Abstract
It is now 23 years since Lieberman first reported that serum angiotensin converting enzyme (SACE) levels were raised in patients with sarcoidosis.1 He concluded that raised SACE levels appeared to be associated with the active disease process and not a familial inherited enzyme abnormality. The paper by Takemoto and colleagues in this issue of Thorax 2 provides new evidence that the sarcoid granuloma load in patients is not the only factor to account for circulating SACE levels in sarcoidosis and that polymorphisms in both the ACE and angiotensin II receptor genes may also play a part. Angiotensin converting enzyme (ACE), a zinc metalloproteinase, catalyses the hydrolysis of carboxyterminal dipeptides, particularly the largely inactive peptide angiotensin-1 to the active angiotensin-2. This enzyme has been hypothesised to be a marker of disease activity in sarcoidosis. It is thought that ACE is produced by epithelioid …
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