oxidants, CTAP III and NAP2 have already been described [17,18].Transferrin (TF) not only transports iron in all extracellular fluids but also exerts many additional properties, including cell growth stimulation, bacteriostatic action and inhibition of histamine release from mast cells and basophils [19][20][21][22][23]. TF is a 75 kDa glycoprotein containing 679 amino acids and two glycan chains. For each, the last residue is a sialic (N-acetyl neuraminic) acid which can be hydrolyzed by neuraminidase. Circulating TF mainly originates from hepatocytes, its intracellular precursor being asialoapotransferrin. Transferrin receptors, which are present throughout the body, are abundant (10 6 /cell) on the basophil plasma membrane [24]. They are also involved in the development of the nervous system [25].Because of the known relationships between TF and histamine release, we decided to investigate the histamine-releasing ability of this glycoprotein in the plasma of MO patients.
Jean-Marie Launay François Tabuteau André PradalierAbstract Patients with migraine without aura (MO), either during or between attacks, present elevated histamine levels in platelet-poor plasma but normal whole blood histamine levels, compared with controls. This finding is usually interpreted as an increased histamine release from basophils due to unidentified histamine-releasing factors. Compared with 10 control plasma samples, each sample from 12 MO patients (5 during and 7 between in attacks) contained normal amounts of iron and immunologically reactive transferrin but decreased transferrin iron-binding capacity. As transferrin inhibits histamine release in vitro, such a functional abnormality, probably due to modifications of the transferrin glycan moiety (desialylated transferrin), may well account for the increased histamine release observed in MO patients. We suggest that glycanmodified transferrin may be related to migraine histamine-releasing factors.