Open AccessAnti‐cholesterol antibody levels in hereditary angioedema
Author(s) -
Varga Lilian,
Bíró Adrienn,
Széplaki Gábor,
Tóth Luca,
Horváth Anna,
Füst George,
Farkas Henriette
Publication year - 2007
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/j.1582-4934.2007.00124.x
Subject(s) - danazol , hereditary angioedema , medicine , angioedema , cholesterol , endocrinology , lipoprotein , antibody , immunology , endometriosis
Hereditary angioedema (HAE) is a rare disorder caused by the deficiency of the C1‐inhibitor gene ( C1INH ) and characterized by recurrent bouts of angioedema. Autoimmune disorders frequently occur in HAE. Previously we found, that danazol has an adverse effect on serum lipid profile: reduced high‐density lipoprotein (HDL) and elevated low‐density lipoprotein (LDL) cholesterol levels are associated with long‐term prophylactic use, whereas total cholesterol levels are unchanged. Our aim was to study the anti‐cholesterol antibody (ACHA) production in HAE patients and compare it with those of healthy blood donors, and to investigate the possible associations between ACHA levels and serum lipid profile alterations caused by danazol. Anti‐cholesterol IgG levels were measured by ELISA and their correlation with serum concentrations of total cholesterol, HDL, LDL, triglycerides was determined in HAE patients receiving/not receiving danazol. Serum ACHA levels were significantly higher in HAE patients, compared to healthy blood donors ( P < 0.0001). Longterm danazol prophylaxis had no effect on serum ACHA levels in HAE patients. However, we found a significant, negative correlation between ACHA levels and serum total cholesterol (r =−0.4033, P = 0.0200), LDL (r =−0.4565, P = 0.0076) and triglyceride (r =−0.4230, P = 0.0121) levels only in danazol‐treated patients, but not in HAE patients who did not receive long‐term prophylaxis. Patients with HAE have higher baseline ACHA levels compared to healthy subjects, and this might reflect polyclonal B‐cell activation. The latter would be a potential explanation for the lack of an increased incidence of infectious diseases in HAE patients, but might lead to increased autoimmunity.