Polymyalgia rheumatica in patients with a normal erythrocyte sedimentation rateComment on the article by Helfgott and Kieval.код для вставкиСкачать
1725 AR1 HRITIS & RHEUMATISM Vol 40, No 9, September 1997, pp 1725-1734 0 1997, American College of Rheumatology LETTERS Updating the American College of Rheumatology Revised Criteria for the Classification of Systemic Lupus Erythematosus To the Editor: In 1982, the Diagnostic and Therapeutic Criteria Committee of the American College of Rheumatology (ACR) published revised criteria for the classification of systemic lupus erythematosus (SLE) (1). During the ensuing decade, several investigators, including Drs. Graham Hughes and Donato Alarcon-Segovia, among others, have described the presence and clinical associations of antiphospholipid antibodies in patients with SLE, as well as the occurrence of the primary antiphospholipid syndrome (2-5). In 1992, Piette and colleagues suggested that the ACR revised criteria be reevaluated in light of the above discoveries (6). At the request of Dr. Eng Tan, the Diagnostic and Therapeutic Criteria Committee of the ACR reviewed the 1982 revised criteria for SLE and recommended the following revisions to criterion number 10 (“Immunologic disorder”), which were approved by the Council on Research and the Board of Directors: 1. Delete item lO(a) (“Positive LE cell preparation”), and 2. Change item 10(d) to “Positive finding of antiphospholipid antibodies based on 1) an abnormal serum level of IgG or IgM anticardiolipin antibodies, 2) a positive test result for lupus anticoagulant using a standard method, or 3) a false-positive serologic test for syphilis known to be positive for at least 6 months and confirmed by Treponema pallidum immobilization or fluorescent treponemal antibody absorption test.” Standard methods should be used in testing for the presence of antiphospholipid (7-10). Publication of this letter will allow basic and clinical investigators in SLE to not only use, but also cite, the modification of the 1982 criteria. Marc C. Hochberg, MD, MPH for the Diagnostic and Therapeutic Criteria Committee of the Amencun College of Rheumatology Tan EM, Cohen AS, Fries JF, Masi AT, McShane DJ, Rothfield NF, Schaller JG, Tala1 N, Winchester RJ: The 1982 revised criteria for the classification of systemic lupus erythematosus. Arthritis Rheum 25:1271-1277, 1982 Harris EN, Gharavi AE, Boey M, Patel BM, Mackworth-Young CG, Loizou S, Hughes GRV: Anticardiolipin antibodies: detection by radioimmunoassay and association with thrombosis in systemic lupus erythematosus. Lancet 2:1211-1214, 1983 Alarcon-Segovia D, Deleze M, Oria CV, Sanchez-Guerrero J, Gomez-Pacheco L, Cabiedes J, Fernandez L, Ponce de Leon S: Antiphospholipid antibodies and the antiphospholipid syndrome in systemic lupus erythematosus: a prospective analysis of 500 consecutive patients. Medicine (Baltimore) 68:353-365, 1989 Asherson RA, Khamashta MA, Ordi-Ros J, Derksen RHWM, Machin SJ, Barquinero J, Out HH, Harris EN, Vilardell-Torres M, Hughes GRV: The primary antiphospholipid syndrome: major 5. 6. 7. 8. 9. 10. clinical and serological features. Medicine (Baltimore) 68:366374, 1989 Alarcon-Segovia D: Antiphospholipid syndrome within systemic lupus erythematosus. Lupus 3:289-291, 1994 Piette JC, Wechsler 13, Frances C, Godeau P: Systemic lupus erythematosus and the antiphospholipid syndrome: reflections about the relevance of ARA criteria. J Rheumatol 19:1835-1837, 1992 Harris EN, Gharavi AE, Patel BM, Hughes GRV: Evaluation of the anticardiolipin antibody test: report of an international workshop held 4 April 1986. Clin Exp Immunol 68:215-222, 1987 Harris EN, Phil M: The second international anticardiolipin standardization workshop: The Kingston Antiphospholipid Antibody Study (KAPS) Group. Am J Clin Pathol 94:474-484, 1990 Exner T, Triplett DA, Taberner D, Machin SJ: Guidelines for testing and revised criteria for lupus anticoagulants: Subcommittee for the Standardization of LUPUSAnticoagulants. Thromb Haemost 65320-322, 1991 Brandt JT, Triplett DA, Alving B, Scharrer I: Scientific and Standardization Committee Communications: criteria for the diagnosis of lupus anticoagulants-an update. Thromb Haemost 74:1185-1190, 1995 Polymyalgia rheurnatica in patients with a normal erythrocyte sedimentation rate: comment on the article by Helfgott and Kieval To the Editor: We read with interest the article by Helfgott and Kieval (l),in which the authors state that 22% of their patients with polymyalgia rheumatica (PMR) were found to have a normal erythrocyte sedimentation rate (ESR; 1 3 0 mmihour), and a significantly higher proportion of these patients were male. To ascertain the frequency of PMR with a normal ESR, we carried out a retrospective chart review study of all patients meeting the Jones and Hazleman criteria for PMR (2). Based on a large series of 2,500 healthy men and women, it was found that the upper limit of normal for the ESR in patients who are over the age of 50 is 20 mm/hour for men and 30 mmihour for women (3). We established a normal cutoff value of 5 3 0 mmihour, with the additional requirement that all patients should have had a normal ESR throughout the course of their disease. The ESR was determined by the Westergren method in all cases, and we used Student’s t-test and Fisher’s exact test to evaluate the data. We excluded patients with a normal ESR pretreatment who developed a rise in the ESR during the course of the disease. Systemic inflammatory diseases, such as rheumatoid arthritis (RA) and systemic lupus erythematosus, fibromyalgia, thyroid disorders, multiple myeloma, remitting seronegative symmetrical synovitis with pitting edema, and cancer were ruled out by clinical evaluation and laboratory testing. The patients’ charts were also reviewed for episodes of fever, weight loss, depression, and peripheral arthritis, and for symptoms of giant cell (temporal) arteritis (GCA) (transient blindness, diplopia, blurring, temporal headache, jaw pain or claudication, and tenderness and/or thickening of a temporal LETTERS 1726 artery). Laboratory test results, such as levels of hemoglobin, rheumatoid factor, and antinuclear antibodies, and serum protein electrophoresis findings were recorded as available. Over an 8-year period, 39 patients with PMR were seen and treated. Thirty-six patients (92%) had an elevated ESR (average ESR 68 mmihour, range 32-120) and 3 patients continued to have a normal ESR (average ESR 16 mmihour, range 10-22) during followup of the disease. All of the latter patients were female, compared with 25 of the 36 patients with an elevated ESR (Pnot significant). The mean age (73 versus 69 years) did not differ significantly between groups. Shoulder and pelvic girdle involvement, peripheral arthritis (oligoarticular involvement), fever, and weight loss showed no differences of statistical significance. One patient in each group had symptoms of GCA. One patient with an elevated ESR was found to have GCA on temporal artery biopsy. All patients were treated with low-dose corticosteroids (prednisone 5 10 mgiday). The response was prompt and striking. There was an improvement in all patients. None of our followup patients developed the peripheral polydrthritis of RA. Based on the findings of several reports, the incidence of PMR in patients with an initial pretreatment ESR considered to be normal was -22% (4,s). We think this frequency is very high. In our study, we found that 8% of patients with PMR had a normal ESR, which was maintained during the followup. The clinical features of our patients with a normal versus elevated ESR were similar. Some authors have noted a normal ESR early in the course of the disease, with subsequent elevation over time. We believe that these patients should not be included in the normal ESR group. Taking into account this observation, further investigation is needed to establish what is dcemed a normal ESR in PMR. We suggest that, to be considered a normal ESR in PMR, the designated range should be maintained throughout the evolution of the illness. A normal ESR in patients with otherwise classic PMR has tended to mislead physicians, resulting in a serious delay in diagnosis. Thus, if there is good clinical evidence for PMR, a normal ESR should be ignored, and the patient should undergo an empirical trial of corticosteroid treatment. L. Caliani, MD Sergio 0. Paira, MD Hospital Jose! M. Cullen Santa Fe, Argentina 1. Helfgott S, l e v a 1 RI: Polymyalgia rheumatica in patients with a normal erythrocyte sedimentation rate. Arthritis Rheum 30:304307, 1996 2. Jones JG, Hazleman BL: The prognosis and management of polymyalgia rheumatica. Ann Rheum Dis 40:l-5, 1981 3. Bottiger LE, Suedberg CA: Normal erythrocyte sedimentation rate and age. BMJ 2:85-87, 1967 4. Ellis ME, Ralston S: The ESR in the diagnosis and management of the polymyalgia rheumatica/giant cell arteritis syndrome. Ann Rheum Dis 42:168-170, 1983 5. Sueiro JLF, Armona J, Rodriguez-Valverde V, Blanco R, Taboada MM: Polymyalgia rheumatica without clinically significant increased ESR (abstract). Arthritis Rheum 37 (suppl 9):S410, 1994 The diagnosis of polymyalgia rheumatica in patients with a low erythrocyte sedimentation rate: comment on the article by Helfgott and Kieval To the Editor: The issue of PMR with a low or normal ESR has revived the interest of rheumatologists. Between 10% and 20% of PMR patients show an ESR below 30 mmihour (1-3). In these cases, the diagnosis is often delayed and the risk of visual disturbanccs increased. Different strategies have been proposed for the diagnosis of PMR in patients with a low ESR. including an evaluation of C-reactive protein levels (l), plasma viscosity (4), symptoms and signs alone (2), concentration of CD8+ T cells (S), or the effect of steroid treatment (6). We have postulated that even a normal ESR may be an indicator of inflammation. To substantiate this hypothesis, we havc evaluated the changes in ESR after steroid treatment, with a view to differentiating between patients with PMR and healthy controls. The ESR was measured in 53 consecutive patients with classic PMR and in 6 patients with PMR and a normal ESR. The ESR was measured at diagnosis and after a median of 24 days of treatment with a mean daily dosage of 1.5 mg of prednisone. PMR was diagnosed according to a modification of the criteria proposed by Jones and Hazleman (7), in which only patients over SO years of age were included and the ESR was not considered in the diagnosis. As controls, 2 young, healthy individuals volunteered to receive prednisone (20 mg daily) after giving their informed consent. ESRs of the 2 controls were measured at baseline and after 10 days of treatment. The ESR significantly declined after treatment, both in patients with a raised baseline ESR and in those with a normal baseline ESR. The percentage differences were similar in both groups (P < 0.00001 and P = 0.0029, respectively. by paired t-test) (Table l), with a ratio between pre- and posttreatment ESRs of 5.7 in patients with a raised ESR at baseline and a ratio of 5.4 in patients with a normal ESR. The controls also showed a decrease in ESR after steroid treatment; however, this decrease was much lower than that observed in PMR patients. The pre- and posttreatment ESR ratio for controls was 1.4. The control subjects were considerably younger than Table 1. Demographic and clinical characteristics of the study population” Age, years Ma1e:female ratio Baseline ESR, mmihour Posttreatment ESR, mm/hour Baseline ESR:posttrcatment ESR ratio Patients with high ESR (n = 53) Patients with normal ESR (n = 6) Controls (n = 2) 70.0 ? 9.6 10:37 76.4 t- 20.4 23.3 2 15.8 5.7 68.8 ? 9.2 4:2 25.8 5 3.7 7.5 ? 6.4 5.4 26 -t 2.8 2:o 10 -t 2.8 7 -t 1.4 1.4 * Except where otherwise indicated, values are the mean i- SD. ESR = erythrocyte sedimentation rate.