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Grossly elevated serum angiotensin-converting enzyme activities are still suppressible with ACE inhibitor therapy

JRAAS 2002;3:138 In the course of a recent clinical trial, we discovered very high serum angiotensin-converting enzyme (ACE) activity in one of our patients. He was an 83-year-old man with moderately impaired left ventricular (LV) function and his serum ACE fluctuated between 670 and 860 U/L (reference range: 17–85 U/L). Thorough clinical assessment, together with chest radiography, routine biochemistry and haematology, revealed no features of sarcoidosis or other disease state associated with elevated serum ACE. In the light of a recent report by Kramers et al., we suspect that he may have a mutation of the stalk region of ACE, leading to increased rates of cleavage and consequently high serum ACE activities. The interesting point about our patient is that one week after commencing perindopril, 2 mg once-daily, for his heart failure, the serum ACE activity fell to 18 U/L. This fall in serum ACE was sustained, and one year later the patient remains well. Thus, even in cases similar to those investigated by Kramers et al., serum ACE activity is still suppressible by ACE inhibitor (ACE-I) therapy to a huge extent – our patient sustained a 98% fall in serum ACE down into the population-based reference interval on commencing perindopril. In clinical practice,measurement of serum ACE is useful for two reasons. Firstly, a high activity can help to diagnose sarcoidosis and secondly, a low activity can be used to monitor compliance with ACE-I therapy. We already know that ACE-I can mask elevations in serum ACE that would be expected with sarcoidosis. Until now, however, we had no information on whether serum ACE was still a useful test of compliance in those individuals with very high ACE activity. Our patient demonstrates that such high serum ACE is still suppressible with ACE-I and this therefore does not preclude the use of serum ACE to monitor adherence, even in such individuals.