M. Pacilio et al., Elevated bioactive prolactin levels in systemic lupus erythematosus - Association with disease activity, J RHEUMATOL, 28(10), 2001, pp. 2216-2221
Objective. To assess the possibility that prolactin (PRL) is involved in th
e pathogenesis of systemic lupus erythematosus (SLE).
Methods. We determined serum PRL levels in 122 serum samples from 78 unsele
cted patients with SLE (73 women, 5 men, age range 16-71 yrs). Disease acti
vity was defined according to Lupus Activity Criteria Count (LACC) and scor
ed by Systemic Lupus Disease Activity Index (SLEDAI). Serum PRL concentrati
ons were determined by immunoradiometric assay (IRMA) and by biological ass
ay (BA) that evaluates Nb2 lymphoma cell proliferation.
Results. Hyperprolactinemia (> 20 ng/ml) was found in 21 patients (26.9%) b
y IRMA and in 31 (39.7%) by BA. A significant correlation between IRMA and
BA PRL levels was found (r(s) 0.46, p < 0.001). According to LACC, SLE was
active in 29 patients and inactive in 49. In those with active disease medi
an PRL levels were higher both by IRMA (18.5 ng/ml, range 2.2-51.2 vs 10.6
ng/ml, range 3.9-29.6; p < 0.001) and BA (21.0 ng/ml, range 12.4-84 vs 14.9
ng/ml, range 4.2-46.1; p <less than> 0.001). Hyperprolactinemia was associ
ated with active disease in 13/21 patients (61.9%) by IRMA and in 18/31 (58
.1%) by BA (p < 0.01). SLEDAI scores correlated with PRL levels both by IRM
A (r(s) 0.5, p < 0.001) and BA (r(s) 0.41, p < 0.02). A followup analysis o
n serum samples from 44 patients seen again after 6-8 mo confirmed the abov
e results. There was no difference in the rate of different clinical manife
stations in hyperprolactinemia and normoprolactinemic subjects, apart from
the increased prevalence of malar rash and central nervous system manifesta
tions in the patients with hyperprolactinemia (p < 0.03 and p < 0.01, respe
ctively).
Conclusion. Hyperprolactinemia was frequently detected in patients with SLE
by IRMA and by BA and was associated with disease activity. Our Findings s
uggest that PRL may play a role in the pathogenesis of SLE.