Serum markers of endothelial dysfunction in prolactinomas before and after normalization of serum prolactin: prospective case control study.
Abstract
Background: Clustering of metabolic abnormalities in untreated hyperprolactinemia leads to chronic low-grade inflammation and endothelial dysfunction (ED). Data on endothelial dysfunction in hyperprolactinemia is limited.
Objective: To study markers of inflammation and endothelial dysfunction in untreated prolactinoma patients
Participants: Fifty-six treatment naïve patients of hyperprolactinemia (because of prolactinoma) and fifty-three apparently healthy age and sex-matched controls were enrolled in the study.
Methodology: All participants’ anthropometric variables, metabolic parameters like blood glucose, HBA1C and lipids, and markers of inflammation (ESR/ high sensitivity C- reactive protein (hsCRP) endothelial dysfunction i.e. Intercellular adhesion molecule (ICAM1) and vascular cell adhesion molecule (VCAM1) were measured. Patients were treated with dopamine agonist (cabergolin) and same parameters were reassessed after 12 weeks.
Results: women constituted 84% of the study population. Overall 37 % patients were obese and 52% had metabolic syndrome. Patients with prolactinoma had higher fasting blood glucose, HBA1c, total cholesterol, Triglycerides, low-density lipoprotein cholesterol and uric acid as compared with healthy matched controls. Mean/median/IQR ESR, hsCRP, ICAM1 and VCAM1 were significantly higher in patients with prolactinoma as compared with healthy controls. Serum prolactin correlated positively with ESR/hsCRP, tumour size, ICAM1 and VCAM1 after controlling for age, sex and BMI. Dopamine agonists normalized serum PRL in almost all patients with a significant decrease in BMI, metabolic parameters, ESR/hsCRP and ICAM1/VCAM1.
Conclusion: Untreated hyperprolactinemia because of prolactinoma is a state of low-grade inflammation with associated metabolic abnormalities and increased levels of endothelial dysfunction molecules.
Implications: Endothelial dysfunction is precursor event in atherosclerosis and may predispose prolactinoma patients to future cardiovascular events.
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