Background Prolactin (PRL) is an anterior pituitary hormone which is known to stimulate humoral and cell mediated immune responses, and may have a role in the pathogenesis of systemic lupus erythematosus (SLE).
Objectives To determine whether elevated serum prolactin associates the SLEDAI activity and/or specific organ involvement in SLE when recent reports have been till now discrepant.
Methods Basal serum PRL levels were determined in 55 consecutive SLE patients (pts) (49 females, 6 males) and in 41 healthy controls (31 females, 10 males) by RIA method. The estimated normal values of serum PRL were 200 mUI/l for males and 450 mUI/l for females.
Results The idiopathic hyperprolactinemia (hyper-PRL) was found in 7 SLE females (14,29%; 828,682 ± 391,410 mUI/l) and in 3 males (50,00%; 305,469 ± 65,751 mUI/l); and in one male in healthy controls (10,00%; 348,352 mUI/l) only. In remaining 42 SLE females and in 3 males PRL serum level was normal (365,783 ± 282,796 mUI/l; 142,854 ± 84,512 mUI/l). After 6 months repeatedly determined serum PRL in 2 females and 2 males with initial hyper-PRL, has shown normalisation in 1 female and 1 male. As to the proposed association between hyper-PRL and disease activity and specific organ involvement and presence of anti-ds-DNA there are some data on the Table 1.
Conclusion There was significantly higher frequency of hyper-PRL in 55 SLE pts compared to 41 healthy controls (p < 0,001). The value of serum PRL has normalised in 2 pts with hyper-PRL from 4 pts with initial hyper-PRL without any specific treatment after 6 months by repeated estimation. We document a new idiopathic hyper-PRL in 1 patient with normal initial serum PRL. The association between hyper-PRL and activity and/or specific organ involvement and presence of anti-ds-DNA was not statistically significant due to low number of observations.
Walker SE, et al. Effect of prolactin in stimulating disease activity in SLE. Proc NY Acad Sci 1998;840:762–72
Neidhart M. Prolactin in autoimmune diseases. Proc Soc Exp Bio Med. 1998;217:408–79
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