Hyperprolactinemia in acromegalic patients may result either from cosecretion of growth hormone and prolactin by the tumour or from pituitary stalk compression. The occurrence of both conditions is possible. This study was designed aiming 1) to estimate the prevalence of each cause of hyperprolactinemia and its respective clinical course; 2) to compare the outcomes of patients with tumours staining only for growth hormone against tumours staining for both growth hormone and prolactin. 75 acromegalic patients submitted to transsphenoidal surgery between 1989 and 2018 were included. Patients were divided based on preoperative prolactin levels and immunostaining pattern. Statistical analysis was performed with SPSS version 23. Hyperprolactinemia was documented in 22 out of 36 patients (61%). Stalk compression was the only underlying cause of hyperprolactinemia in 45% of cases. The levels of prolactin were not associated with the immunostaining pattern for prolactin. Clinical differences were not observed between hyperprolactinemic and normoprolactinemic patients, except for a higher frequency of cavernous sinus invasion (64% vs 29%, p=0,064), that reached the level of significance for the subgroup with macroadenomas staining exclusively for growth hormone (p=0,031). In the present series, no clinical differences were noticed between patients with tumours staining only for growth hormone or staining for both growth hormone and prolactin. Hyperprolactinemia resulting from stalk compression is likely to anticipate a less favourable course of disease, since it is associated with larger tumours and a higher frequency of cavernous sinus invasion. On the contrary, positive immunostaining for prolactin was not a marker of worse prognosis.

Type 2 diabetes (T2D) is a complex, chronic disease with a significant quality of life burden for affected individuals, as well as socio-economic burdens on a population scale. Efforts to mitigate morbidity, mortality, and risks for other acute and chronic diseases have been compromised by a traditional chronic disease model that focuses on tertiary prevention (i.e., waiting until the disease is fully manifest and in many cases with severe complications). More specifically, the role for prevention at an earlier “prediabetes” stage has been questioned. A re-examination of the biology and clinical data on T2D pathogenesis can modulate the way we think about T2D. The new Dysglycemia-Based Chronic Disease (DBCD) model addresses these challenges by positioning T2D and prediabetes along a continuous spectrum from insulin resistance to prediabetes to T2D to vascular complications. It is hoped that by conceptualizing T2D in the DBCD framework, health care professionals can provide more efficient, cost-effective care.