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PubMed1991

Treatment of polymyalgia rheumatica with intramuscular injections of depot methylprednisolone.

Although the treatment of patients with polymyalgia rheumatica by corticosteroids given by mouth is effective, it is often accompanied by multiple side effects. Various studies have shown that the steroid related complications are proportional to the cumulative dose of steroids administered. In a prospective study of 16 patients with polymyalgia rheumatica the effects of regular intramuscular injections of methylprednisolone over 12 months were evaluated. Remission of disease was achieved with injections of 120 mg of methylprednisolone every three weeks for 12 weeks. Subsequent disease remission was maintained by monthly injections of methylprednisolone on a reducing schedule of dose. The treatment was efficacious, safe, well tolerated over one year, and showed no suppression of the hypothalamic pituitary adrenal axis at 12 weeks after initiation of treatment. Such a mode of steroid treatment results in a considerably lower cumulative steroid dose than with conventional doses of prednisolone given by mouth. These results will be further evaluated in a controlled trial using intramuscular injections of methylprednisolone and prednisolone given by mouth for the treatment of polymyalgia rheumatica.

Delayed-Action Preparations↗
PubMed2004

Polymyalgia rheumatica: clinical presentation is key to diagnosis and treatment.

Polymyalgia rheumatica should be considered in the differential diagnosis in patients over 50 years old who present with bilateral achiness and stiffness in the shoulders or hips or both. It usually responds quickly to once-daily, low-dose prednisone, but some patients require treatment for several years. Polymyalgia rheumatica frequently overlaps with giant cell arteritis, and patients must be followed closely for development of complications from this condition, especially aortitis.

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PubMed1985

Polymyalgia rheumatica and giant cell arteritis. The dilemma of therapy.

Polymyalgia rheumatica, next to rheumatoid arthritis the most common inflammatory rheumatic disorder of the elderly, is a nonspecific clinical syndrome involving pain in the shoulder and pelvic girdles. Giant cell arteritis appears to localize in elastin-containing arteries and can cause similar myalgias. A relationship exists between the two diseases, as evidenced by their frequent coexistence in the same patient. The symptoms of polymyalgia rheumatica respond to low-dose corticosteroid therapy, while giant cell arteritis requires higher doses to prevent blindness due to involvement of the temporal artery. The key decision in therapy, therefore, concerns the dose and duration of use of steroid for polymyalgic symptoms. In this decision, prevention of the catastrophic complications of giant cell arteritis and avoidance of needless side effects of high-dose steroid therapy in the elderly are competing considerations.

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PubMed1976

Liver dysfunction and polymyalgia rheumatica. A case report.

Hepatic dysfunction may be a manifestation of polymyalgia rheumatica. We present a second patient with the polymyalgia rheumatica syndrome and a significantly elevated alkaline phosphtase who, on liver biopsy, demonstrated granuloma formation and massive infiltration of the portal spaces with lymphocytes. The alkaline phosphatase elevation was favorably influenced by low dose steroid therapy.

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PubMed1993

Increased RAHA titer and interleukin-6 levels in the synovial fluid in a patient with polymyalgia rheumatica.

We report a patient with polymyalgia rheumatica (PMR) accompanied by an increased Rheumatoid Arthritis Hemagglutinin Test (RAHA) titer and interleukin-6 level in the synovial fluid. A 60-year-old female was admitted because of polymyalgia, a body temperature of 39.2 degrees C, and an erythrocyte sedimentation rate increased to 94 mm/h. Since a muscle biopsy failed to show a specific finding, she was diagnosed as PMR. The titer of RAHA and the interleukin-6 level were increased only in the synovial fluid; prednisolone treatment decreased both. The present case raised the possibility that a similar mechanism in rheumatoid arthritis may involve the development of synovitis in PMR.

Arthritis, Rheumatoid↗
PubMed1993

[Raynaud's syndrome during the course of polymyalgia rheumatica].

A case is described of polymyalgia rheumatica in which Raynaud's sign appeared at the beginning of the disease parallel with changes of rheumatoid arthritis type without other features of arterial system involvement in particular without clinical features of the involvement of the subclavian or axillary artery. The sign of temporal artery involvement appeared only after 18 months of disease duration. Steroid-therapy produced complete regression of both articular muscular and vascular changes.

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PubMedDate not supplied

[Polymyalgia rheumatica].

Giant cell arteritis-mediated polymyalgia rheumatica is a typical disease of old age; though manifestation is rare in patients younger than 50 years, there is no upper age limit. Average disease-onset is at age 70. Typical symptoms and high serological inflammation are found. Laboratory data is nonspecific; temporal artery biopsy is imperative in unclear cases. Only glucocorticoid therapy initiates prompt pain relief, stops the inflammatory process and apprehends vascular complications. Monitoring of therapy requires careful guidance and experience.

Adrenal Cortex Hormones↗
PubMedDate not supplied

[Trouble of liver function in polymyalgia rheumatica (author's transl)].

The possible existence of liver function disease such as cholestasis during temporal arteritis or polymyalgia rheumatica has been recently discovered. Two cases are reported of cholestasis without jaundice during polymyalgia rheumatica. The altérations most frequently observed are the elevation of the alcalin phosphatases, 5' nucleotidases, gamma G.T. and the retention of BSP. The syndrome disappears by treatment as well as the rheumatologic disease. It seems to be interesting to diagnose polymyalgia rheumatica through this trouble of liver funcion.

Cholestasis, Intrahepatic↗
PubMed1988

"Chronic Epstein-Barr virus infection" syndrome and polymyalgia rheumatica.

Twenty-three patients with polymyalgia rheumatica (PMR) followed in an academic rheumatology practice frequently reported symptoms commonly found in the recently described "chronic fatigue syndrome" or "chronic Epstein-Barr infection syndrome." These symptoms persisted for months after treatment had reduced the severity of the myalgias and lowered the sedimentation rate: periodically disabling fatigue (33%), recurrent pharyngitis (30%), sleep disorder (65%) and arthralgias (70%). However, antibody titers to Epstein-Barr virus in the patients with PMR were not significantly different from those in age and sex matched control subjects.

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PubMed2005

Serum amyloid A as a potent therapeutic marker in a refractory patient with polymyalgia rheumatica.

We report a patient with polymyalgia rheumatica (PMR) who showed a relapse soon after tapering of oral prednisolone. C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) were quickly normalized after the re-increase in oral prednisolone, and muscle pain and stiffness gradually improved in parallel with a decrease in serum amyloid A (SAA). Flow cytometry simultaneously demonstrated an increase in CD8+CD25+ cells and a decrease in CD4+CD25+ cells and CD4+CD45RA+ cells. When clinical symptoms remain with negative results for CRP and ESR even after the start of corticosteroid treatment, SAA might be a potent therapeutic marker for disease activity in PMR.

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PubMed2005

[Polymyalgia rheumatica: myalgic syndrome or occult vasculitis?].

Polymyalgia rheumatica (PMR) is a chronic inflammatory disorder of unknown etiology which typically presents with symmetric myalgias in the shoulder and pelvic girdles. Other clinical signs include the rapid onset of symptoms and the almost exclusive manifestation in the elderly population. In around 20% of cases, PMR is associated with giant cell arteritis (GCA). However, new imaging techniques suggest that the prevalence of subclinical GCA (e. g. aortitis) in PMR is probably higher. Acute phase reactants like erythrocyte sedimentation rate and c-reactive protein are usually elevated. Myalgias are accompanied by synovitis and bursitis of the large proximal joints and can be visualized by ultrasound or magnetic resonance imaging. While the diagnosis of GCA can be verified by temporal artery biopsy, pathognomonic findings for PMR like specific autoantibodies are lacking. Typical for PMR is the rapid response to corticosteroids. Usually the therapy needs to be continued for at least 2 years. Due to adverse events in many cases a corticosteroid saving therapy like methotrexate is needed.

Adrenal Cortex Hormones↗
PubMed2006

Glucocorticoid effects on adrenal steroids and cytokine responsiveness in polymyalgia rheumatica and elderly onset rheumatoid arthritis.

Polymyalgia rheumatica (PMR) usually exhibits a good clinical response to glucocorticoid (GC) treatment, but early clinical symptoms may create some difficulties in the differential diagnosis with elderly onset rheumatoid arthritis (EORA), particularly in patients complaining of shoulder and pelvic girdle involvement at onset (PMR-like clinical onset) (EORA/PMR). Since neuroendocrine mechanisms seem to play a pathogenetic role in these clinical conditions, the aim of this study was to evaluate hormone and cytokine responsiveness to GC treatment in these patients. Cortisol (CO), dehydroepiandrosterone sulphate (DHEAS), 17-OH-progesterone (PRG), interleukin-1 receptor antagonist (IL-1Ra), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) were evaluated at base line, and 1 month after GC treatment (prednisone 10 mg/day), in 14 PMR, 11 EORA/PMR, and 13 EORA patients (mean age 73 +/- 5 years, +/- SD, mean disease duration 3 +/- 2 months, +/- SD). No patient was taking GCs or immunosuppressive agents at base line. Following GC treatment, CO, DHEAS, and PRG decreased significantly in both PMR and EORA/PMR patients (P < 0.05), but not in EORA patients. On the contrary, IL-1Ra was significantly increased in both PMR and EORA/PMR patients (P < 0.05). IL-6 and TNF-alpha serum levels were significantly decreased in all groups of patients (P < 0.05). In conclusion, PMR and EORA/PMR seem to exhibit similar hormonal variations after GC administration, when compared to EORA patients. These differences suggest a deficient function of the hypothalamic-pituitary-adrenal (HPA) axis in PMR and EORA/PMR patients, with a related higher responsiveness to GC treatment. Interestingly, in PMR and EORA/PMR patients, GC treatment was found to downregulate PRG serum levels.

Adrenal Glands↗
PubMed1999

[Prevalence of antiphospholipid antibodies in Horton's disease and in polymyalgia rheumatica].

PURPOSE: Antiphospholipid antibodies (APL) are frequently observed in the course of giant cell arteritis and polymyalgia rheumatica. However, their role and relationships with potential ischemic events are still debated. METHODS: To determine the prevalence of APL in relation with ischemic events, 62 patients with giant cell arteritis and/or polymyalgia rheumatica were retrospectively studied. RESULTS: Before corticosteroid treatment 41% of the 51 patients with giant cell arteritis and 64% of the 11 patients with isolated polymyalgic rheumatica had high IgG ACL levels, with a frequency significantly higher than that (15.6%) of the control group which was composed of healthy elderly. IgM ACL were found in only two patients with giant cell arteritis. There was no correlation between the occurrence of an ischemic event (22 ischemic events in the 51 patients with giant cell arteritis) and the presence of ACL, even though the latter were more frequently observed in the giant cell arteritis group (52% versus 41% in non ischemic patients). The prevalence of ACL increased, reaching 59% if lupus anticoagulant was associated, but the difference was not significant. ACL disappeared soon after corticosteroid therapy had been initiated. CONCLUSION: Though ACL are frequently seen in giant cell arteritis and/or polymyalgia rheumatica, they are not related to ischemic events and disappear rapidly after corticosteroid treatment.

Adrenal Cortex Hormones↗
PubMed1995

Polymyalgia rheumatica or Lyme disease? How to avoid misdiagnosis in older patients.

This case report demonstrates the need to consider Lyme disease in older patients who present with nonspecific signs and symptoms often seen in polymyalgia rheumatica, particularly a markedly elevated erythrocyte sedimentation rate (ESR). ESRs greater than 100 mm/hr are common in polymyalgia rheumatica, but rates higher than 85 mm/hr are also possible in Borrelia infection. Because positive serologic findings for Lyme disease have been noted in patients with polymyalgia rheumatica who have been exposed to endemic areas, differential diagnosis must be based on clinical manifestations. Response to therapy should be monitored closely to confirm the diagnosis and avoid the adverse consequences of inappropriate treatment. The potentially deleterious effect that corticosteroids can have on Lyme disease must be considered in the decision to treat polymyalgia rheumatica.

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PubMed2004

Prednisone plus methotrexate for polymyalgia rheumatica: a randomized, double-blind, placebo-controlled trial.

BACKGROUND: Steroids are the standard treatment for polymyalgia rheumatica. The efficacy of the candidate drug methotrexate has not yet been demonstrated in controlled studies. OBJECTIVE: To compare the efficacy and safety of prednisone plus methotrexate and prednisone alone in patients with polymyalgia rheumatica. DESIGN: Multicenter randomized, double-blind, placebo-controlled trial. SETTING: 5 Italian rheumatology clinics. PATIENTS: 72 patients with newly diagnosed polymyalgia rheumatica. MEASUREMENTS: The proportion of patients no longer taking prednisone, the number of flare-ups, and the cumulative prednisone dose after 76 weeks. INTERVENTION: Prednisone dosage (25 mg/d) was tapered to 0 mg/d within 24 weeks and was adjusted if flare-ups occurred. Oral methotrexate (10 mg) or placebo, with folinic acid supplementation (7.5 mg), was given weekly for 48 weeks. RESULTS: Twenty-eight of 32 patients in the methotrexate group and 16 of 30 patients in the placebo group were no longer taking prednisone at 76 weeks (P = 0.003). The risk difference was 34 percentage points (95% CI, 11 to 53 percentage points). Similar results were obtained after adjustment for C-reactive protein level and duration of symptoms in a multivariate model. Fifteen of 32 patients in the methotrexate group and 22 of 30 patients in the placebo group had at least 1 flare-up by the end of follow-up (P = 0.04). The median prednisone dose was 2.1 g in the methotrexate group and 2.97 g in the placebo group (P = 0.03). The rate and severity of adverse events were similar. LIMITATIONS: Follow-up was short, and a high dose of folinic acid and a relatively high starting dosage of prednisone were used. Ten of 72 patients (14%) discontinued treatment or were lost to follow-up. CONCLUSIONS: Prednisone plus methotrexate is associated with shorter prednisone treatment and steroid sparing. It may be useful in patients at high risk for steroid-related toxicity.

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PubMed1999

Bronchiolitis obliterans organizing pneumonia associated with polymyalgia rheumatica.

The association of bronchiolitis obliterans organizing pneumonia (BOOP) with polymyalgia rheumatica is rare, and only one case has previously been described. This study reports on the case of an 80 yr-old male who presented with malaise, nonproductive cough and exertional dyspnoea for several weeks, along with a history of bilateral shoulder and pelvic girdle pain of several months' duration. The chest radiograph revealed a pneumonic infiltrate in the right lower lobe, which was unresponsive to antibiotics. Bronchoscopy, bronchoalveolar lavage and a transbronchial lung biopsy established the diagnosis of BOOP. The patient improved consistently on steroids. As in other connective diseases, organizing pneumonia may be one of the early manifestations of polymyalgia rheumatica.

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PubMed1980

Hepatitis B virus and polymyalgia rheumatica: a search for HBsAg, HBsAb, HBcAb, HBeAg, and HBeAb.

Forty-three consecutive patients with polymyalgia rheumatica were studied for serological markers of actual or previous hepatitis B virus infection. Signs of active virus replication, which include HBsAg supported by the presence of HBeAg and anti-HBc in high titres, were not found in any cases. Anti-HBs, a serological sign of previous hepatitis B virus exposure, was present in 16.8%. The prevalence of anti-HBs is strongly age-dependent in the normal population, and its prevalence in polymyalgia rheumatica was not significantly different from the incidence found in other hospital patients. No significantly raised incidence was found in any subgroups, including patients without liver dysfunction. These results do not support the concept that current or previous hepatitis B virus infection plays any role in the pathogenesis of the majority of cases of polymyalgia rheumatica.

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