Effects of the Luteinizing Hormone-Releasing Hormone Agonist Leuprolide on Lipoproteins, Fibrinogen and Plasminogen Activator Inhibitor in Patients with Benign Prostatic Hyperplasia

Eri, Lars M.; Urdal, Petter; Bechensteen, A. G.

doi:10.1016/s0022-5347(01)67239-2

Cited by 81 publications

(39 citation statements)

References 23 publications

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“…ADT has been associated with prothrombotic changes including increases in fibrinogen, plasminogen activator inhibitor 1, and tissue plasminogen activator antigen 47–48 that may also explain a reported increase in venous thromboembolism. 49 Platelet counts are unaffected by ADT, 50 but platelet activation has yet to be characterized. In addition, this study did not include a placebo group because withholding ADT from men with prostate cancer and giving it to men without prostate cancer to enable a placebo group are both unethical because of the risks of morbidity and mortality.…”

Section: Discussionmentioning

confidence: 99%

Androgen Deprivation Therapy Reversibly Increases Endothelium‐Dependent Vasodilation in Men With Prostate Cancer

Nguyen

Jarolím

Basaria

et al. 2015

JAHA

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BackgroundAndrogen deprivation therapy (ADT) is a standard treatment for patients with aggressive prostate cancer. Although ADT improves survival, it increases the risk of diabetes. Emerging evidence suggests that ADT increases adverse cardiovascular events as early as 3 months after initiation in patients with cardiovascular disease, but the mechanism is unknown. We hypothesized that ADT may impair endothelium‐dependent vasodilation due to increases in lipids and insulin resistance and may provide a link for heightened cardiovascular risk in this population.Methods and ResultsWe prospectively evaluated conduit artery endothelium‐dependent and ‐independent vasodilation, lipids, and insulin resistance in 16 consecutively treated men (mean age 66±7 years; 25% with diabetes) with prostate cancer before and after 3 months of ADT. High‐resolution B‐mode ultrasound was used to assess flow‐mediated (endothelium‐dependent) and nitroglycerine‐mediated (endothelium‐independent) brachial artery vasodilation. ADT significantly increased insulin resistance, total cholesterol, HDL, and LDL. Endothelium‐dependent vasodilation was greater at 3 months than at baseline (10.8% [interquartile range: 7.7% to 14.6%] versus 8.9% [interquartile range: 4.0% to 12.6%], respectively; P=0.046, allometric P=0.037). Nitroglycerine‐mediated vasodilation did not change from baseline (P>0.2). The subset of participants on ADT for 6 months returned for reevaluation at 1 year. In this group, endothelium‐dependent vasodilation increased from baseline to 3 months and returned to baseline 6 months after ADT withdrawal (9.4% [interquartile range: 6.9% to 10.9%], 11.6% [interquartile range: 7.9% to 15.2%], and 9.0% [interquartile range: 5.1% to 12.5%], respectively; P=0.05).ConclusionsIn contrast to our expectation, ADT improved endothelium‐dependent vasodilation and its cessation returned endothelium‐dependent vasodilation to baseline. Determining the mechanism of this change requires further investigation.

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Section: Discussionmentioning

confidence: 99%

Androgen Deprivation Therapy Reversibly Increases Endothelium‐Dependent Vasodilation in Men With Prostate Cancer

Nguyen

Jarolím

Basaria

et al. 2015

JAHA

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“…Alterations in lipid profiles are highly variable during ADT use; however, many studies have reported increases in total cholesterol, triglycerides and HDL-C. 40,44,45 The increase in HDL-C observed while on ADT is a beneficial consequence, although it is unknown whether this improvement provides a cardio-protective effect. Regardless, increases in HDL-C are seen as early as 3-6 months within initiation of treatment.…”

Section: Mets and Androgen Deprivation Therapymentioning

confidence: 99%

“…Regardless, increases in HDL-C are seen as early as 3-6 months within initiation of treatment. 44,45 Due to the variability in lipid profile changes following ADT use, further investigation is warranted to determine the overall impact of ADT on cardio-metabolic risk in this population.…”

Section: Mets and Androgen Deprivation Therapymentioning

confidence: 99%

A review of clinical effects associated with metabolic syndrome and exercise in prostate cancer patients

Kiwata

Dorff

Schroeder

et al. 2016

Prostate Cancer Prostatic Dis

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Androgen deprivation therapy (ADT), a primary treatment for locally advanced or metastatic prostate cancer, is associated with adverse effects on numerous physiologic parameters, including alterations in cardio-metabolic variables that overlap with components of the metabolic syndrome (MetS). As MetS is an established risk factor for cardiovascular mortality and treatment for prostate cancer has been associated with the development of MetS, interventions targeting cardio-metabolic factors have been investigated in prostate cancer patients to attenuate the detrimental effects of ADT. Much support exists for exercise interventions in improving MetS variables in insulin resistant adults, but less evidence is available in men with prostate cancer. Regular exercise, when performed at appropriate intensities and volumes, can elicit improvements in ADT-related adverse effects, including MetS, and contributes to the growing body of literature supporting the role of exercise in cancer survivorship. This review 1) discusses the biologic interrelationship between prostate cancer, ADT, and MetS, 2) evaluates the current literature in support of exercise in targeting MetS, and 3) describes the physiological mechanisms by which exercise may favorably alter MetS risk factors in prostate cancer patients on ADT.

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“…Hepatic insulin resistance is shown to be sufficient to produce dyslipidemia and increase the susceptibility to atherosclerosis in mice (50,51). In human clinical studies, GnRH agonists to suppress androgen/AR signaling cause increases in total cholesterol and triglycerides (52,53). It is therefore likely that functional deficiency of AR in the liver caused by GnRH agonists leads to these lipid alterations.…”

Section: Cell Type–specific Arko Mouse Modelsmentioning

confidence: 99%

Androgen Receptor Roles in Insulin Resistance and Obesity in Males: The Linkage of Androgen-Deprivation Therapy to Metabolic Syndrome

Lin

Sparks

et al. 2014

Diabetes

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Prostate cancer (PCa) is one of the most frequently diagnosed malignancies in men. Androgen-deprivation therapy (ADT) is the first-line treatment and fundamental management for men with advanced PCa to suppress functions of androgen/androgen receptor (AR) signaling. ADT is effective at improving cancer symptoms and prolonging survival. However, epidemiological and clinical studies support the notion that testosterone deficiency in men leads to the development of metabolic syndrome that increases cardiovascular disease risk. The underlying mechanisms by which androgen/AR signaling regulates metabolic homeostasis in men are complex, and in this review, we discuss molecular mechanisms mediated by AR signaling that link ADT to metabolic syndrome. Results derived from various AR knockout mouse models reveal tissue-specific AR signaling that is involved in regulation of metabolism. These data suggest that steps be taken early to manage metabolic complications associated with PCa patients receiving ADT, which could be accomplished using tissue-selective modulation of AR signaling and by treatment with insulin-sensitizing agents.

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Effects of the Luteinizing Hormone-Releasing Hormone Agonist Leuprolide on Lipoproteins, Fibrinogen and Plasminogen Activator Inhibitor in Patients with Benign Prostatic Hyperplasia

Cited by 81 publications

References 23 publications

Androgen Deprivation Therapy Reversibly Increases Endothelium‐Dependent Vasodilation in Men With Prostate Cancer

Androgen Deprivation Therapy Reversibly Increases Endothelium‐Dependent Vasodilation in Men With Prostate Cancer

A review of clinical effects associated with metabolic syndrome and exercise in prostate cancer patients

Androgen Receptor Roles in Insulin Resistance and Obesity in Males: The Linkage of Androgen-Deprivation Therapy to Metabolic Syndrome

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