ADA2 is the predominant form present in human blood plasma and is increased in many diseases, particularly those associated with the immune system: for example rheumatoid arthritis, psoriasis and sarcoidosis. The plasma ADA2 isoform is also increased in most cancers. ADA2 is not ubiquitous but co-exists with ADA1 only in monocytes-macrophages.
Total plasma ADA can be measured using high performance liquid chromatography, enzymatic or colorimetric techniques. Perhaps the simplest system is the measurement of the ammonia released from adenosine when broken down to inosine. After incubation of plasma with a buffered solution of adenosine the ammonia is reacted with a Berthelot reagent to form a blue colour which is proportionate to the amount of enzyme activity. To measure ADA2, erythro-9-(2-hydroxy-3-nonyl) adenine (EHNA) is added prior to incubation so as to inhibit the enzymatic activity of ADA1[4]. It is the absence of ADA1 that causes SCID.
ADA can also be used in the workup of lymphocytic pleural effusions, in that such specimens with low ADA levels essentially excludes tuberculosis from consideration. Ref: http://erj.ersjournals.com/cgi/content/abstract/21/2/220 .
Adapted from the Wikipedia article Adenosine deaminase, under the G. N. U. Free Documentation License. Please also see http://en.wikipedia.org/wiki
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Adenosine deaminase – Clinical significance
ADA2 is the predominant form present in human blood plasma and is increased in many diseases, particularly those associated with the immune system: for example rheumatoid arthritis, psoriasis and sarcoidosis.
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