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Several lines of evidence suggest that the anterior pituitary hormone prolactin has a stimulatory roIe on immune function and that pharmacological suppression of prolactin secretion with the dopamine-agonist bromocriptine suppresses both humoral and cellular immunity. Here, we describe the effects of prolactin-suppression on the course of experimental allergic encephalomyelitis in female Lewis rats. Initiation of continuous bromocriptine treatment before immunization reduced both the severity and incidence of clinical signs of acute experimental allergic encephalomyelitis. Experimental allergic encephalomyelitis-immunized rats experienced a threefold rise in basal prolactin levels on day 4 after immunization and maintained elevated prolactin levels on day 10, before the onset of neurological signs of experimental allergic encephalomyelitis. Bromocriptine treatment reduced prolactin levels to those of shamimmunized rats. In viva bromocriptine pretreatment inhibited splenic lymphocyte proliferative responses in vitro to the immunizing antigen and to concanavalin A. Moreover, bromocriptine therapy was protective when initiated 1 week after the initial immunization and w a s also effective in suppression of late disease. These results indicate that (1) prolactin levels are elevated after immunization and before the onset of experimental allergic encephalomyelitis, (2) bromocriptine inhibits both prolactin secretion and the severity of acute experimental allergic encephalomyelitis, and (3) inhibition is also present when treatment is begun after sensitization, suggesting an effect of prolactin on the effector limb of the immune response during experimental allergic encephalomyelitis.Riskind PN, Massacesi L, Doolittle TH, Hauser SL. The role of prolactin in autoimmune demyelination: suppression of experimental allergic encephaiomyelitis by bromocriptine. Ann Neurol 199 1; Prolactin (PRL), the major hormonal stimulus to lactation, is a 24-kd polypeptide hormone that is synthesized and secreted by the anterior pituitary gland. The importance of PRL to normal immune homeostasis was first shown by Nagy and Berczi 111, who found that hypophysectomized rats were severely immunocompromised, with profoundly depressed antibody titers to administered antigen and virtually absent delayed hypersensitivity responses. Surprisingly, in such animals, immunocompetence could be restored by exogenous PRL, and to a lesser extent by growth hormone, but not by other pituitary hormones 121. Later work demonstrated that bromocriptine (BCR), a dopaminergic agonist that selectively inhibits PRL release, mimics the effect of hypophysectomy {33. Treatment with PRL reversed the effect of BCR, indicating that its activity was due to specific inhibition of PRL release.Other studies indicated that excessive PRL levels maj7 stimulate immune responses. PRL treatment of normal mice resulted in a dose-dependent increase in splenic cell responses to mitogens such as concanavalin A (ConA) [4, S}. In rodent splenic lymphocytes, PRL also induced the expres...

A previously healthy 35 year old woman presented with bilateral uveitus associated with multiple, evolving, non-enhancing white matter lesions consistent with a progressive leukoencephalopathy such as multiple sclerosis. Thirty months after her initial presentation, she was diagnosed with primary CNS lymphoma and died 14 months later. The unusual clinical course preceding the diagnosis suggests that a demyelinating disease may have preceded, and possibly heralded, the development of primary CNS lymphoma. Cases of "sentinel lesions" heralding the diagnosis of primary CNS lymphoma have been reported, and this case further corroborates such instances and raises further issues regarding possible neoplastic transformation occurring in inflammatory diseases such as multiple sclerosis. (J Neurol Neurosurg Psychiatry 1998;65:917-920)

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