Key result
Familial S-ACE elevation appears inherited as an autosomal dominant trait.
Case Report
Identifies a familial, likely autosomal dominant, congenital elevation of serum ACE activity due to a lack of intrinsic ACE inhibitor, which should be considered in patients with unexplained high ACE levels.
May warrant consideration in unexplained ACE elevations; leaves open the genetic mechanism and prevalence.
A clustering of high levels of serum angiotensin converting enzyme (S-ACE) was found in an Italian family. The elevation affected five subjects, two of whom were completely healthy and free from known causes of S-ACE increase. The values of S-ACE in hyperACEmic subjects exceeded the values found in normal relatives severalfold. HyperACEmia seemed to be inherited as an autosomal dominant trait. Immunogenetic studies were performed, but we did not find a genetic marker for this condition. The S-ACE activity was inhibited in vitro by edetic acid (EDTA) and SQ 14,225 (captopril). The S-ACE activity was also determined after 1:8 dilution and dialysis against saline of sera. From these experiments we deduced that Lieberman's intrinsic ACE inhibitor was lacking in the hyperACEmic sera. In the presence of remarkable S-ACE increase, a congenital elevation of S-ACE should be considered and it would be useful to perform a familial investigation.
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Luisetti et al. (1990) conducted a case report in Familial elevation of serum angiotensin converting enzyme activity (HyperACEmia). Familial hyperACEmia vs. Normal relatives was evaluated on Serum angiotensin converting enzyme (S-ACE) levels and inheritance pattern. Familial elevation of serum angiotensin converting enzyme (S-ACE) was identified in five subjects of an Italian family, appearing to be inherited as an autosomal dominant trait.
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