title: Endothelial function, insulin sensitivity and inflammatory markers in hyperprolactinemic pre-menopausal women.
abstract: BACKGROUND
  Hyperprolactinemia has been reported to be associated with abnormalities of carbohydrate metabolism. The aim of this study was to evaluate the effects of hyperprolactinemia and bromocriptine (Brc) treatment on endothelial function, insulin sensitivity and inflammatory markers in pre-menopausal women.
  
  
  METHODS
  Sixteen hyperprolactinemic pre-menopausal women with pituitary adenomas were recruited and 20 healthy subjects were included as controls. Patients were given Brc in doses of 2.5-20 mg/dl until normal levels of prolactin were reached. Prior to treatment and 2 months after prolactin levels were normalized, the following tests were performed. Insulin sensitivity was determined by an oral glucose tolerance test based on a formula named the insulin sensitivity index (ISI composite). Endothelial function was measured as flow-mediated dilatation (FMD) on a brachial artery using high resolution ultrasound.
  
  
  RESULTS
  Serum glucose, insulin, estrogen, highly sensitive C-reactive protein (hsCRP), fibrinogen, homocysteine and uric acid levels were measured. Calculated ISI composite and FMD were significantly lower in the hyperprolactinemic group in comparison with the controls and improved after Brc treatment. Serum homocysteine, hsCRP and uric acid levels were significantly higher in hyperprolactinemic patients than in the controls and returned to normal levels with Brc treatment. Serum prolactin concentrations were inversely correlated with FMD measurements (r=-0.68; P<0.0001), ISI composite (r=-0.48; P<0.005) and serum estrogen (r=-0.54; P<0.005), and positively correlated with serum homocysteine concentrations (r=0.55; P<0.0001) in the hyperprolactinemic group.
  
  
  CONCLUSIONS
  The hyperprolactinemic state is associated with impaired endothelial function and decreased insulin sensitivity, which are early markers of atherosclerosis. These alterations may predispose to the development of atherosclerosis in non-treated cases. Correction of the hyperprolactinemic state is associated with improved endothelial function and insulin sensitivity.
authors.affiliation: Department of Internal Medicine, Section of Endocrinology and Metabolism, Marmara University, Istanbul, Turkey. dyavuz@tnn.net
authors.forename: Dilek
authors.initials: D
authors.lastname: Yavuz
authors.forename: Oğuzhan
authors.initials: O
authors.lastname: Deyneli
authors.forename: Ihsan
authors.initials: I
authors.lastname: Akpinar
authors.forename: Erdem
authors.initials: E
authors.lastname: Yildiz
authors.forename: Hülya
authors.initials: H
authors.lastname: Gözü
authors.forename: Ozlem
authors.initials: O
authors.lastname: Sezgin
authors.forename: Goncagül
authors.initials: G
authors.lastname: Haklar
authors.forename: Sema
authors.initials: S
authors.lastname: Akalin
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D001971:Bromocriptine / Q000627:therapeutic use*; D002097:C-Reactive Protein / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D004730:Endothelium, Vascular / Q000378:metabolism / Q000502:physiology*; D004967:Estrogens / Q000097:blood; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D005951:Glucose Tolerance Test; D006710:Homocysteine / Q000097:blood; D006727:Hormone Antagonists / Q000627:therapeutic use*; D006801:Humans; D006966:Hyperprolactinemia / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology*; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance / Q000502:physiology*; D017697:Premenopause / Q000097:blood / Q000502:physiology; D011388:Prolactin / Q000097:blood; D014527:Uric Acid / Q000097:blood; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology
chemical_list: D001786:Blood Glucose; D004967:Estrogens; D006727:Hormone Antagonists; D007328:Insulin; D006710:Homocysteine; D014527:Uric Acid; D001971:Bromocriptine; D005340:Fibrinogen; D011388:Prolactin; D002097:C-Reactive Protein; D002784:Cholesterol