It is argued that the coupling of peripheral tryptophan levels and cerebral serotonin levels has physiological significance. The clinical implications and therapeutic consequences of changes in tryptophan and consequently serotonin metabolism are discussed.

Aggressive impulse dysregulation is highly prevalent in patients receiving interferon treatment. This is associated with decreased plasma tryptophan levels which may lead to attenuated peripheral and central serotonergic neurotransmission.

In two groups, each consisting of five healthy volunteers, 7 ml blood/kg body weight were exchanged with equal amounts of hydroxyethyl starch (HES) and dextran 60 solutions, respectively. Dextran 60 plasma levels, determined by the anthrone method, were undetectable after 4 weeks. The elimination of HES from the blood, determined by an immunological technique and by the anthrone method, had a very protracted course. Two weeks after infusion the HES plasma concentrations were 9% of the initial value and after 17 weeks they were still above the l% level. The prolonged intravascular persistence of HES in its commercially available preparation, and the possibility of tissue accumulation after repeated HES infusions were considered undesirable. The hypothesis that HES infusion causes an augmentation of serum α-amylase concentrations in man was confirmed. This effect should be borne in mind when HES solutions are given to patients in whom the diagnosis of acute pancreatitis might be considered.

Impulse control disorders are prevalent in patients with carcinoid syndrome. The serotonin production by the tumor possibly decreases the tryptophan pool in the cerebrospinal fluid, which is the essential substrate for the production of brain serotonin as a pivotal neurotransmitter.

No abstract