Abstract
Individuals with heterozygous Pi M subtypes were found to have higher serum levels of α1-antitrypsin (α1-AT) than homozygotes. The α1-AT levels in heterozygotes showed a unimodal distribution. Among homozygotes, a tendency towards a bimodal distribution was found. The mechanism behind this difference is not known. The result can apparently not be explained as the result of a hitherto undiscovered deficiency gene.

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