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Home > Archive > Lupus Support > April 2005 > lab stuff
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| Hi there, this is what is printed on one of my ANA labwork's...which
showed a low titre of ANA 1:40 and Speckled.
I'm just posting this in case it helps someone else. (check your lab
reports)
Sure doesn't help me, because they don't say which type of "speckled" mine
was. <g>
Hugs
J
Antinuclear autoantibodies (ANA) produce fluorescence patterns according
to the target nuclear antigen, and are often characteristic of a
particular disease.
Low titre autoantibodies (<1:80) are found in up to 5% of healthy
populations, increasing to 30% of healthy elderly patients.
The coarse speckled pattern is common in SLE, MCTD, and other overlap
syndromes.
Antigens are ribonuclear proteins.
The fine speckled pattern is associated with SLE, Sjogren's syndrome, and
scleroderma.
Antigens are nuclear proteins like SS-A(Ro) and SS-B(La).
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| I thought speckled was speckled. Homogenous was homogenous. And so on and
so on.
Mine is 1:640 and has not changed much over the years.
Now the other lab stuff jumps around like fleas on hounddogs!
I am MCTD by the way.
Always,
...· ´¨¨)) -:¦:-
¸.·´ .·´¨¨))
((¸¸.·´ ..·´ cloud -:¦:-
-:¦:- ((¸¸.·´*
> Hi there, this is what is printed on one of my ANA labwork's...which
> showed a low titre of ANA 1:40 and Speckled.
> I'm just posting this in case it helps someone else. (check your lab
> reports)
> Sure doesn't help me, because they don't say which type of "speckled" mine
> was. <g>
> Hugs
> J
>
> Antinuclear autoantibodies (ANA) produce fluorescence patterns according
> to the target nuclear antigen, and are often characteristic of a
> particular disease.
> Low titre autoantibodies (<1:80) are found in up to 5% of healthy
> populations, increasing to 30% of healthy elderly patients.
>
> The coarse speckled pattern is common in SLE, MCTD, and other overlap
> syndromes.
> Antigens are ribonuclear proteins.
> The fine speckled pattern is associated with SLE, Sjogren's syndrome, and
> scleroderma.
> Antigens are nuclear proteins like SS-A(Ro) and SS-B(La).
>
| |
|
| cloud wrote:
[vbcol=seagreen]
> I thought speckled was speckled. Homogenous was homogenous. And so on and
> so on.
> Mine is 1:640 and has not changed much over the years.
> Now the other lab stuff jumps around like fleas on hounddogs!
> I am MCTD by the way.
>
>
I'm adding more
http://rheumatology.oupjournals.org...t/full/41/3/343
Rheumatology 2002; 41: 343-345
© 2002 British Society for Rheumatology
Autoantibodies to nuclear antigens, including DNA, were discovered over 40 yr
ago and have become the hallmark of systemic rheumatic disease. Antinuclear
antibodies (ANA) are present in the sera of 95–99% of patients with the
prototypic autoimmune disease, systemic lupus erythematosus (SLE), but may also
be found frequently in many other connective tissue disorders. ANAs are useful
aids in the diagnosis of many rheumatic diseases, but have also shed light on
the role of nuclear antigens in autoimmune disease. In this short article, we
will highlight the key experiments that led to the discovery of these
antibodies.
The LE cell phenomenon was first observed in 1948 by Hargraves et al. [1] in
blood from patients with SLE. It was noted that, when leucocytes were incubated
with serum from such patients, nuclear alterations developed together with
phagocytosis of nuclear remnants by mature polymorphonuclear leucocytes. This
crucial observation went on to receive considerable attention in the ensuing
years.
<skipped some here, but some may want to copy and paste it all into a message or
text file and save the whole thing>
The early techniques of indirect immunofluorescence used in the discovery of
antinuclear factor have evolved and remain widely used in the detection of ANAs.
Whilst early methods made use of cryopreserved tissues and organs as substrates,
tissue culture cell lines have now replaced them. Figure 1 shows some of the
common staining patterns obtained with different sera. Multiple staining
patterns have been described, and it has been noted that these can often occur
with the same sera as a result of ANAs reacting with different nuclear or
nucleolar antigens. Other key developments include the discovery of anti-Sm
antibodies specific for SLE [17] and the description by Pincus et al. of the
DNA-binding assay [18, 19]. Numerous antibodies to non-histone nuclear proteins
and RNA–protein complexes were described in the 1970s and 1980s, some of which
were also found to be relatively disease-specific. A description of the
discovery of various antibodies to extractable nuclear antigens is beyond the
scope of this article, but the interested reader is directed to a review by Tan
[20].
FIG. 1. Common ANA patterns on Hep-2000 cell line substrate. (a) Homogeneous
pattern with chromatin staining. (b) Coarse speckled pattern. (c) Nucleolar
pattern. (d) Fine speckled pattern.
The observations by Friou and others in the late 1950s clearly demonstrated an
autoimmune pathological process underlying SLE, and this paved the way for a new
area of research into the pathogenesis of this disease. ANA profiles have become
very useful in the differential diagnosis of rheumatic disease with atypical
presentations and, in the case of antibodies to DNA, a potential role for
certain ANAs in the pathogenesis of tissue injury has been proposed. Together
with Hargraves’ demonstration of the LE cell phenomenon, the discovery of
antinuclear factor remains one of the most important findings in the history of
SLE and autoimmune disease.
| |
| janers 2005-04-05, 6:28 pm |
| WELCOME back J
nice seeing you post.
janers
| |
|
| Yeah, and that too!
Hi J, I do not think we have ever been formerly introduced. Sorta difficult
to do this online though so I will just say Hi.
Always,
...· ´¨¨)) -:¦:-
¸.·´ .·´¨¨))
((¸¸.·´ ..·´ cloud -:¦:-
-:¦:- ((¸¸.·´*
>
> I'm adding more
> http://rheumatology.oupjournals.org...t/full/41/3/343
> Rheumatology 2002; 41: 343-345
> © 2002 British Society for Rheumatology
> Autoantibodies to nuclear antigens, including DNA, were discovered over 40
> yr
> ago and have become the hallmark of systemic rheumatic disease.
> Antinuclear
> antibodies (ANA) are present in the sera of 95-99% of patients with the
> prototypic autoimmune disease, systemic lupus erythematosus (SLE), but may
> also
> be found frequently in many other connective tissue disorders. ANAs are
> useful
> aids in the diagnosis of many rheumatic diseases, but have also shed light
> on
> the role of nuclear antigens in autoimmune disease. In this short article,
> we
> will highlight the key experiments that led to the discovery of these
> antibodies.
>
> The LE cell phenomenon was first observed in 1948 by Hargraves et al. [1]
> in
> blood from patients with SLE. It was noted that, when leucocytes were
> incubated
> with serum from such patients, nuclear alterations developed together with
> phagocytosis of nuclear remnants by mature polymorphonuclear leucocytes.
> This
> crucial observation went on to receive considerable attention in the
> ensuing
> years.
>
> <skipped some here, but some may want to copy and paste it all into a
> message or
> text file and save the whole thing>
>
> The early techniques of indirect immunofluorescence used in the discovery
> of
> antinuclear factor have evolved and remain widely used in the detection of
> ANAs.
> Whilst early methods made use of cryopreserved tissues and organs as
> substrates,
> tissue culture cell lines have now replaced them. Figure 1 shows some of
> the
> common staining patterns obtained with different sera. Multiple staining
> patterns have been described, and it has been noted that these can often
> occur
> with the same sera as a result of ANAs reacting with different nuclear or
> nucleolar antigens. Other key developments include the discovery of
> anti-Sm
> antibodies specific for SLE [17] and the description by Pincus et al. of
> the
> DNA-binding assay [18, 19]. Numerous antibodies to non-histone nuclear
> proteins
> and RNA-protein complexes were described in the 1970s and 1980s, some of
> which
> were also found to be relatively disease-specific. A description of the
> discovery of various antibodies to extractable nuclear antigens is beyond
> the
> scope of this article, but the interested reader is directed to a review
> by Tan
> [20].
>
> FIG. 1. Common ANA patterns on Hep-2000 cell line substrate. (a)
> Homogeneous
> pattern with chromatin staining. (b) Coarse speckled pattern. (c)
> Nucleolar
> pattern. (d) Fine speckled pattern.
>
> The observations by Friou and others in the late 1950s clearly
> demonstrated an
> autoimmune pathological process underlying SLE, and this paved the way for
> a new
> area of research into the pathogenesis of this disease. ANA profiles have
> become
> very useful in the differential diagnosis of rheumatic disease with
> atypical
> presentations and, in the case of antibodies to DNA, a potential role for
> certain ANAs in the pathogenesis of tissue injury has been proposed.
> Together
> with Hargraves' demonstration of the LE cell phenomenon, the discovery of
> antinuclear factor remains one of the most important findings in the
> history of
> SLE and autoimmune disease.
>
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