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A 62-year-old woman developed symptoms of polymyalgia rheumatica (PMR), but without clinical evidence of concomitant giant cell arteritis (GCA). A single blind, placebo-controlled trial of prednisolone confirmed the diagnosis, but in addition unwittingly exposed clinically silent giant cell arteritis.
A 70-year-old woman presenting with typical polymyalgia rheumatica (PMR) and a normal temporal artery biopsy appeared to respond completely to low-dose prednisone therapy. A subsequent biopsy showing temporal arteritis with a normal sedimentation rate and no recurrence of myalgic symptoms emphasizes the unpredictable course of treated PMR and the need for continued clinical as well as laboratory follow-up.
Giant cell (temporal) arteritis and polymyalgia rheumatica are related conditions that primarily affect older persons. They are among the most common chronic inflammatory disorders in this age group. In recent years, several new insights have been gained about the clinical features of these illnesses as well as their underlying pathophysiology. In addition, a great deal of study is underway to find better ways of detecting, monitoring, and treating them. This article provides a general review of these conditions, including their diagnosis and treatment.
Giant cell arteritis (GCA) and polymyalgia rheumatica (PMR) are closely related disorders found predominantly in older patients. These disorders, which are being recognized more frequently, are more common in women, in Caucasians, and in various geographic locations. Early recognition and treatment may prevent possible catastrophic consequences of GCA, such as blindness, stroke, or dissection of the aorta. Although diagnosis is fairly easy with the classic presentation, it may be missed when the patient presents with nonspecific constitutional symptoms. An increased awareness among primary care physicians will aid in the prevention of much of the morbidity and mortality related to these diseases.
OBJECTIVE: To review the data on the epidemiology of polymyalgia rheumatica (PMR), in particular geographical and temporal differences in incidence and its risk factors including the actinic hypothesis. METHODS: Evaluation of the literature. RESULTS: Epidemiological data show that the incidence of PMR varies between 12.7/100,000 in Italy and 112.6/100,000 in Norway with a geographical gradient of increased frequency in the northern hemisphere. The incidence of PMR and giant cell arteritis (GCA) have increased in recent years. This observation may be related to a greater awareness of the disease but also to real epidemiological changes. Risk factors for PMR/GCA include infections, smoking, sun exposure, and nulliparity. CONCLUSION: Epidemiological studies have helped to unravel the etiopathogenic factors at work in PMR/GCA. More data are needed on the correlation between the incidence of PMR/GCA and epidemics of infectious diseases and on environmental and biological risk factors.
A differential diagnosis of polymyalgia rheumatica (PMR) and rheumatoid arthritis (RA) can be difficult in elderly patients, especially at the prodromal phase of RA. Furthermore, it was felt that there might be a diagnostic criteria for PMR specific to the Japanese. Accordingly, we have retrospectively studied the PMR patients who had come to our hospital, for making a diagnostic criteria. We especially stressed the distinguishing of PMR from RA in elderly patients. The criteria proposed are as follows: 1. Bilateral muscular pain persisting for 2 weeks at least in more than two of the following areas; neck, shoulders or shoulder girdle, upper arms, hips or pelvic girdle and thighs. 2. Normal serum myogenic enzymes. 3. ESR of more than 40 mm/h. 4. No swelling in the hand joints. PMR is defined by the presence of all of the 4 items. The criteria demonstrated a 93.1% sensitivity and 98.3% specificity for PMR.
OBJECTIVES: To investigate the association between the onset of polymyalgia rheumatica (PMR) and prior or persistent infection with Chlamydia pneumoniae or cytomegalovirus (CMV) (both known to infect the vessel wall) enteroviruses (EV) or respiratory syncytial virus (RSV). METHODS: Serum samples were collected from 48 patients with newly-diagnosed PMR and from 22 controls of the same age. The presence of IgG, IgA and IgM antibodies to C. pneumoniae, IgG and IgM antibodies to CMV and EV, and complement fixing antibodies to RSV were analysed. RESULTS: Clinical symptoms of infection preceding PMR symptoms were associated with the presence of synovitis at the first visit. There were no significant differences in the seroprevalence rates of antibodies to C. pneumoniae, CMV, EV or RSV between PMR patients and controls. IgM antibodies to EV were found in two patients and IgM antibodies to CMV in another two patients. CONCLUSION: Serological evidence of an association between newly-diagnosed PMR and prior or chronic infection with C. pneumoniae was not found. IgM antibodies to EV in two patients, consistent with ongoing or recent infection, suggest that EV could represent one of perhaps several microbes which are able to trigger PMR.
Forty-four patients with polymyalgia rheumatica and/or giant cell arteritis (PMR/GCA) were followed from presentation, through remissions and relapses for a median duration of 36 months. Clinical disease activity, ESR, CRP and alpha 1-antichymotrypsin (alpha 1-ACT) were measured. Before treatment ESR, CRP and alpha 1-ACT were all significantly raised, compared with age- and sex-matched controls. On clinical remission with prednisolone treatment, ESR and CRP fell to control levels but alpha 1-ACT behaved quite differently, remaining raised for 18 months or until prednisolone treatment could be withdrawn. At 18 month follow-up of PMR/GCA, and alpha 1-ACT level of < or = 0.7 g/l was associated with a reduced risk of subsequent relapse (P = 0.006). At clinical relapse during treatment, ESR was not raised compared with controls, and CRP, although significantly higher than controls (P = 0.015), remained less than 6 mg/l in the majority of patients. The three laboratory investigations were, therefore, of limited value in confirming relapses of PMR/GCA during prednisolone treatment, but alpha 1-ACT may be useful as an indicator of underlying disease activity and hence as a guide to the speed that the prednisolone dosage should be reduced.
The influence of non-steroidal anti-inflammatory drugs (NSAIDs) and of disease activity on the serum alkaline phosphatase concentration was examined in patients with rheumatoid arthritis, osteoarthritis, and polymyalgia rheumatica. Concentrations of serum alkaline phosphatase were similar both in patients with rheumatoid arthritis taking NSAIDs and in those not taking NSAIDs. In patients with osteoarthritis NSAID use was not associated with a significant increase in serum alkaline phosphatase. In rheumatoid arthritis no correlation was found between clinical indices of disease activity and serum alkaline phosphatase concentrations. There was significant correlation with plasma viscosity in rheumatoid arthritis, both in those taking and not taking NSAIDs, and in polymyalgia rheumatica. Serum alkaline phosphatase concentrations are not influenced by NSAIDs. Concentrations correlate with laboratory parameters, but not clinical indices of disease activity.
Two elderly patients presented with generalized aches and pains (particularly in the shoulders and the pelvic girdle), stiffness, fatigue, anemia, and an elevated erythrocyte sedimentation rate, but there were no signs or symptoms directly referable to the joints. Two and five months later respectively, pain, swelling, and signs of synovitis appeared in several joints in a symmetrical pattern, and a diagnosis of rheumatoid arthritis was made. Rheumatoid arthritis in the elderly may resemble polymyalgia rheumatica. On the other hand, synovitis in many patients with polymyalgia rheumatica may resemble rheumatoid arthritis. In the elderly, the differentiation of these two entities may be difficult. Moreover, patients initially presenting with the signs and symptoms of polymyalgia may eventually manifest typical rheumatoid arthritis.
We report three patients with giant cell arteritis but no clear clinical signs of temporal artery involvement, during an episode of polymyalgia rheumatica. In the first case a biopsy performed upon an apparently normal temporal artery showed a typical hortonian arteritis. The same finding was obtained from a pulseless right temporal artery in the second patient, who suffered a sudden blindness of right eye after a trigeminal neuralgia. In the third case the polymyalgic symptoms developed together with a syndrome of the aortic arc. The histologic findings of the temporal artery were normal, whereas the biopsy performed on both the subclavian arteries during surgical revascularization demonstrated a typical giant-cell arteritis in the acute stage. The cases mentioned above confirm that there is a close relation between polymyalgia rheumatica and Horton arteritis. In the latter the temporal localization could be inconstant.
Levels of three factor VIII-von Willebrand factor components (von Willebrand antigen, ristocetin cofactor, and factor VIII coagulant) were higher in specimens of plasma from 27 patients with giant cell arteritis and 18 patients with polymyalgia rheumatica than in specimens from 21 normal control subjects. Values in patients with active giant cell arteritis were higher than those in patients with either inactive giant cell arteritis or active polymyalgia rheumatica. Levels of factor VIII-von Willebrand factor components tended to decline gradually after disease activity had been suppressed by corticosteroid therapy and therefore may be indicators of vascular damage. These levels, however, did not revert to normal rapidly in response to corticosteroid therapy as did the patients' symptoms and the usual laboratory measurements indicative of inflammation; thus, measurements of these components are unlikely to be useful in day-to-day management of these diseases. Electrophoretic analysis suggested that the elevated values are due to increased amounts of normal factor VIII-von Willebrand factor rather than to the presence of an abnormal molecule.
The use of steroid therapy in polymyalgia rheumatica and temporal arteritis is necessary and usually effective, but may mask coexisting disease. The importance of early consideration of other disorders in such patients is illustrated by three case histories.
Fresh sera from patients with active polymyalgia rheumatica and/or giant cell arteritis are fixing the complement components C4 and C3 to structures of the medulla of rat kidney tissue as demonstrated by the indirect immunofluorescent technique. This PMR-associated reaction is also a useful tool in monitoring disease activity, as it becomes negative under effective treatment with steroids.
The central joints of 19 patients identified as suffering from polymyalgia rheumatica were examined using ultrasonography (US). At US 13 patients (68%) were found to have an effusion in the hip and/or glenohumeral joints. Synovial fluid analyses were conducted on the central joints of four patients. These findings suggest that at least one patient group with the syndrome of PMR could better be designated as having axial arthritis and this synovitis might play an important role in the understanding of their symptoms.
Fifty-five Caucasoid patients with polymyalgia rheumatica or giant cell arteritis were typed for HLA, A, B, C and DR locus antigens. In the total patient group, DR4 had a significantly increased frequency. The prevalence of CW3 and CW6 was also significantly increased, the rise of CW3 possibly being attributable to its well-documented linkage disequilibrium with DR4. The rise in CW6 cannot be attributed to its known linkage disequilibrium with DR7.
The nosological relationship between Polymyalgia rheumatica (PMR) and Cranial Arteritis has been studied by comparing 46 cases of PMR with 21 cases of cranial arteritis. Symptoms consistent with cranial arteritis were present in 83% of the PMR patients, but only 32% showed giant cell arteritis in the biopsy of temporal arteries. The difference is explained by the segmental involvement of the arteritis. The patients with cranial arteritis had symptoms of PMR in 48%. It is concluded, that PMR and cranial arteritis are both manifestations of the same disease. Temporary signs of generalized arteritis seem to occur often in PMR and may lead to fatal complications. PMR may last up to ten years. Because of the potential fatality of this disease, a temporal artery biopsy is indicated in every suspicious case in order to provide a sound basis for the required long term therapy with corticosteroids.
A 63-year-old man with polymyalgia rheumatica (PMR) with cytoplasmic bodies (CB) in biopsied muscle was reported. He was referred to our hospital in June 1988 because of myalgia of four extremities. The ESR was 114 mm/hr and the serum CPK level was normal. Needle EMG and nerve conduction velocities showed normal findings. On light microscopic examination in biopsied muscle, the inclusion bodies which appeared on HE stained sections as deep reddish masses were present in 10% of all fibers. By electron microscopy the core of the bodies consisted of a dense tangle of thin filaments which were intermixed with granular material. Around the core a network of irregularly or radially oriented filaments was observed. These bodies were identified with cytoplasmic bodies. Since there has been no previous report of PMR with CB, our case is important to discuss the relationship between the pathogenesis of PMR and CB.