CRP - C-reactive protein
http://www.nlm.nih.gov/medlineplus/ency/article/003356.htm
C-reactive protein is a test that measures the concentration of a
protein in serum that indicates acute inflammation.

http://tinyurl.com/2qyo
Actually it indicates inflammation and can also be raised in conditions
like auto-immune disease, cancer and infection.

http://www.labtestsonline.org/understanding/analytes/crp/glance.html
When your doctor suspects that you might be suffering from an
inflammatory
disorder (as with certain types of arthritis and autoimmune disorders or

inflammatory bowel disease) or to check for the possibility of
infection.[]

http://www.drmirkin.com/heart/2074.html (various causes of elevated CRP)

http://www.ucl.ac.uk/~regfjxe/CLINICALASSESSMENT.htm
<long bunch not posted here>
this part is at the end

Erythrocyte sedimentation rate (ESR) and acute phase proteins

The ESR is commonly used in rheumatology, but needs to be interpreted
with care. It is affected by several changes in blood chemistry, but
chiefly by globulin levels. Globulins such as immunoglobulin and
fibrinogen, in contrast to albumin, encourage red cells to stick
together. Anaemia also encourages red cell sedimentation, but the effect

is small.

A high ESR is often assumed to be a by-product of inflammation, but this

is not necessarily so. In inflammatory joint disease the extent of
synovitis and the level of the ESR show a very variable relationship.
The ESR may be 100 with only trivial inflammation at one site and
widespread destructive synovitis may be associated with an ESR of 10. In

polymyalgia the ESR is very high in the absence of any true
inflammation.

A likely explanation is that the ESR partly reflects changes in quantity

and type of immunoglobulin (as it does in myeloma). In rheumatoid
patients a significant proportion of circulating IgG is in the form of
complexes, which may favour red cell clumping. These complexes are
likely to be the primary cause of synovitis. Thus, the ESR may reflect a

potential for inflammation, not inflammation itself.

The rise in ESR in association with inflammatory joint disease is also
likely to be partly due to raised fibrinogen levels secondary to the
release of cytokines such as tumour necrosis factor and interleukin 6.
This rise in fibrinogen will parallel other acute phase proteins such as

C-reactive protein (CRP) synthesised by the liver. Blockade of tumour
necrosis factor in rheumatoid patients can reduce the CRP to normal
levels. ESR and CRP levels may, therefore reflect the degree of joint
disease. However, in rheumatoid arthritis small immune complexes
probably activate Kuppfer cells in the liver as well as synovial
macrophages. Kuppfer cell activation may contribute to CRP levels, to
the mild rises in liver enzymes often seen, and, in Felty’s syndrome to
hepatomegaly from nodular hyperplasia. This is another reason to think
that the ESR may not reflect synovitis directly. In Felty’s syndrome the

ESR is usually very high and extra-articular disease is prominent, but
joint disease may be minimal.

The CRP has the potential advantage over the ESR that it reflects only
the response to cytokine release and not immunoglobulin levels or the
presence of complexes. However, as indicated above, it cannot be taken
to reflect joint disease specifically. Moreover, if the objective is to
assess remission of the underlying immune disturbance, the ESR may have
the advantage of reflecting complex-forming immunoglobulins.

In lupus the ESR is frequently elevated but the CRP only rises in the
presence of frank synovitis or serositis. This may indicate that the ESR

is reflecting immunoglobulin changes and the CRP the effects of small
complexes capable of activating Kuppfer cells. However, it may also be
that different autoantibody populations have differential effects on
acute phase proteins so that fibrinogen and CRP levels are dissociated
under some circumstances.

Several types of autoantibody are associated with disease which is not
truly inflammatory. Examples are membranous glomerulonephritis in lupus,

the microvascular obliteration in systemic sclerosis, the glandular
changes of sicca syndrome and the coagulation changes associated with
antiphospholipid antibodies. In systemic sclerosis both CRP and ESR tend

to be near normal. Thus, the ESR is not a screen for this type of
autoimmune rheumatic disease.

In general, the ESR and CRP should be interpreted with caution. They are

poor screening tests but within an individual patient can assist in
monitoring the progress of certain aspects of disease and response to
therapy.

Autoantibodies

Autoantibodies can be of diagnostic value, but only under limited
circumstances, because the important pathology can usually be recognised

clinically. In the absence of a good clinical assessment autoantibody
results can be very misleading. It is doubtful whether a rheumatoid
factor test should ever alter clinical management. Nevertheless, a
positive anti-nuclear antibody is of key importance in recognising that
joint disease may be the presenting feature of multisystem lupus.
Anti-neutrophil cytoplasmic antibodies are of value to identify
necrotising arteritis, which may produce life-threatening problems, the
cause of which may be difficult to define acutely.

see more there...