Different effects of fenofibrate on cardiometabolic risk factors in young women with and without hyperprolactinemia.


Journal

Pharmacological reports : PR
ISSN: 2299-5684
Titre abrégé: Pharmacol Rep
Pays: Switzerland
ID NLM: 101234999

Informations de publication

Date de publication:
Feb 2019
Historique:
received: 02 05 2018
revised: 31 07 2018
accepted: 05 09 2018
pubmed: 24 11 2018
medline: 4 4 2019
entrez: 24 11 2018
Statut: ppublish

Résumé

Elevated prolactin levels are associated with increased cardiometabolic risk. No previous study has compared the effect of hypolipidemic therapy on plasma levels of lipids and other cardiometabolic risk factors in patients with and without hyperprolactinemia. The study included three age-, weight-, blood pressure- and lipid-matched groups of premenopausal women: 18 women with untreated hyperprolactinemia, 19 women with bromocriptine-treated hyperprolactinemia and 20 drug-naïve women with normal prolactin levels. Because of concomitant atherogenic dyslipidemia, all patients were treated with fenofibrate (200 mg daily) for 12 weeks. Plasma lipids, glucose homeostasis markers, as well as plasma levels of uric acid, high-sensitivity C-reactive protein (hsCRP), homocysteine and fibrinogen were assessed at baseline and at the end of hypolipidemic treatment. Unlike similar baseline lipid levels, plasma concentrations of the remaining investigated cardiometabolic risk factors were higher in women with elevated prolactin levels than in patients with normal prolactin levels. The impact of fenofibrate on total cholesterol, LDL cholesterol, HDL cholesterol and triglyceride levels, as well as on uric acid, hsCRP, homocysteine, and fibrinogen was less pronounced in women with untreated hyperprolactinemia than in women with bromocriptine-treated hyperprolactinemia and drug-naïve women with normal prolactin levels. The results of our study indicate that cardiometabolic effects of fenofibrate depend on plasma prolactin levels.

Sections du résumé

BACKGROUND BACKGROUND
Elevated prolactin levels are associated with increased cardiometabolic risk. No previous study has compared the effect of hypolipidemic therapy on plasma levels of lipids and other cardiometabolic risk factors in patients with and without hyperprolactinemia.
METHODS METHODS
The study included three age-, weight-, blood pressure- and lipid-matched groups of premenopausal women: 18 women with untreated hyperprolactinemia, 19 women with bromocriptine-treated hyperprolactinemia and 20 drug-naïve women with normal prolactin levels. Because of concomitant atherogenic dyslipidemia, all patients were treated with fenofibrate (200 mg daily) for 12 weeks. Plasma lipids, glucose homeostasis markers, as well as plasma levels of uric acid, high-sensitivity C-reactive protein (hsCRP), homocysteine and fibrinogen were assessed at baseline and at the end of hypolipidemic treatment.
RESULTS RESULTS
Unlike similar baseline lipid levels, plasma concentrations of the remaining investigated cardiometabolic risk factors were higher in women with elevated prolactin levels than in patients with normal prolactin levels. The impact of fenofibrate on total cholesterol, LDL cholesterol, HDL cholesterol and triglyceride levels, as well as on uric acid, hsCRP, homocysteine, and fibrinogen was less pronounced in women with untreated hyperprolactinemia than in women with bromocriptine-treated hyperprolactinemia and drug-naïve women with normal prolactin levels.
CONCLUSIONS CONCLUSIONS
The results of our study indicate that cardiometabolic effects of fenofibrate depend on plasma prolactin levels.

Identifiants

pubmed: 30469130
pii: S1734-1140(18)30258-5
doi: 10.1016/j.pharep.2018.09.004
pii:
doi:

Substances chimiques

Biomarkers 0
Dopamine Agonists 0
Hypolipidemic Agents 0
Lipids 0
Bromocriptine 3A64E3G5ZO
Prolactin 9002-62-4
Fenofibrate U202363UOS

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

61-66

Informations de copyright

Copyright © 2018. Published by Elsevier B.V.

Auteurs

Robert Krysiak (R)

Department of Internal Medicine and Clinical Pharmacology, Medical University of Silesia, Katowice, Poland. Electronic address: r.krysiak@interia.pl.

Witold Szkróbka (W)

Department of Internal Medicine and Clinical Pharmacology, Medical University of Silesia, Katowice, Poland.

Bogusław Okopień (B)

Department of Internal Medicine and Clinical Pharmacology, Medical University of Silesia, Katowice, Poland.

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Classifications MeSH