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Abstract
Several studies have demonstrated zinc (Zn), prolactin (PRL) and thymulin (Zn-FTS) interplay: Zn inhibits, in a dose related manner, PRL release from lactotropes in vitro and stimulates thymulin synthesis in vivo both in humans and in animals. PRL receptors are present on thymic epithelial cells (TEC); PRL stimulates TEC trophism and activity. Little is known about the influence of PRL on Zn metabolism, though in prolactinomas we found reduced Zn and thymulin circulating levels. For this reason, we evaluated PRL, Zn, bioactive thymulin (Zn-FTS) and total thymulin (T-FTS: Zn-bound plus Zn-unbound form) serum levels in 58 patients with prolactinomas (PRL: 253 ± 263 ug/L). Zn (82 ± 23 ug/dl), Zn-FTS (2.2 ± 0.20log-1) and T-FTS (3.7 ± 0.25 log2−1) were significantly lower (p <. 01) than those found in age matched controls. Zn-unbound bioinactive thymulin form (FTS) levels were in the normal range. Bromocriptine administration (Brc) (2.5–5 mg p.o., b.i.d. for 9 months) to 20 patients with microprolactinomas lowered serum PRL levels (10.5 ± 6.2 ug/L) and significantly increased (p <. 01) Zn (118.6 ± 14.7 ug/dl). Zn-FTS (3.96 ± 0.7log2-1) and T-FTS (4.66 ± 0.7log2-1) circulating levels. ZnSO4 administration (400 mg p.o. daily for 3 months) to 6 patients with microprolactinomas, significantly increased (p <. 01) Zn (136 ± 18 ug/dl), Zn-FTS (4.5 ± 0.5log2-1) and T-FTS (5.6 ± 0.9log2-1) levels, while caused only a slight decrease in serum PRL concentrations (from 95 ± 8 to 75 ± 9ug/l: p: NS). In conclusion: in prolactinomas Zn and Zn-FTS titers are low. They are normalized after bromocriptine-induced PRL decrease within the normal range. ZnSO4 administration is ineffective in lowering serum PRL levels. Since ZnSO4 p.o. is able to increase Zn and Zn-FTS circulating levels, but not to decrease PRL values, it is possible to assume that the hyperprolactinemia reduces thymulin secretion by modifying Zn turnover rather than acting directly on thymic epithelial cells.