lower extremities as well as in the erector spinae muscles. Investigation failed to reveal abnormalities in either creatinine phosphokinase (CPK), aldolase, or muscle obtained at biopsy. The presence of these EMG findings in the PMR-GCA syndrome is unusual. Response to therapy with systemic corticosteroids and normalization of the EMG are documented.
Seventy patients with polymyalgia rheumatica (PMR) were seen at a suburban rheumatology practice from July 1983 to December 1987. Six of these patients presented without the typical limb girdle features associated with PMR. Presenting symptoms included peripheral synovitis or unilateral shoulder pain (3 patients), lower leg pain (3 patients), carpal tunnel syndrome (1 patient), and abdominal pain (1 patient). The disease evolved into the recognizable syndrome of PMR over a period of 2-12 months. We suggest that PMR may present in a variety of guises, or have a "stuttering evolution" to the full syndrome. The presenting manifestations of these atypical cases result from peripheral synovitis and thus represent a variant of the more common subclinical proximal synovitis seen in PMR. Increased clinical awareness of atypical presentations may assist earlier diagnosis and effective treatment.
Evidence suggests that polymyalgia rheumatica (PMR) may be an immune-mediated disease. Therefore, the role of HLA class II genes, the switch region of immunoglobin mu and alpha 1 heavy chain as the T-cell receptor (TcR) genes were investigated by Southern blot analysis. The frequency of DR4 specificity was increased in PMR (67.4% versus 30.3%; P = 0.00017). No association was found with the DQA and DQB genes, the switch region of immunoglobulin mu and alpha 1 heavy chain genes, and the TcR alpha, beta and gamma genes. This study suggests that HLA-DR4 is an important susceptibility factor for PMR. Further studies are needed to elucidate the role of Ig and TcR genes.
Thirteen patients with polymyalgia rheumatica (P.M.R.) were examined for evidence of viral infection. Hepatitis-B surface antibody (HBsAb) was detected in nine out of twelve patients tested prior to therapy. The antibody persisted up to six months in four patients but reverted to negative in the other five. HBsAb was found in only one of twelve age-matched controls. Hepatitis-B surface antigen was not detected in any patient or control. No significant elevation of antibody titre was detected to a panel of twelve other organisms. Immunoglobulin levels were elevated prior to treatment in several patients. With steroid therapy the IgG and IgA levels fell serially but the IgM levels increased in six patients. These results suggest that hepatitis B is an important trigger for P.M.R. In view of the association with giant-cell arteritis, P.M.R. may represent an abnormal immunological response to infection in elderly patients.
Management of the polymyalgia rheumatica syndrome (PMR) is controversial. Gratifying symptomatic response usually occurs after treatment with nonsteroidal antiinflammatory drugs or low doses of corticosteroids. However, some PMR patients are at risk of sudden blindness from an associated disease, giant cell arteritis (GCA). Blindness can be prevented by using higher and more toxic doses of corticosteroids. Temporal artery biopsy can be an aid in diagnosis, though it is not a completely sensitive test for GCA. This study employs decision analysis and derived risk-benefit ratios (equivalent to utility ratios) to evaluate five possible PMR management strategies. The incremental risk-benefit analysis provides a means for weighing intangible trade-offs without a formal utility analysis. Given base case assumptions derived from the literature, empirical treatment with high-dose steroids cannot be justified for PMR patients who have no cranial arteritic symptoms, because the acceptable risk-benefit ratio associated with this strategy is more than 90 cases of severe medication side effects per case of monocular blindness averted.
Polymyalgia rheumatica (PMR) typically manifests as inflammatory pain in the shoulder and/or pelvic girdles in a patient over 50 years of age. This condition was long underrecognized and therefore underdiagnosed. Today, however, overdiagnosis may occur. Physicians must be aware that many conditions may simulate PMR, including diseases that carry a grim prognosis or require urgent treatment. PMR may be the first manifestation of giant cell arteritis, and a painstaking search for other signs is mandatory. PMR may inaugurate other rheumatologic diseases such as rheumatoid arthritis, RS3PE syndrome, spondyloarthropathy, systemic lupus erythematosus (SLE), myopathy, vasculitis, and chondrocalcinosis. Finally, PMR may be the first manifestation of an endocrine disorder, a malignancy, or an infection. Failure to respond to glucocorticoid therapy should suggest giant cell arteritis, malignant disease, or infection. Ultrasonography may assist in the diagnosis by showing bilateral subdeltoid bursitis. Glucocorticoids are the mainstay of the treatment of PMR. Although the optimal starting dosage and tapering schedule are not agreed on, a low starting dosage and slow tapering may decrease the relapse rate. Methotrexate is probably useful when glucocorticoid dependency develops. In contrast, TNF-alpha antagonists are probably ineffective.
Polymyalgia rheumatica (PMR) and giant cell arteritis (GCA) are closely related and frequently occurring inflammatory diseases with an incidence of 50 and 18 per 100,000 per year, respectively, in people aged 50 years or over. The most frequent symptom of PMR is aching and morning stiffness lasting more than 1 month and exacerbated by movement, occurring in the shoulder and pelvic girdles and in the neck region. GCA is vasculitis of the large and medium-sized arteries that originate from the aortic arch, causing new and marked headache localised over the temporal or occipital areas, jaw claudication, visual impairment or claudication of the arms. GCA is characterised by histopathological panarteritis with a predominantly lymphohistiocytic cell infiltrate. Activation of macrophages is central to the arteritis. Standard treatment for PMR and GCA is glucocorticoids, which may consist of prednisone 10-20 mg/day or its equivalent for PMR patients and prednisone 30-40 mg to 1 mg/kg body weight for GCA patients. For GCA patients with recently impaired vision, treatment should start with high doses of intravenously administered glucocorticoids, such as methylprednisolone 1 g/day for 3 consecutive days. A treatment duration of 1-2 years is often required for patients with PMR or GCA; because of the side effects associated with long-term use of glucocorticoids, osteoporosis prophylaxis with oral calcium supplementation, vitamin D and bisphosphonates is appropriate.
OBJECTIVE: In untreated polymyalgia rheumatica (PMR), high levels of circulating soluble intercellular adhesion molecule-1 (ICAM-1) have been observed. To investigate the clinical implication of ICAM-1 polymorphisms in isolated PMR, we examined their potential influence in an unselected series of patients. METHODS: We studied 72 patients with isolated PMR and 129 ethnically matched controls from Lugo, Spain. Patients and controls were genotyped for HLA-DRB1 and ICAM-1 polymorphism at codons 241 and 469 by molecular methods. RESULTS: The distribution of alleles and genotypes for each ICAM-1 polymorphism did not show significant differences between patients with isolated PMR and controls. There were also no associations between ICAM-1 polymorphisms and relapses of the disease. The latter was primarily associated with carriage of an HLA-DRB1*0401 allele (OR 7.2, p = 0.01), although all relapsed patients with HLA-DRB1*0401 also carried the GG genotype of the ICAM-1 polymorphism at codon 241. The presence of both HLA-DRB1*0401 and the GG241 ICAM-1 genotype gave an OR of 15.2 (p = 0.005) after correction for age and sex. CONCLUSION: Although ICAM-1 polymorphisms alone do not appear to be associated with disease severity in isolated PMR, the presence of both HLA-DRB1*0401 and the ICAM-1 codon 241 GG homozygosity was significantly associated with increased risk of relapses in these patients.
BACKGROUND: Studies of polymyalgia rheumatica and temporal arteritis have shown that a low initial dose of oral corticosteroids should be preferred. It is, however, uncertain whether or not the suggested recommendations have been implemented by practising physicians. MATERIAL AND METHODS: Questionnaires were mailed to members of the Norwegian association for patients with polymyalgia rheumatica or temporal arteritis. RESULTS: The average initial dose of prednisolone in polymyalgia rheumatica was 35 mg; 51 of 62 patients were given a starting dose exceeding 15 mg. INTERPRETATION: The recommended low initial dose of prednisolone has still been not implemented by the majority of general practitioners and rheumatologists.
OBJECTIVE: To analyze temporal artery specimens from patients with giant cell arteritis and polymyalgia rheumatica for the presence of inflammatory cytokines and to ascertain whether a specific cytokine pattern exists for the two conditions. DESIGN: Case series of patients having temporal artery biopsy procedures. SETTING: The outpatient clinic and the research laboratories of the Division of Rheumatology, Mayo Clinic. PATIENTS: 34 patients having temporal artery biopsy procedures: 15 patients had giant cell arteritis, 9 had polymyalgia rheumatica without evidence of vasculitis, and 10 had neither polymyalgia rheumatica nor vasculitis. MEASUREMENT: Temporal artery specimens were analyzed for in vivo presence of cytokine messenger RNA (mRNA) by polymerase chain reaction with cytokine-specific primer sets. RESULTS: Vasculitic lesions in giant cell arteritis samples were characterized by in situ production of interleukin-1 beta, interleukin-6, and transforming growth factor-beta 1 mRNA (indicative of macrophage activation) and by interferon-gamma and interleukin-2 mRNA (indicative of selective T-cell activation). However, macrophage- and T-cell-derived cytokines were also detected in temporal artery biopsy specimens from patients with polymyalgia rheumatica. Tissue-infiltrating T cells in giant cell arteritis and polymyalgia rheumatica samples each had distinctive lymphokine profiles. Although interferon-gamma was found in 67% of giant cell arteritis samples, polymyalgia rheumatica samples had only interleukin-2. CONCLUSIONS: Patients with polymyalgia rheumatica have vascular involvement. Patients with polymyalgia rheumatica and giant cell arteritis share in situ production of mRNA specific for macrophage-derived cytokines. T cells recruited to vasculitic lesions in patients with giant cell arteritis predominantly produce interleukin-2 and interferon-gamma. Patients with polymyalgia rheumatica do not have interferon-gamma production, suggesting that interferon-gamma may be involved in the progression to overt arteritis.
Polymyalgia rheumatica developed in a 71-year-old patient within 2 years of the onset of acute sarcoidosis with biopsy-verified involvement of the thyroid, and concomitant autoimmune thyroiditis with hyperthyroid symptoms. Three years after the onset of muscle symptoms a non-metastasizing breast carcinoma was discovered and treated surgically. Neither the long interval between the onset of polymyalgia rheumatica and the discovery of the breast tumour, nor the good response of muscle symptoms to a one-year maintenance treatment with corticosteroids, was consistent with a paraneoplastic mechanism of the polymyalgia rheumatica syndrome. It was therefore hypothesized that the various disorders suffered by this patient might be related to a partly age-dependent depression of T-lymphocyte function, leading to an altered immunological reactivity to which the various clinical manifestations could be attributed. Such a hypothesis is supported by recent reports showing that in old people and in ageing experimental animals, a decrease in T-lymphocyte function and in the number of circulating T-cells occurs concomitantly with an increase in the incidence of a variety of neoplasms and autoimmune disorders.
Polymyalgia rheumatica and Fibromyalgia are probably not distinct clinical entities. Rather polymyalgia rheumatica is the common denomiator of a large spectrum of different diseases. The historical separation between Polymyalgia rheumatica and Giant-Cell Arteritis is no more clinically applicable in most cases. A better clinical approach is to view them as extrems of a continuum. Similarly, fibromyalgia is one manifestation of chronic pain syndromes of undetermined etiology. In addition, fibromyalgia can often not be delineated clearely from functional disorders, including depression.
Polymyalgia rheumatica (PMR) is a relatively common disorder in the elderly. Whereas the relationship between polymyalgia rheumatica and giant cell arteritis (GCA) is well recognized, there is still controversy about PMR and malignancy. We are presenting a patient with PMR and adenocarcinoma of the sygmoid colon and hypothesize a paraneoplastic relationship.
Reports of polymyalgia rheumatica and temporal arteritis in blacks are rare. We analyzed five cases of polymyalgia rheumatica and one case of temporal arteritis appearing in blacks. Polymyalgia rheumatica and temporal arteritis in blacks have the same presentation, course, and response to treatment as in Caucasians. A previously unrecorded case of polymyalgia rheumatica and biopsy-proven temporal arteritis in a black had a similar presentation and course as cases in whites. HLA typing of five cases of polymyalgia rheumatica in blacks revealed an increased incidence of AW30 and BW16 in comparison to whites and polymyalgia.