ergoline and Inflammation

The aim of this study was to evaluate the effect of Cabergoline on insulin sensitivity, inflammatory markers, and carotid intima media thickness in prolactinoma patients. Twenty-one female, newly diagnosed patients with prolactinoma were included in the study. None of the patients were treated previously. Cabergoline was given as treatment, starting with 0.5 mg/day and tapered necessarily. Blood samples were taken for prolactin, highly sensitive C-reactive protein, homocysteine, total cholesterol, low density lipoprotein (LDL) cholesterol, fasting glucose, insulin, and HOMA (homeostasis model assessment of insulin resistance) score was calculated, prior to and 6 months after starting treatment. The body mass index (BMI) was measured and carotid intima media thickness (CIMT) was evaluated for each patient prior to and 6 months after the treatment. The prolactin levels and LDL decreased significantly after cabergoline treatment. Insulin sensitivity improved independently from the decrease in prolactin levels and BMI. The significant decrease in homocysteine and hs-CRP was not related with the decrease in prolactin levels. The significant decrease in CIMT was independent from the decrease in prolactin levels, HOMA score, and BMI. Our data suggest that cabergoline treatment causes an improvement in insulin sensitivity and inflammatory markers and causes a decrease in CIMT independent from the decrease in prolactin, LDL cholesterol, and BMI. We conclude that short term cabergoline treatment can improve endothelial function independently from the changes in metabolic disturbances and inflammatory markers.

Topics: Adolescent; Adult; Antineoplastic Agents, Hormonal; Biomarkers; Cabergoline; Carotid Intima-Media Thickness; Ergolines; Female; Glucose Tolerance Test; Humans; Inflammation; Insulin Resistance; Middle Aged; Pituitary Neoplasms; Prolactinoma; Young Adult

In view of the association of hyperprolactinaemia with insulin resistance, we hypothesized that patients with hyperprolactinaemia may present increased cardiovascular risk markers.. Descriptive clinical trial.. Serum glucose, insulin, insulin resistance, lipids, high sensitivity C-reactive protein (hsCRP), interleukin (IL)-6, tumour necrosis factor (TNF)-alpha and soluble E-selectin (sELAM-1) serum levels were determined in 15 patients with hyperprolactinaemia at baseline (compared with 20 healthy subjects) and after 12 weeks of cabergoline therapy (0.5-1 mg twice per week). We also measured mononuclear cell NF-kappaB activation and TNF-alpha production in a subset of subjects.. Serum levels of prolactin (PRL), insulin, insulin resistance (HOMA-IR) index and hsCRP were significantly higher in patients than in control subjects. Markers of mononuclear cell activation did not differ between the groups. Hyperprolactinaemia, BMI and age were predictors of hsCRP. BMI was the only predictor of HOMA-IR. Cabergoline therapy significantly reduced serum PRL, insulin, hsCRP and sELAM-1 levels.. These data suggest that hyperprolactinaemia is associated with insulin resistance related to increased BMI and low-grade inflammation independently of BMI. Short-term cabergoline therapy can reduce the inflammatory markers.

Topics: Adult; Biomarkers; Blood Glucose; C-Reactive Protein; Cabergoline; Cardiovascular Diseases; E-Selectin; Enzyme-Linked Immunosorbent Assay; Ergolines; Female; Humans; Hyperprolactinemia; Inflammation; Insulin; Insulin Resistance; Interleukin-6; Linear Models; Lipids; Male; Middle Aged; Obesity; Risk Factors; Tumor Necrosis Factor-alpha

The dysfunction of immune regulation plays a critical role in the pathogenesis of a number of chronic inflammatory disorders, such as IBD. A close relationship between psychological stress and intestinal inflammation has been noted; the underlying mechanism remains elusive. This study aims to elucidate a pathological pathway between psychological stress and the dysfunction of regulatory T cells (Treg), and its effect on facilitating intestinal inflammation.. A restraint stress model was employed to induce psychological stress in mice. The functions of Tregs were determined by assessing the immune suppressor effects in the intestine. A mouse model of intestinal inflammation was established using a low dose of trinitrobenzene sulfonic acid (TNBS) or dextran sulfate sodium (DSS) together with the challenge of chronic stress.. After treating mice with restraint stress, the suppressor function of intestinal Treg was compromised, although the frequency of Treg was not changed in the intestine. Further observation revealed that stress induced Tregs in the intestine to differentiate into foxhead box P3(+) interleukin (IL)-17(+) tumour necrosis factor (TNF)-α(+) T cells. We also observed that exposure to stress-derived prolactin induced dendritic cells (DC) to produce IL-6 and IL-23 in vitro and in vivo, which played a critical role in altering Treg's phenotypes. Treating mice with chronic stress facilitated the initiation of intestinal inflammation by a low dose of TNBS or DSS, which was abolished by pretreatment with an inhibitor of prolactin, the cabergoline.. Psychological stress-derived prolactin alters DC and Treg's properties to contribute to intestinal inflammation.

Topics: Animals; Cabergoline; Colitis; Dextran Sulfate; Disease Models, Animal; Dopamine Agonists; Ergolines; Forkhead Transcription Factors; Immunity, Mucosal; Inflammation; Interleukins; Mice; Mice, Inbred BALB C; Prolactin; Stress, Psychological; T-Lymphocytes, Regulatory; Trinitrobenzenesulfonic Acid; Tumor Necrosis Factor-alpha

Topics: Antineoplastic Agents, Hormonal; Biomarkers; Carotid Intima-Media Thickness; Ergolines; Female; Humans; Inflammation; Insulin Resistance; Pituitary Neoplasms; Prolactinoma