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All carbonic anhydrase isoenzymes catalyze the reversible hydration of dissolved CO2 to form carbonic acid.
Under physiological conditions carbonic acid is primarily in the bicarbonate (HCO3–) form, and the CO2 / bicarbonate buffering system is the most important one in the human body1. The transport of CO2 from the tissues to the lungs and the subsequent release of CO2 into the alveolar air space relies on the rapid equilibration of the above reaction, thus carbonic anhydrase is an important enzyme in facilitating respiration2. Therefore it is not surprising that carbonic anhydrase is a major constituent of erythrocytes, being the most abundant protein in these cells after hemoglobin3.
There are many isoenzymes of carbonic anhydrase4, but the most common ones and the earliest forms to be extensively studied are variously referred to by the confusing designations: CA-I (or CA-B), CA-II (or CA-C) and CA-III (or CA-A). The first two are the primary forms found in erythrocytes, carbonic anhydrase-I being the most abundant in mass and carbonic anhydrase-II by activity3. The latter enzyme is considered to be one of the fastest enzymes known to man, if not actually the fastest5.
However one of the most interesting isoenzymes from a clinical point of view is carbonic anhydrase III (CA-A). It is the most abundant soluble protein in the red fibers of skeletal muscle5. Although not a particularly fast catalyst, it is found only at extremely low levels (if at all) in other tissues7, and therefore is a reliable serum marker for skeletal muscle damage7. Because of this fact, for a time carbonic anhydrase III was in serious consideration as a useful cardiac marker for acute myocardial infarction (AMI). Not because it’s found in cardiac tissue, rather for the opposite reason. Since virtually no carbonic anhydrase III is found in cardiac muscle, a lack of elevation of the serum level of carbonic anhydrase III could be used to make the myoglobin marker more specific. Myoglobin has been considered to be among the earliest of the major cardiac markers to elevate in serum after AMI9. It is an extremely sensitive marker for AMI, but the problem is its almost complete lack of specificity, the cardiac and skeletal muscle forms of myoglobin being identical10. The simultaneous measurement of carbonic anhydrase III with myoglobin would allow the clinician to understand what the source of the elevated serum myoglobin was. If it was due to skeletal muscle damage, both analytes, carbonic anhydrase III and myoglobin would be elevated, whereas if only myoglobin was elevated that would be extremely strong evidence for myocardial tissue damage11,12,13. An elevation in both analytes would be inconclusive for AMI since this could indicate either only skeletal muscle damage or both myocardial and skeletal muscle damage. This could be one reason carbonic anhydrase III has not gained acceptance as part of a cardiac marker panel. Aside from its possible role in AMI diagnosis, there is no dispute that carbonic anhydrase III is an excellent marker for skeletal muscle pathologies14-17, although it has not gained commercial acceptance in this field either.
|ADULT CAIII REFERENCE RANGE11:Â||< 38 Âµg/L (not clinically established)|