We measured peripheral blood mononuclear cells (PBMC) beta-endorphin (BE) in patients suffering from hereditary angioneurotic edema (HANE), a disease attributed to C1-esterase inhibitor (C1INH) deficiency inherited as an autosomal dominant trait. Two orders of considerations prompted us to undertake the study reported herein: the presence of elevated plasma BE concentrations in HANE and the demonstration of BE-immunoreactivity in human unstimulated peripheral blood leukocytes obtained from healthy volunteers. Our results show that patients suffering from HANE have a very high BE presence in uncultured, unstimulated PBMC and in unstimulated PBMC cultured for 48 h. At this time high BE concentrations are detected in the culture supernatants. These observations suggest that in HANE patients the same factor(s) involved in causing increased secretion and release of BE from the pituitary (and, in turn, increased plasma BE levels) can play a relevant role also in the determination of high BE presence in PBMC and BE release from the cells.