Cirrhosis of the liver is associated with profound endocrinological disturbances. Until recently it was thought that these disturbances were caused mainly by ineffective elimination of hormones by the diseased liver. It is now known that the pathogenesis of disturbed hormonal function in liver cirrhosis is rather more complex, as, in many instances, it involves disturbed secretion and feedback mechanisms as well. In fact, in liver disease the metabolic clearance rate of sex-steroids for instance is not significantly altered (1,2). The most striking hormonal syndrome associated with cirrhosis of the liver is the feminization process which occurs in up to 40-50% of male patients (1,3). This syndrome is characterized by gynecomastia, a feminine distribution of hair, palmar erythema, the formation of spider nevi, disturbed gonadal function, impotence and infertility. The role of changes in androgen and estrogen metabolism in causing this syndrome has been the subject of extensive research in recent years and has been elucidated to a large extent (4,5,6,7,8,9,10,11,12). It is by no means certain, however, that the disturbed androgen and estrogen metabolism accounts for all the signs and symptoms found in this syndrome. It seemed interesting in this respect to look at possible disturbances in the synthesis, release and metabolism of prolactin (PRL). Prolactin, a polypeptide hormone, secreted by the anterior pituitary, plays a physiological role in breast development and lactation. When produced in excess it may lead to sterility, amenorrhea and loss of libido. In recent years sensitive radioimmunoassays for the determination of prolactin in plasma have become available, thus facilitating the study of prolactin metabolism and function in health and disease. This thesis describes an attempt to elucidate the effect of liver disease on the synthesis, release and metabolism of prolactin.