CASE REPORT Multiple sclerosis attacks triggered by hyperprolactinemia V. Nociti • G. Frisullo • T. Tartaglione • A. K. Patanella • R. Iorio • P. A. Tonali • A. P. Batocchi Received: 31 August 2009 / Accepted: 16 November 2009 / Published online: 3 December 2009 Ó Springer Science+Business Media, LLC. 2009 Abstract Multiple sclerosis (MS) is a T-cell autoimmune disease of the central nervous system (CNS). Predomi- nance of women in autoimmune diseases suggests that sex hormones may play a role in disease susceptibility. A possible role for prolactin, a neuroendocrine peptide with powerful immunomodulatory properties, is suggested in MS. We describe the case of a 32-year-old man affected by relapsing-remitting MS who experienced the first MS clinical event during the development of a prolactin- secreting adenoma and the only two MS relapses during adenoma recurrence. Prolactin may have facilitated the inflammatory process and triggered MS clinical attacks, suggesting a role of prolactin in immunomodulation and therefore in autoimmune disease course. Keywords Multiple sclerosis Á Prolactin Á Prolactin-secreting adenoma Á Cytokines Á Immune system Introduction MS is a T-cell autoimmune disease characterized by a relapsing-remitting (RR) course followed by a progressive phase. Factors that initiate inflammation are unknown, but it is believed that MS is caused in a genetically susceptible host by environmental factors that trigger a T-cell auto- immune response against the CNS [1]. Although many aspects of the pathogenesis of MS are still to be fully defined, the role of effector T helper (Th) cells in the ini- tiation of autoimmune tissue inflammation is fairly well established. Relapses, in particular, are driven by the adaptive immune system and involve waves of Th1, Th17, and CD8 ? T cells that infiltrate the CNS [2]. Predominance of women in autoimmune diseases sug- gests that female sex hormones may play a role in disease susceptibility. A possible role for prolactin is suggested by some clinical evidence. Prolactin is a neuroendocrine peptide with potent immunomodulatory properties. It can stimulate and inhibit immune response, with type of response related to prolactin dosage [3]. The role of prolactin in MS is presently being debated. In experimental autoimmune encephalomyelitis, an animal model of MS, prolactin levels were higher before disease onset, and bromocriptine attenuated disease severity [4]. Hyperprolactinemia was found in 30% of MS patients and was speculated to be related to hypothalamic lesions [5]. A role of bromocriptine in therapy for MS was suggested, but an open-label pilot study did not show therapeutic effects on MS activity [6]. Intravenous high-dose methylprednis- olone (IVMP) therapy caused a reduction of T2-lesion volume with a decrease of plasma prolactin in nine RRMS patients [7], but these findings could not be confirmed by others. We describe the case of a 32-year-old man affected by RRMS who experimented three MS attacks in coinci- dence with increased prolactin serum levels due to a prolactin-secreting adenoma, suggesting that hyperprolac- tinemia could facilitate induction of inflammatory process triggering MS clinical exacerbation. V. Nociti Á G. Frisullo Á A. K. Patanella Á R. Iorio Á P. A. Tonali Á A. P. Batocchi (&) Institute of Neurology, Department of Neurosciences, Catholic University, Largo Agostino Gemelli, 8, 00168 Rome, Italy e-mail: annapaola.batocchi@rm.unicatt.it T. Tartaglione Institute of Radiology, Department of Bioimaging and Radiological Sciences, Catholic University, Rome, Italy V. Nociti Á A. K. Patanella Á P. A. Tonali Á A. P. Batocchi Fondazione Don Gnocchi, Rome, Italy 123 J Neurooncol (2010) 98:407–409 DOI 10.1007/s11060-009-0076-1