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Polymyalgia rheumatica in patients with a normal erythrocyte sedimentation rateComment on the article by Helfgott and Kieval.

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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.
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