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Reference reagents for antinuclear antibodies.

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1331
LETTERS
Destructive spondylarthropathy and chronic renal
failure
Reference reagents for antinuclear antibodies
To the Editor:
Autoantibodies to nuclear and other intracellular
antigens, often called antinuclear antibodies (ANA), have
been useful as diagnostic aids in clinical medicine and as
immunologic probes in molecular and cell biology. Recently,
two international organizations, the International League
Against Rheumatism and the International Union of Immunological Societies, agreed to the formation of the International Committee on Antinuclear Antibodies, at a meeting at
the World Health Organization in Geneva. The charge of this
international committee was to standardize reference sera
containing ANA of different immunologic specificities and,
in collaboration with the Arthritis Foundation (AF) and the
Centers for Disease Control (CDC) in Atlanta, GA, make
these reference reagents available to bona fide clinical laboratories and research investigators throughout the world.
This communication is a preliminary announcement concerning the availability of certain reference ANA (see
Table 1).
Researchers interested in obtaining these reagents
should write to AF/CDC ANA Reference Laboratory, Immunology Branch, 1-1202 A25, Centers for Disease Control,
Atlanta, GA 30333.
ILAWIUIS International ANA Committee:
E. M. Tan, MD (Chair), USA
T. E. W. Feltkamp, MD (Vice-Chair), The Netherlands
D. Alarcon-Segovia, MD, Mexico
R. L. Dawkins, MD, Australia
M. Homma, MD, Japan
J. R. Kalden, MD, FRG
P. H. Lambert, MD, Switzerland
A. Lange, MD, Poland
R. N. Maini, MD, U K
F. C. McDuffie, MD, U SA
J. S. McDougal, MD, U SA
R. Norberg, MD, Sweden
M. Wilson. MD USA
Table 1.
Reference antinuclear antibodies (ANA) available
Reagent
Immunologic features
AF/CDC 1
Homogeneous-pattern ANA (doubles as
anti-native DNA)
Anti-La (SS-B)
Speckled-pattern ANA
Anti-UI R N P (U1 small nuclear RNP)
Anti-Sm (U1, U2, U5, U416 small nuclear RNP)
Nucleolar-pattern ANA
Anti-Ro (SS-A)
Centromere-pattern ANA
Anti-Scl-70 (DNA topoisomerase I)
Anti-Jo-1 (histidyl-transfer RNA synthetase)
AFlCDC2
AF/CDC3
AF/CDC4
AFICDC5
AFlCDC6
AFlCDC7
AF/CDC8
AFlCDC9
AF/CDC10
Arthritis and Rheumatism, Vol. 31, No. 10 (October 1988)
To the Editor:
There have been several reports in Arthritis and
Rheumatism of "destructive spondylarthropathy" occurring
in patients with chronic renal failure (1-3). The most recent
(3) suggests that hyperparathyroidism is responsible for this
condition, a view with which we agree. Readers should be
reminded of the elegant studies reported in 1963 by Bywaters
et a1 (4), illustrating the joint damage and the associated
histopathologic changes which may occur in primary or
secondary hyperparathyroidism. The lesions described include a spondylarthropathy that appears indistinguishable
from those described in Arthritis and Rheumatism (1-3).
This is not a new syndrome (I), but an old one "rediscovered."
N. P. Hurst, MRCP, PhD
R. Van den Berg, BM, BS
The Queen Elizabeth Hospital
Woodville, South Australia
Kuntz D, Naveau B, Bardin T, Drueke T, Treves R, Dryll A:
Destructive spondylarthropathy in hemodialyzed patients: a new
syndrome. Arthritis Rheum 27:369-375, 1984
Sebert J-L, Fardellone P, Marie A, Deramond H, Lambrey G ,
Legars D, Galibert P, Smajda A, Fournier A: Destructive
spondylarthropathy in hemodialyzed patients: possible role of
amyloidosis (letter). Arthritis Rheum 29:301-303, 1986
Alcalay M, Goupy M-C, Azais I , Bontoux D: Hemodialysis is not
essential for the development of destructive spondylarthropathy
in patients with chronic renal failure. Arthritis Rheum
30:1182-1186, 1987
Bywaters EGL, Dixon ASTJ, Scott JT: Joint lesions of hyperparathyroidism. Ann Rheum Dis 22: 171-187, 1963
Unusual features of iliopsoas bursitis
To the Editor:
Enlargement of the iliopsoas bursa is an unusual
clinical event. When present, it is almost always seen in a
patient with underlying rheumatoid arthritis ( 1 4 ) . Clinical
manifestations may include a mass in the groin area, pain
referred to the knee, and unilateral edema of the leg on the
affected side (1,3). The patient described below had no
underlying rheumatic disease, nor any of the typical clinical
features of iliopsoas bursitis.
The patient, a 65-year-old previously healthy man,
presented to the rheumatology clinic with a 6-month history
of left hip and left leg pain. The pain was diffuse, but it
seemed to emanate from the left lateral hip region. He had
had extreme difficulty with sleeping on his left side. The pain
was persistent and was not affected by rest or physical
activity.
Findings of a general examination were unremarkable. Examination of the patient's left hip region revealed
exquisite tenderness to palpation over the left trochanteric
bursa. The left hip could be flexed to 95", externally rotated
15", and internally rotated 10". The right hip could be flexed
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antibodies, reagents, references, antinuclear
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