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Prevalence of monosodium urate and calcium pyrophosphate dihydrate crystals in postmortem knee synovial fluid.

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LETTERS
1319
These observations lead us to propose that local
factors in the synovium must play a major role in the
development of chronic inflammation in this model. With
regard to what these local factors are, we can only speculate
at this time. For example, we are now examining synovial
mast cells (number, function), but vascular endothelial cells
(type, function) or the peripheral nervous system are other
potentially important areas for investigation. The peripheral
nervous system is particularly interesting in light of recent
reports on the role of synovial innervation and substance P,
a peptide neurotransmitter, in regulating the severity of
adjuvant-induced arthritis (4). In any event, our observations with this experimental model emphasize the potential
complexity underlying the development of chronic proliferative and erosive synovitis.
Figure 1. Ankle synovium from an F344/N female rat, 9 weeks after
intraperitoneal injection of an aqueous suspension of group A
streptococcal cell walls. The slide demonstrates positive staining for
antigens (black precipitate) in blood vessels of various sizes. Appropriate control slides showed negative findings.
the extremities of both chronic arthritis-susceptible LEWM
and -resistant F344/N female rats (4), we have reexamined
the effects of streptococcal cell wall injection in F344/N
female rats, using a more sensitive in situ immunoperoxidase
staining technique. Ankle synovial specimens from F344/N
femalt: rats intraperitoneally injected with an aqueous suspension of group A streptococcal cell walls were sectioned
and sequentially incubated with rabbit anti-group A streptococcal cell wall antibody, followed by biotin-conjugated goat
anti-rabbit IgG and then by an avidin-peroxidase complex
(ABC Vectastain Kit; Vector Laboratories, Burlingame,
CA). Color was developed by immersing the sections in a
solution of 0.05% (weightholume) 3,3-diaminobenzidine
tetrahydrochloride, 0.04% (w/v) nickel chloride, and 0.003%
hydrogen peroxide in O.OSM Tris-saline buffer, pH 7.4. The
section was counterstained with 2% methyl green.
By this technique, as shown in Figure 1, group A
streptococcal cell wall antigens were, indeed, demonstrable
in the synovium of F344/N female rats. More specifically,
they were deposited in the walls of blood vessels of various
sizes. The obviously interesting and important observation,
however, was that in contrast to the LEW/N and other
arthrit is-susceptible rat strains, no chronic inflammatory
reaction (i.e., mononuclear cell infiltration, synovial ceil
hyperplasia, erosions, etc.) was induced in the F344/N rats.
These observations have important implications with
regard to the mechanisms regulating the development of
chronic inflammation in response to arthritogenic cell walls
and possibly other etiologic agents. Our published and
unpublished data indicate that the F344lN female rats can
mount an excellent inflammatory response to cell walls in
vitro (as indicated by cytokine secretion), and in vivo in the
spleen and peritoneum if cell walls are injected into the
peritoneum (2), or in the skin if cell walls are injected locally
(5). The F344/N female rat does not, however, mount a
chronic inflammatory response in the joints.
Ronald L. Wilder, MD, PhD
Janice B. Allen
NIADDK, NIH
Bethesda, MD
I . Wilder RL, Calandra GB, Garvin AJ, Wright KD, Hansen C T
Strain and sex variation in the susceptibility to streptococcal cell
wall-induced polyarthritis in the rat. Arthritis Rheum 25: 10641072, 1982
2. Lehman TJA, Allen JB, Plotz PH, Wilder RL: Polyarthritis in
rats following the systemic injection of Lactobacillus casei cell
wall in aqueous suspension. Arthritis Rheum 26: 1259-1265, 1983
3. Wilder RL, Allen JB, Wahl LM, Calandra GB, Wahl SM: The
pathogenesis of group A streptococcal cell wall-induced polyarthritis in the rat: comparative studies in arthritis resistant and
susceptible inbred rat strains. Arthritis Rheum 26:1442-1451,
1983
4. Lehman TJA, Allen JB, Plotz PH, Wilder RL: Lactobacillus
casei cell wall-induced arthritis in rats: cell wall fragment distribution and persistence in chronic arthritis-susceptible LEW/N
and -resistant F344lN rats. Arthritis Rheum 27~939-942, 1984
5. Allen JB, Calandra GB, Wilder RL: Cutaneous inflammatory
reactions to group A streptococcal cell wall fragments in Fisher
and Lewis inbred rats. Infect Immun 42:796-801, 1983
6. Levine JD, Clark R, Devor M, Helms C, Moskowitz MA,
Basbaum A: Interneuronal substance P contributes to the severity of experimental arthritis. Science 226547-549, 1984
Prevalence of monosodium urate and calcium
pyrophosphate dihydrate crystals in postmortem knee
synovial fluid
To the Editor:
In December 1983, Wall and collaborators published
their results of a study of the prevalence of monosodium
urate (MSU) and calcium pyrophosphate dihydrate (CPPD)
crystal deposition in- first metatarsophalangeal joints at autopsy (Wall B, Agudelo CA, Tesser JRP, Mountz J, Holt D,
Turner RA: An autopsy study of the prevalence of monosodium urate and calcium pyrophosphate dihydrate crystal
deposition in first metatarsophalangeal joints. Arthritis
Rheum 24:1522-1524, 1983).
LETTERS
1320
Of 70 subjects, 1 1 showed MSU deposits and 1 had
CPPD crystals. This suggested that the high proportion of
patients with MSU crystals was due to the fact that the
population studied was not typical, but a population of
acutely ill patients who died in a hospital.
We studied the postmortem knee synovial fluid samples of subjects who had donated their bodies to the Department of Anatomy of the University of Louvain. Between
October 1983 and February 1985, we studied 138 specimens
from 70 men and 68 women, ranging in age from 52-95 years.
Eleven patients died in a hospital and 127 died at home.
When death occurred at home, 2 or 3 days elapsed before the
body arrived at the Department of Anatomy, so the joint was
aspirated between 48 and 72 hours after death. Aspiration
was done with a 20-gauge needle and a 5-cc syringe. We
examined the fluid with a compensated polarized Zeiss
microscope. Of the 138 specimens studied, 3 contained MSU
crystals and 11 contained CPPD crystals.
Despite several letters to family members and/or the
home physician, it was not possible to collect sufficient data
on premortem blood analysis, medical history, and more
specifically, on acute arthritis attacks in the past to make any
correlation between the medical history and our findings.
Wall and coworkers found a majority of MSU crystals. McCarty et al, in 1966, found CPPD crystals in 7 of 215
cadavers (McCarty DJ, Hogan JM, Gatter RA, Grossman M:
Studies on pathological calcifications in human cartilage. J
Bone Joint Surg 48A:309-325, 1966). Our study found more
CPPD crystals than MSU crystals. Since the majority of our
subjects died at home and did not receive all the therapeutic
treatment that would have been received if in a hospital, we
are inclined to say that our group might better reflect reality
and that in a normal population, there would be approximately 12% with CPPD crystals and 4% with MSU crystals.
But the difference between our results and those of Wall et a1
may also be due to the fact that 48 to 72 hours elapsed
between the time of death and our examination.
Chr. Moens, MD
D. Moens
Ph. Moens
Centre Medico-Social de Bruxelles
Brussels, Belgium
References from the classical rheumatologic literature
To the Editor:
We very often observe in medical literature, rheumatologic literature included, the citation of references to
articles published many years ago, e.g., 1900-193Os, which
are difficult to find in the libraries.
We recently wrote a review of massive pulmonary
hemorrhage in patients with systemic lupus erythematosus
(SLE) (1). It was most difficult for us to find the first
description of this complication in SLE, which was written
by William Osler in 1904 (2). We have also had this problem
when trying to locate the first descriptions of Reiter’s
syndrome, by the German author Hans Reiter (3) and the
French authors Fiessinger and Leroy (4), as well as descriptions of Sjogren’s syndrome, by Hadden (S), Schirmer (6),
Gougerot (7), and Sjogren (8). These are only a few examples, but in general, this is a common problem when original
descriptions of any disease are needed for an in-depth study
or for a literature review.
In our country, at least, it is impractical and time
consuming to search for the original, old medical references.
Moreover, this problem is frequently compounded because
many of these articles, when located, are found to be
published in the original languages, e.g., German, French,
Finnish, Turkish, Japanese, etc. Nevertheless, we think that
the study of the “first teachers” is very interesting from a
historical as well as an academic perspective, and a system
for obtaining such remote citations would be of great practical utility to the investigator.
We believe it would be very useful to produce a book
that is a compilation of the more quoted classical references
in the field of rheumatology. If these references were translated from their original languages and published in English,
that would be even better. We suggest that such a compilation would be a good supplementary edition of Arthritis and
Rheumatism.
G. Herrero-Beaumont, MD
S . Castafieda, MD
Fundacibn JimPnez Diaz
Universidad Autbnoma
Madrid, Spain
1. Castafieda S, Herrero-Beaumont G, Valenzuela A, Vidal J ,
Fernttndez-Vallado P: Massive pulmonary hemorrhage: fatal
comolication of svstemic luous ervthematosus. J Rheumatol
12:186-187, 1985 .
2. Osler W: On the visceral manifestations of the erythema group of
skin disease. Am J Med Sci 127:l-23, 1904
3. Reiter H: Ueber eine bisher unerkannte Spirochaeteninfektion
(Spirochaetosis arthritica). Dtsch Med Wochenschr 42: 15351536, 1916
4. Fiessinger N, Leroy ME: Contribution ti I’ttude d’une Cpidtmie
de dysenterie dans la Somme. Bull Mem SOCMed Hop Pans
40~2030-2069, 1916
5. Hadden WB: On “dry mouth” or suppression of the salivary and
buccal secretions. Trans Clin SOCLondon 27:176-182, 1888
6. Schirmer 0: Studien zur Physiologie und Pathologie der Tranenabsonderung und Tranenabfulis. Graefes Arch Ophthalmol
56~197-291, 1903
7. Gougerot H: Insuffisance progressive et atrophie des glandes
salivaires et muqueuses de la bouche, des conjunctives (et parfois
des muqueuses nasale, laryngte, vulvaire): “secheresse” de la
bouche, des conjunctives, etc. Bull SOC Franc Derm Syph
32~376-379, 1925
8. Sjogren H: Zur Kenntnis der Keratoconjunctivitis sicca (Keratitis filiformis bei Hypunfunktion der Tranendrussen). Acta Ophthalmol (suppl) 11:1-151, 1933
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crystals, dihydrate, urate, postmortem, monosodium, pyrophosphate, knee, calcium, synovial, prevalence, fluid
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