Effect of Dopamine Agonists on Lactotroph Adenomas of the Human Pituitary

Endocrine Pathology
|July 13, 2002
PubMed

Insights

Dopamine agonists shrink lactotroph adenomas by reducing cell proliferation, indicated by lower mitotic and MIB-1 indices. Apoptosis and p27 expression do not significantly contribute to this tumor shrinkage.

Area of Science:

  • Endocrinology
  • Oncology
  • Cell Biology

Background:

  • Lactotroph adenomas are pituitary tumors often treated with dopamine agonists.
  • Dopamine agonists effectively reduce prolactin levels and induce tumor shrinkage.
  • The precise cellular mechanisms underlying dopamine agonist-induced tumor shrinkage require further elucidation.

Purpose of the Study:

  • To investigate the cellular mechanisms responsible for tumor shrinkage in lactotroph adenomas treated with dopamine agonists.
  • To compare cellular parameters including proliferation, apoptosis, and microvessel density between treated and untreated adenomas.

Main Methods:

  • Analysis of surgically removed lactotroph adenomas from 29 patients (19 treated, 10 untreated).
  • Assessment of mitotic index, MIB-1 labeling index, p27 expression, apoptotic index, microvessel density (MVD), surface microvessel density (SMD), and DNA ploidy.
  • Comparison of these parameters between adenomas treated with bromocriptine (oral/injectable) or quinagolide and untreated adenomas.

Main Results:

  • Treated adenomas exhibited significantly lower mitotic and MIB-1 indices compared to untreated ones, indicating reduced cell proliferation.
  • MIB-1 labeling significantly decreased with quinagolide treatment.
  • Apoptotic indices were not significantly higher in treated adenomas.
  • Microvessel density (MVD) was significantly lower in treated adenomas, but surface microvessel density (SMD) showed no significant difference.
  • p27 expression was reduced in the bromocriptine long-acting injectable (BEC-LAR) group but not significantly different overall.
  • DNA ploidy and other nuclear parameters did not differ significantly between groups.

Conclusions:

  • Suppression of cell proliferation, evidenced by decreased mitotic and MIB-1 indices, is a key mechanism for dopamine agonist-induced lactotroph adenoma shrinkage.
  • p27 protein expression and apoptosis play minor roles in the involution of these tumors.
  • Further research is needed to understand the impact of dopamine agonists on microvessel density (MVD) and surface microvessel density (SMD).

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