Evidence suggests that neurohormones such as GH and IGF-I are involved in the neuroreparative processes in multiple sclerosis (MS). GH and IGF-I blood levels in na？ve MS patients with different disease courses were investigated in this study. Serum GH and IGF-I in untreated MS patients ( ), healthy controls (HC, ), and patients affected by other neurological diseases (OND, ) were evaluated with a solid-phase-enzyme-labeled-chemiluminescent-immunometric assay. No differences were detected in GH across MS, OND, and HC ( ？ng/mL; ; and ; ) when considering gender, disease duration, and disease course. However, GH was lower ( ) in patients with more severe disease (expanded disability scale score, ) compared with milder forms ( ). IGF-I l did not differ across the 3 groups ( ), as far as concern disease course, disability, and gender were. Lower IGF-I levels were detected in subjects older than 50 years compared to younger ones for all 3 groups. Lower GH was detected in patients with more severe MS, and age was confirmed as the main factor driving IGF-I levels in all subjects. These findings, relying on the natural course of the disease, could help in shedding lights on the mechanisms involved in autoreparative failure associated with poorer prognosis in MS. 1. Introduction Multiple sclerosis (MS) is a chronic demyelinating disease of the central nervous system with an unpredictable time course. Among the plethora of factors affecting the clinical heterogeneity of MS, autoreparative mechanisms are of particular importance. Remyelination is largely known to occur in MS [1], but it is still unclear why its adequacy differs so largely among patients. Many factors have been proposed to influence remyelination, including several neuroendocrine factors [2, 3]. Unresponsiveness to these factors and/or their insufficient release could possibly be involved in reparative mechanism failure, and studies focusing on these molecules have attracted a great deal of attention. Growth hormone and IGF-I have been recognised as factors that can affect survival of myelin and central nervous system (CNS) cells [3, 4]. Several studies [2–4] have focused on these growth factors, unfortunately with equivocal results. Heterogeneity is not largely dependent on the different methodologies used but also on the disease’s natural history. Growth factor bioavailability can vary in the different phases of the disease leading to a permissive or, on the contrary, an inadequate microenvironment supporting remyelination. Moreover, another putative confounding factor could be the different
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