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PubMed1992

[Polymyalgia rheumatica and malignant neoplasms. A report of 3 cases].

Polymyalgia rheumatica (PMR) is an inflammatory disease which mainly affects elderly patients and is highly responsive to steroid therapy. PMR can be associated with giant cell arteritis and, less frequently, with malignancy. The authors describe three cases of paraneoplastic PMR. In one patient PMR has been the initial manifestation of a B-cell non-Hodgkin lymphoma, in two of a malignant neoplasm of the gastrointestinal system. In two patients the response to steroid therapy was documented. A careful clinical evaluation and a long term follow-up is needed before considering PMR an idiopathic disease.

Adenocarcinoma↗

PubMed1994

Multiple deletions of the mitochondrial DNA in polymyalgia rheumatica.

We analyzed the mitochondrial DNA of patients with polymyalgia rheumatica, a disease frequently associated with mitochondrial myopathy. In an attempt to study the deletions, we have developed a qualitative PCR method using a highly thermostable polymerase in order to amplify multiple mitochondrial DNA large fragments (up to 12 kb). PCR serves to observe both deleted and normal fractions of the mitochondrial DNA. We found multiple deletions of the mitochondrial DNA in all of the patient muscles. Although these muscles harbored many ragged red fibers, we found no point mutations of the tRNA(Leu)(UUR)) and the mutation at nucleotide position 8344 was not present.

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PubMed1995

The relationship of anti-endothelial cell antibodies to anti-phospholipid antibodies in patients with giant cell arteritis and/or polymyalgia rheumatica.

Sera from patients with giant cell arteritis and/or polymyalgia rheumatica were tested for the presence of IgG, IgM and IgA antibody to endothelial cells (AEC), cardiolipin (ACL) and phosphatidylethanolamine (APE) using enzyme-linked immunosorbent assays. There were strong correlations between ACL and APE, but also between AEC and ACL IgM (p < 0.02) and between AEC and APE IgA (p < 0.003). Inhibition of AEC binding was achieved by absorption onto EC, but ACL and APE binding was also significantly reduced. In contrast, the binding of AEC antibody could not be inhibited by incubation with CL. Our data suggest that AEC constitute a heterogeneous population of autoantibodies.

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PubMed1995

Polymyalgia rheumatica and giant cell arteritis.

The original descriptions of polymyalgia rheumatica (PMR) and giant cell arteritis (GCA) in the medical literature date back to 1888 and 1890, respectively. Classification criteria for PMR and GCA are not standardized since most authors used subjective criteria based on their personal experience. Only one study has evaluated criteria for PMR and has found seven variables with high discriminant value. Criteria for GCA are less varied because a positive biopsy of the temporal artery is diagnostic. However, combinations of different clinical and laboratory features have been used for diagnosis when biopsy is negative or missing. Assessment of PMR/GCA is based on the serial determination of markers of acute phase such as ESR, CRP, or plasma viscosity. However, their value in predicting recurrence of the diseases is poor. New immunological factors including soluble interleukin-2 receptors, interleukin-6, serum soluble CD8, and serum soluble intercellular adhesion molecule-1 are presently under investigation.

Giant Cell Arteritis↗

PubMed1986

[Ultrastructural changes in skeletal muscle in polymyalgia rheumatica].

Skeletal muscle from 21 patients with clinical confirmed polymyalgia rheumatica (PMR) were examined electronmicroscopically. The changes were classified according to 15 ultrastructure criteria. The focal changes have a regressive character and, while they are nonspecific, the systematic assessment of all criteria produced a characteristic pattern in which the ultrastructural picture of skeletal muscles provided a certain profile in cases of PMR. The functionally most important ultrastructural change concerns the mitochondria. Deposition and deformation of crystals result in mitochondrial changes which are structurally definable and are harmful to cell respiration. They are compensated by new formation and accumulation of mitochondria. Comparative analysis of regressive skeletal changes and of processes in the region of the media of the muscular arteries demonstrates analogous morphological changes which point to a common harmful and overlying systemic process in PMR and giant cell arteritis. Changes in the ultrastructure of the kind and degree described cannot be explained by inflammatory or noninflammatory arterial occlusions.

Humans↗

PubMed2001

Polymyalgia rheumatica and giant cell arteritis. Avoiding management traps.

BACKGROUND: Polymyalgia rheumatica (PMR) needs to be considered in the patient over 55 years of age who presents with stiffness and pain. It appears to exist in a continuum with giant cell arteritis (GCA), and the differential diagnosis is large. It may affect one in 200 patients in this age group. Corticosteroid toxicity is a major problem, either because of inappropriate dosage or prolonged disease. OBJECTIVE: To provide an up to date understanding of the concepts of this group of disorders in order to allow rapid recognition, better management, and to minimise toxicity of the necessary treatment. The most important of these are the appropriate dose of corticosteroid and instituting preventive therapy for potential complications such as osteoporosis. DISCUSSION: As there is no specific test for PMR, the diagnosis is still made on clinical grounds from the presentation, symptoms and signs, and the presence of serological markers of inflammation. Because these are all nonspecific, alternative diagnoses must be actively excluded. Certain newer investigations, such as high resolution ultrasound of the temporal arteries may be very helpful in directing temporal artery (TA) biopsies. When the response to treatment does not follow the usual course (and this may be prolonged: 18 months to five years or more), then re-evaluation is imperative.

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PubMed2006

Giant cell arteritis and polymyalgia rheumatica: pathophysiology and management.

Giant cell arteritis (GCA) and polymyalgia rheumatica (PMR) are common and often concurrent diseases in Western countries in individuals aged >50 years. Clinical features of GCA are mainly due to involvement of the cranial arteries. PMR is clinically characterised by pain, aching and morning stiffness involving the neck, shoulder and hip girdles. Both conditions are generally associated with elevation of erythrocyte sedimentation rate and C-reactive protein. A temporal artery biopsy is the gold standard test for the diagnosis of GCA. Some diseases may mimic PMR or present with polymyalgic symptoms. Corticosteroids are the cornerstone of the management of GCA and PMR. An initial dosage of prednisone 10-20 mg/day yields a dramatic improvement of PMR symptoms in most cases. In GCA, the initial prednisone dosage required is higher (40-60 mg/day). However, once established, visual loss, which is the most feared complication of GCA, does not usually improve following corticosteroid therapy. Some patients exhibit a chronic-relapsing course and may need low doses of corticosteroids for several years. Alternative corticosteroid-sparing therapies and some therapeutic agents aimed at restoring balanced bone cell activity in patients taking corticosteroids are potentially useful in the management of GCA and PMR.

Adrenal Cortex Hormones↗

PubMedDate not supplied

[Electronoptical, morphometric and histochemical studies on skeletal muscles of patients with polymyalgia rheumatica].

1. Skeletal muscle biopsies from 21 patients with polymyalgia rheumatica (PMR) were examined morphometrically, histochemically, and by electron microscopy. 2. Ultrastructural changes in the PMR specimens have been classified according to 15 criteria including nucleus, myofilaments, mitochondria, T-system, glycogen deposition, lipid, lipofuscin and myelin figures. 3. The described focal muscle changes are of regressive character and nonspecific in themselves. 4. The described recording of these criteria shows an extraordinarily high incidence of skeletal muscle changes in PMR. This constellation of characteristics gives a distinctive profile to the ultrastructural picture of the skeletal musculature in PMR. 5. The most important ultrastructural changes concern the mitochondria. Crystalline inclusions and deformations lead to structural changes of the mitochondria which threaten the breathing of the cells. This, however, is compensated by the reproduction and accumulation of the mitochondria. 6. A similar analysis of the regressive muscle changes and the processes in the field of muscular artery media shows morphological analogies pointing to an identical systemic process in PMR and arteritis gigantocellularis. 7. Ultrastructural changes of this kind cannot be explained by inflammatory or noninflammatory arterial occlusions. The same applies to the light microscopic muscle findings. 8. Minor type II fiber atrophy and some moth-eaten and whorled fibers were demonstrated histochemically. These findings are not specific to PMR, being found in skeletal muscle diseases of varying origin.

Adenosine Triphosphatases↗

PubMed1998

Deltoid muscle in patients with polymyalgia rheumatica.

OBJECTIVE: To investigate muscle tissue in patients with polymyalgia rheumatica (PMR). METHODS: Deltoid muscle biopsies obtained from 10 female patients with PMR before corticosteroid therapy and from 5 healthy female controls of similar age were studied using light microscopy. Serial cryosections were stained for the activity of myofibrillar ATPases at various pH and for oxidative and glycolytic enzymes. Sections were also incubated with antibodies against different myosin heavy chain (MyHC) isoforms, and the laminin alpha1 chain, identifying capillaries and cell borders, and against ligands for selected adhesion molecules. RESULTS: The muscle fibers in patients and controls were mainly of type I containing slow MyHC, or type II AB containing both fast A and fast B MyHC isoforms. The oxidative capacity of the muscle fibers was in general low. In the patients with PMR the numbers of capillaries per unit area of type I and type II fibers were higher than in controls (p = 0.05 and p < 0.5, respectively). No accumulation of inflammatory cells or increased expression of adhesion molecules in the muscle sections from patients with PMR was found. CONCLUSION: There is increased microvascularization of the deltoid muscle fibers in patients with PMR. Whether this is directly associated with the systemic inflammation and the musculoskeletal symptoms or is mainly due to muscle fiber atrophy could not be determined.

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PubMed1997

P-31 magnetic resonance spectroscopy demonstrates unaltered muscle energy utilization in polymyalgia rheumatica.

OBJECTIVE: To characterize muscle metabolic anomalies associated with polymyalgia rheumatica (PMR) using P-31 magnetic resonance spectroscopy (MRS). METHODS: Seventeen patients with PMR and 9 age-matched control subjects were investigated. The forearm flexor muscles were examined by P-31 MRS in a 4.7 T superconducting horizontal magnet (Biospec Bruker 47/30) during a rest-exercise-recovery protocol. The intracellular pH and the relative concentrations of phosphocreatine (PCr), inorganic phosphate (Pi), ATP, and phosphomonoesters were measured every minute during the protocol. Based on the PCr and pH time-dependent changes during exercise and recovery, the rates of ATP production from PCr hydrolysis, glycogenolysis, and aerobic metabolism were calculated for each minute of exercise. RESULTS: At rest, the metabolic parameters [PCr]:[Pi], pH, and [PCr]:[ATP] were not significantly different between the PMR patients and the control subjects. During exercise, the energetic cost and the contribution of anaerobic and oxidative pathways to energy supply were similar in the 2 groups, as were the recovery kinetics of the phosphorylated compounds and pH. CONCLUSION: Muscle MRS does not confirm the findings of histologic and biochemical studies that suggest an alteration of mitochondrial function in PMR. No other modifications in glycolytic or glycogenolytic pathways or in proton handling were found that could indicate an alteration of muscle energetics in patients with PMR.

Adenosine Triphosphate↗

PubMed2003

Genetic markers of disease susceptibility and severity in giant cell arteritis and polymyalgia rheumatica.

BACKGROUND AND OBJECTIVES: Giant cell arteritis (GCA) and polymyalgia rheumatica (PMR) are common and often overlapping diseases that generally occur in elderly patients. In this article, we examine the role of different genes as markers of disease susceptibility and severity in GCA and PMR. METHODS: The influence of human leukocyte antigen (HLA)-DRB1 and tumor necrosis factor alleles, as well as the different allelic polymorphisms, on the susceptibility and severity to GCA and PMR was examined. A review of the literature was conducted. RESULTS: Most studies have described an association of GCA with HLA-DRB1(*)04 alleles. However, HLA-DRB1 association in patients with PMR varies from one population to another. In Northwest Spain, patients with GCA and PMR exhibited different tumor necrosis factor microsatellite polymorphism associations. Studies of intercellular adhesion molecule-1 biallelic polymorphisms have yielded contradictory results. Interleukin 1 cluster and tumor necrosis factor alpha polymorphisms increased susceptibility to GCA and PMR slightly. In Northwest Spain, interleukin 6 promoter polymorphism at position -174 modulated the phenotypic expression of PMR in biopsy-proven GCA. In the same population, regulated upon activation, normal T cell expressed and presumably secreted gene promoter biallelic polymorphism at position -403 was a marker for PMR susceptibility but not for GCA, and corticotropin-releasing hormone polymorphism appeared to be implicated in the risk of severe ischemic complications in patients with GCA. CONCLUSIONS: The present analysis confirms that GCA and PMR are polygenic diseases. The search for additional genes is necessary to better understand the pathogenesis of these conditions.

Animals↗

PubMedDate not supplied

Absence of the association with CC chemokine receptor 5 polymorphism in polymyalgia rheumatica.

OBJECTIVE: Elevated RANTES serum levels are present in polymyalgia rheumatica (PMR) patients with active disease. Chemokines may contribute to the inflammatory PMR process through their binding to CC chemokine receptor 5 (CCR5). The aim of this study was to examine if the 32 base pair deletion allele in CCR5 (CCR5 delta 32 allele) might be associated with PMR susceptibility and influence the disease outcome. METHODS: We enrolled 88 consecutive patients with PMR residing in the Reggio Emilia area (Italy) who had a follow-up duration of at least one year. As a control group we used 86 healthy blood donors from the same geographic area. The CCR5 genotype of all PMR patients and controls was studied by polymerase chain reaction amplification of the region which includes the 32 deletion (CCR5 delta 32). RANTES serum levels were measured by commercial ELISA kits in CCR5 delta 32 heterozygous and CCR5 homozygous PMR patients at diagnosis before starting corticosteroid therapy and again after 6 months of therapy, as well as in 28 healthy subjects over 50 years of age. RESULTS: Frequencies of the CCR5 and CCR5 delta 32 alleles in patients and controls did not differ significantly. Homozygosity for CCR5 delta 32 was not detected in PMR patients and was detected in only one of the controls. No significant differences were observed between the patients carrying the CCR5 delta 32 allele and those homozygous for the normal CCR5 allele when we compared sex, presence of distal synovitis and systemic signs and/or symptoms, initial and cumulative prednisone dose, duration of therapy, ESR at diagnosis, frequency of relapse/recurrence and RANTES serum levels at diagnosis and after 6 months of corticosteroids. CONCLUSION: These results indicate that the frequency of the 32 deletion of the CCR5 receptor was not significantly different between PMR patients and healthy controls, and this genotype does not appear to be associated with the susceptibility to or severity of PMR.

Adrenal Cortex Hormones↗

PubMed1985

Polymyalgia rheumatica. Duration of therapy and long-term outcome.

The duration of therapy and outcome were examined in 76 patients with polymyalgia rheumatica without evidence of temporal arteritis at presentation. Seventy-five patients received corticosteroids, with a mean prednisone dosage of 22.8 mg per day initially. Duration of therapy was assessed using life-table methods. No significant difference could be ascertained between groups segregated on the basis of age, sex, or initial steroid dosage. The median duration of therapy was 37.3 months. It was estimated that 40 percent of patients will require therapy longer than four years. Corticosteroids were permanently discontinued in 31 patients after a mean of 23.7 months of therapy. The data support the concept of two patient populations--one with limited disease and another requiring long-term therapy. Relapses were frequent, occurring in 56 percent of patients. Evolution of arteritis during the course of therapy was infrequent, occurring in only one patient. Steroid-related adverse effects occurred in 22.7 percent of patients and were more common in females. The data suggest that, although corticosteroids may be discontinued in some patients with polymyalgia rheumatica, prolonged therapy is required in a significant number.

Actuarial Analysis↗

PubMed2002

Myelodysplastic and myeloproliferative syndromes associated with giant cell arteritis and polymyalgia rheumatica: a coincidental coexistence or a causal relationship?

A variety of systemic autoimmune disorders have been reported in patients with myelodysplastic and myeloproliferative syndromes. A possible association with polymyalgia rheumatica and giant cell arteritis has also been recognised. We report another case of polymyalgia rheumatica and one of giant cell arteritis associated with a myelodysplastic syndrome and the two first cases of giant cell arteritis associated with essential thrombocytaemia and chronic myelomonocytic leukaemia, respectively. It seems that there is a relationship between these entities, but the nature of this association is still unknown.

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PubMed1997

[Bone loss during low dose glucocorticoid treatment in patients with polymyalgia rheumatica. A double-blind, prospective comparison between prednisolone and deflazacort].

The aim of the study was to compare the long term effects of low dosage prednisolone or deflazacort treatment on bone mass in patients with polymyalgia rheumatica. The subjects were 30 patients with newly diagnosed polymyalgia rheumatica, who were allocated to treatment with prednisolone or deflazacort. Bone Mineral Content (BMC) was measured in the lumbar spine (L-BMC) and distal forearm (A-BMC) before treatment and three, six and 12 months after the start of treatment. After three months the decrease in L-BMC was significantly greater in the deflazacort group than in the prednisolone group (p < 0.05), but at six and 12 months there was not a significant difference between the two groups. There was a significant loss of BMC in all patients after 12 months: a 6.4% loss in L-BMC and a 1.8% loss in A-BMC. In conclusion, this low dose study failed to reveal any calcium sparing property of deflazacort compared with prednisolone.

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PubMed1997

[A case of non-specific interstitial pneumonia associated with psoriasis vulgaris and polymyalgia rheumatica].

We describe the first case, to the best of our knowledge, of non-specific interstitial pneumonia associated with psoriasis vulgaris and polymyalgia rheumatica (PMR). A 50-year-old woman was admitted with a dry cough and a bilateral basilar reticulonodular shadows on chest X-ray. Bronchoalveolar lavage fluid analysis revealed lymphocytosis and a decreased CD4/CD8 ratio. A thoracoscopic lung biopsy specimen showed evidence of non-specific interstitial pneumonia. During her clinical course, she began suffering from psoriasis vulgaris and polymyalgia rheumatica. Corticosteroid therapy had no effect, but maintained a stable condition during a follow-up period of 4 years.

Female↗

PubMed1993

Renal cell carcinoma presenting as polymyalgia rheumatica. Resolution after nephrectomy.

Renal cell carcinoma can present as a variety of paraneoplastic, nonmetastatic conditions, including vasculitis. We describe a patient who presented with the polymyalgia rheumatica syndrome but did not respond to a trial of prednisone. An asymptomatic, nonmetastatic renal cell carcinoma was found during this patient's evaluation. Nephrectomy led to resolution of the systemic complaints. Malignancy, in this case, renal cell carcinoma, can present as polymyalgia rheumatica and resolve after surgical removal of the underlying tumor.

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PubMed1992

Giant cell arteritis and polymyalgia rheumatica in a region of Finland: an epidemiologic, clinical and pathologic study, 1984-1988.

The occurrence of giant cell arteritis (GCA) (considering temporal arteritis and polymyalgia rheumatica as its manifestations) was investigated in Western Nyland, Finland. Between 1984 and 1988 54 patients were diagnosed in a population of about 44,500. Fourteen patients (26%) had biopsy proven arteritis at the initial evaluation, and 2 patients became biopsy positive during followup. The retrospectively determined annual incidence of GCA in a 44 month period was 22.5/10(5) in the whole population, and 69.8/10(5) in residents aged 50 years or older. The corresponding figures of a prospective 16 month study were 30.4/10(5) and 94.4/10(5). The incidence rates of the prospective study are higher than those reported in comparable studies. Polymyalgia rheumatica, occurring alone or combined with cranial symptoms, was the most frequent manifestation of GCA, being present in 87% of patients.

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