Context: Little systematic data on male prolactinomas treated with surgery are available. Objective: To clarify the clinical features and confirm the efficacy of transsphenoidal surgery for male prolactinomas and predictive factors after initial surgery. Patients and methods: This retrospective study included 87 male patients with prolactinoma treated by transsphenoidal surgery at an academic medical center. Hormonal and visual status, remission rates, and the rate of tumor relapse, as well as predictive factors, were evaluated. Results: Postoperative initial remission was achieved in 52.9% of patients. The remission rate was markedly higher in microadenomas (83.3%) than in macroadenomas (44.9%). Logistic regression analysis showed that the predictive factors of the early negative outcomes were high preoperative prolactin (PRL) levels and tumor invasion. After a median follow-up of 45 months, the long-term remission rate was 42.5%, and relapse of hyperprolactinemia occurred in 19.6% of the cured patients. The 5-year recurrence-free survival was 78.2% (95% confidence interval, 62.3-88.1%). When surgery was followed by adjuvant treatment in uncured and recurrent patients, 78.8% of patients in the entire group in the absence of dopamine agonists obtained biochemical remission at the end of follow-up. Conclusion: Transsphenoidal surgery is a viable treatment alternative for male prolactinomas. The remission rates of male patients with microadenomas and/or intrasellar macroprolactinomas by surgery alone remain excellent, and surgery followed by adjuvant therapy as necessary is required for optimizing management of male prolactinomas, especially for extrasellar macroprolactinomas. The early negative results are associated with preoperative PRL levels and tumor invasion.

Objective: The aim of this study is to evaluate clinical data from a large cohort of acromegalic patients with and without hyperprolactinemia. Design and methods: Between January 2002 and June 2010, a set of data on 279 acromegalic patients undergoing transsphenoidal surgery was available. Based on preoperative GH and prolactin (PRL) levels, patients were divided into GH and GHCPRL groups. A stabilization or a further improvement of postoperative changes in clinical, hormonal, immunohistochemical, and magnetic resonance imaging parameters was observed in all patients throughout the follow-up period. Results: The GH group had significantly more coarse facial features, large hands and feet, hypertension, and diabetes mellitus compared with the GHCPRL group but significantly less menstrual disorders (13.8 vs 54.3%, P!0.001) and galactorrhea (3.1 vs 22.4%, P!0.001). The GH group had a higher age at diagnosis compared with the GHCPRL group (45.6G13.9 vs 40.4G11.4 years, PZ0.001). The GH group had a smaller mean maximal diameter of the adenomas (2.2G0.9 vs 2.6G1.1 cm, PZ0.004). There were no significant correlations between hormone levels and the immunohistochemical results. According to the criteria for hormonal cure of acromegaly, the surgical control rates in the GH and GHCPRL groups were 68.4 and 59.7% respectively (PZ0.187). Tumor size was an important factor that affected the results of the operations. The rates of surgical control in GH and GHCPRL groups were 80.7 and 69.1% respectively (PZ0.037), and the recurrence rates in the two groups were 7.1 and 11.3% respectively (PZ0.185). Conclusions: Compared with patients with merely GH-secreting adenomas, acromegalic patients with hyperprolactinemia are characterized by an earlier onset of disease, lesser acromegalic features, lower GH levels, but larger tumor sizes, whereas in female patients, GH-PRL secreting adenomas are associated with higher incidences of menstrual disorders and galactorrhea.

Background: How the activity of GLI2 transcriptional factor is regulated is not well understood. Results: Loss of SUMO modification in GLI2 results in an increase in GLI2 transcriptional activity in cultured cells and in vivo. Conclusion: SUMO modification inhibits GLI2 transcriptional activity. Significance: The activation of GLI2 by Hedgehog signaling may be through the inhibition of GLI2 sumoylation.