Relationship of acetyl transferase activity to antinuclear antibodies and toxic symptoms in hypertensive patients treated with hydralazine.

Abstract

Abstract Fifty-seven hypertensive patients who ingested from 200 to 3,000 Gm. of hydralazine during 1 to 15 years were studied in search of factors related to delayed hydralazine toxicity, minimal manifestations of which were considered to be arthralgia plus elevated cephalin cholesterol flocculation of the plasma. Throughout the study blood pressure was measured and circulating cells and proteins were examined. At the end of the study the presence of serum antinuclear antibodies (ANA) was determined by a fluorescent antibody technique and the activity of hepatic acetyl transferase, an enzyme which metabolizes hydralazine, was assayed. The patients could be divided into 33 and 24 fast acetylators of hydralazine, and 31 of the 57 were found to have ANA. During the study 12 patients had symptoms of hydralazine toxicity; all 12 belonged to the Caucasian race, were slow acetylators, and had ANA. Almost half of the nontoxic patients also had ANA, with the incidence being the same for Negro as for Caucasian patients. The data suggested that ANA might develop with less exposure to hydralazine in than fast acetylators. Good control of blood pressure accompanied drug toxicity, but toxic symptoms could not be related to severity of hypertension before treatment or to anemia, leukopenia, or hyperglobulinemia during treatment.