al. 2015 ). A loss-of-function pathogenic germline PRLR variant (His188Arg), which affected a highly conserved His188 residue within the D2 domain that is important for hormone binding, was described in a family with hyperprolactinaemia ( Kulkarni
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Caroline M Gorvin, Paul J Newey, and Rajesh V Thakker
M V Legorreta-Haquet, K Chávez-Rueda, E Montoya-Díaz, L Arriaga-Pizano, R Silva-García, L Chávez-Sánchez, M Moreno-Lafont, E Zenteno-Galindo, and F Blanco-Favela
between hyperprolactinaemia and disease activity in lupus ( Blanco et al . 1999 , Jara et al . 2008 , 2009 , Nociti et al . 2010 ) because, by down-regulating the suppressive activity of T reg cells, PRL could favour the activation of T eff cells
L J Moran, P A Mundra, H J Teede, and P J Meikle
, Cushing’s syndrome, hyperprolactinaemia, thyroid dysfunction and adrenal disorders). All participants had ceased insulin-sensitising or reproductive hormonal medication for at least 3 months prior to baseline measurements. The studies received ethics
