In this issue of the Annals Eijsbouts and coworkers¹ show that the prolactin (PRL) response to hypoglycaemia is lower in patients with early untreated rheumatoid arthritis (RA) than in healthy controls. Furthermore, the unique design of their study allowed the authors to compare the PRL response before the test, after 2 weeks of treatment with a non-steroidal anti-inflammatory drug (NSAID) and, then again, after 6 months of conventional antirheumatic treatment with NSAIDs and disease modifying antirheumatic drugs (DMARDs). After 6 months they found that the PRL response to hypoglycaemia was significantly normalised, which correlated positively with the Disease Activity Score. The results of the study¹ suggest that disease activity and/or treatment with DMARDs significantly affects the central regulation of PRL secretion resulting from stimulation in patients with RA.

A possible involvement of PRL in the pathogenesis of inflammatory diseases has been intensively studied, including a hypothesis about dysregulated secretion of this pituitary hormone in patients with RA.² It has been shown that about one third of patients with RA are hyperprolactinaemic under basal conditions.² However, controversy remains about whether stimulated secretion of PRL is up regulated or …