Prolactin in human systemic lupus erythematosus

In the last decade. evidence has accumulated to support the hypothesis that both mild and moderate elevations of serum prolactin (PRL) participate in the clinical expression and pathogenesis of systemic lupus erythematosus (S LE). Hyperprolactinemia (HPRL) has been found in 20-30% of patients with SL E. HPRL seems to be associated with clinical activity of SLE during pregnan cy. Although the relationship between HPRL and active SLE in non-pregnant p atients is controversial. recent clinical and experimental studies support the potential role of prolactin (PRL) as a promoter of clinical activity an d severity of SLE. Mild elevations of serum PRL secondary to microadenoma c ould trigger the onset of SLE in a subset of patients. Elevated PRL and interleukin (IL)-6 have been found in the urine of patient s with active lupus nephritis and in cerebrospinal fluid (CSF) of patients with active central nervous system (CNS) SLE. PRL may therefore participate in the pathogenesis of lupus nephritis and cerebritis. and the presence of PRL may reflect an abnormal communication between the immune system and th e neuroendocrine system in active SLE, Lymphocytes from patients with activ e SLE produce increased amounts of PRL. and this extrapituitary PRL may par ticipate in aberrant immune processes in SLE. There is exciting new evidenc e that HPRL in SLE may be explained by Stimulation of pituitary PRL secreti on by cytokines. In addition, defects in peptidergic modulators and dopamin e metabolism have been described in patients with SLE. The interactions bet ween PRL, cytoquines. autoantibodies and organ involvement suggest that PRL participates in local and generalized immune and inflammatory processes an d acts as a bridge between the neuroendocrine and immune systems in SLE. Un derstanding the interactions between these systems in SLE will help us to u nderstand and treat this important autoimmune disease.