Primary Biliary Cirrhosis (cont.)
In this Article
What is the role of blood tests?
The key blood test abnormality in PBC and all liver diseases associated with
cholestasis is an elevated alkaline phosphatase enzyme level in the blood. The
finding of a concurrent elevation of the gamma glutamyl transpeptidase (ggt)
blood level proves that the elevated alkaline phosphatase is from the liver,
rather than from bone (another source of alkaline phosphatase). Other liver
enzymes, such as aspartate aminotransferase (AST) and alanine aminotransferase
(ALT), may be either normal or only slightly elevated at the time of diagnosis.
As the duration of disease increases, both of these liver enzymes (the
aminotransferases) usually become elevated to a mild to moderate degree, while
the alkaline phosphatase can become very high. For more information about liver
blood tests, please read the Liver Blood Tests article.
Other blood tests may also be helpful in the diagnosis of PBC. For example,
serum immunoglobulin M (IgM) is frequently elevated. Also, just about all
patients with cholestasis develop increased cholesterol levels (as noted
previously), and some also develop elevated triglycerides. Moreover, testing the
levels of these fats (lipids) can identify patients who might form cholesterol
deposits in the skin or nerves. (See the section on xanthomas above.)
What is the role of testing for antimitochondrial antibodies?
AMA are detectable in the serum in 95 to 98% of patients with PBC, as noted
earlier. The most economical test for AMA applies diluted samples of a patient's
serum onto tissue sections from rat stomach or kidney in the laboratory.
(Remember that the mitochondria are present in all cells, not just the cells of
the liver and bile ducts.) Serum antibodies that attach (bind) to mitochondrial
membranes within the tissue cells can then be observed with a microscope. The
most dilute sample of serum showing this binding reaction is reported, using the
term titer. The titer indicates the most dilute serum sample that reacts with
the tissue mitochondria. A higher titer means there is a greater amount of AMA
in the serum.
The AMA titers in PBC are almost universally greater than or equal to 1 to
40. This means that a serum sample diluted with 40 times its original volume
still contains enough antimitochondrial antibodies to be detected in the binding
reaction. A positive AMA with a titer of at least 1:40 in an adult with an
elevated alkaline phosphatase is highly specific for a diagnosis of PBC. The
antigen recognized by AMA in patients with PBC is now known to be PDC-E2 and is
also often referred to as the M2 antigen, as discussed earlier. So, newly
developed tests for antibodies that bind to PDC-E2 are more specific and are now
available to confirm the diagnosis of PBC.
It is noteworthy that approximately 20% of patients with AMA also have
antinuclear (ANA) and/or anti-smooth muscle (SMA) autoantibodies in their blood.
The ANA and SMA are more characteristically found in a disease called chronic
autoimmune hepatitis. It turns out that patients who have persistently
undetectable AMA but otherwise have clinical, laboratory, and liver biopsy
evidence of PBC, all have either ANA or SMA. These patients have been referred
to as having AMA-negative PBC, autoimmune cholangiopathy, or autoimmune
cholangitis. The natural history, associated diseases, laboratory test
abnormalities, and liver pathology are indistinguishable between the
AMA-positive and AMA-negative patients. Thus, it seems inappropriate, for now at
least, to classify this AMA-negative disease as different from PBC. Accordingly,
this situation should be referred to as AMA-negative PBC. Rarely, some other
patients appear to concurrently have features of both PBC and chronic autoimmune
hepatitis. Such patients are said to have an overlap syndrome.
Next: What is the role of imaging tests? »
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