Manejo terapéutico de la hiperprolactinemia. Therapeutic management of hyperprolactinemia. Visits. J M. Cabezas Agrícolaa, J. Cabezas-Cerratoa. Num. Pages Manejo clínico de las hiperprolactinemias. Clinical management of hyperprolactinemia. Visits. Download PDF. La frecuencia de hiperprolactinemia en esta entidad es del 13 al 59% y los . Artículo. B. Farzati,G. Mazziotti,G. Cuomo,M. Ressa,F. Sorvillo,G. Amato.
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Normal endocrine function is essential for cardiovascular health. Disorders of the endocrine system, consisting of hormone hyperfunction and hypofunction, have multiple effects on the cardiovascular system. In this review, we discuss the epidemiology, diagnosis, and management of disorders of the pituitary, thyroid, parathyroid, and adrenal glands, with respect to the impact of endocrine dysfunction on the cardiovascular system.
We also review the cardiovascular benefits of restoring normal endocrine function. The objective of this review is to explore the various cardiovascular changes that occur in endocrine dysfunction. We will also assess the cardiovascular benefits hiperprolactlnemia correcting endocrine disorders.
Diabetes is specifically excluded, as the hkperprolactinemia relationship between diabetes and cardiovascular risk is beyond the scope of this review. The anterior pituitary gland contains five cell types that synthesize and hiperprolacfinemia hormones growth hormone [GH], prolactin, follicle stimulating hormone, luteinizing hormone, thyroid stimulating hormone [TSH], adrenocorticotropic hormone [ACTH]that participate in hypothalamic-pituitary-target organ regulation.
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The posterior pituitary contains nerve hiperlrolactinemia that secrete vasopressin antidiuretic hormone and oxytocin. Of the pituitary hormones secreted by the anterior pituitary, disorders of prolactin, GH, and ACTH may be associated with cardiac disease.
Prolactin is synthesized and secreted by lactotroph cells of the anterior pituitary gland, and stimulates lactation in the postpartum period. Prolactin biperprolactinemia tonically inhibited by hypothalamic dopamine.
Prolactin levels are physiologically elevated in pregnancy, the postpartum period, and in states of stress. Pathologic hyperprolactinemia may be caused by decreased dopaminergic inhibition, such as when the pituitary stalk is disrupted, or by prolactin secretion from prolactinomas benign pituitary adenomas. The prevalence of hyperprolactinemia ranges from 0. Dopamine agonists, including cabergoline, bromocriptime, and quinagolide not approved for use in the United Statesare the primary treatment for prolactinomas.
Cabergoline is most commonly used, due to its clinical efficacy, tolerability, and favorable pharmacokinetic profile. This treatment duration hiperprolactinsmia concern for increased risks of articylo, including tricuspid regurgitation, mitral regurgitation, and aortic regurgitation.
Peripartum cardiomyopathy is a rare clinical entity. It has been suggested that a 16 kDa prolactin fragment may play a role in its pathophysiology. GH is synthesized and secreted by somatotroph cells in the anterior pituitary gland. It acts directly on peripheral tissues via interaction with the GH receptor, and indirectly via stimulation of insulin-like growth factor type 1 IGF-1 synthesis. In virtually all cell types, IGF-1 promotes glucose uptake and cellular protein synthesis.
GH and IGF-1 regulate somatic growth, including cardiac development and function Adults with GHD can be grouped into three categories: GHD is associated with increased body fat and central adiposity, dyslipidemia low high density lipoprotein cholesterol [HDLc], high total cholesterol, and high low density lipoprotein cholesterol [LDLc]endothelial dysfunction, and insulin resistance 1617 Figure 1. Increased carotid arterial intima-media thickness IMTa marker of early atherosclerotic development, has also been described in GHD.
Effect of growth hormone deficiency on atherosclerosis. Adapted with permission from Colao A. Echocardiography in patients with childhood- or adolescent-onset GHD has revealed significant reductions in left ventricular LV posterior wall thickness and interventricular septal thickness, with resultant decreases in LV mass index and LV internal diameter.
The mean age at diagnosis is years, hi;erprolactinemia with years of symptoms prior to diagnosis. Diagnosis of acromegaly is suggested by elevated IGF-1 levels, and confirmed by elevated GH levels after administration of an oral glucose tolerance test. Treatments for acromegaly aim to reduce or control adenoma growth, inhibit GH hypersecretion, and normalize IGF-I levels.
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Surgery is first-line therapy for acromegaly. The three drug classes available for acromegaly treatment are somatostatin analogs, dopamine agonists, and GH receptor antagonists. Possible mechanisms include increased arterial stiffness due to hypertrophy and fibrosis of the arterial muscular tunica. Cardiac histological abnormalities in acromegaly include myocyte hypertrophy, interstitial fibrosis, inflammatory cell infiltration, reduced capillary density, myofibril derangement, and extracellular collagen deposition.
In the early stage of acromegaly, there is enhanced myocardial contractility, decreased systemic vascular resistance, increased cardiac output, and overall increased cardiac performance. In the intermediate stage, after about 5 years of hipfrprolactinemia disease, there is hiperproactinemia hypertrophy, diastolic dysfunction, and impaired exertional cardiac performance.
Late-stage acromegalic cardiomyopathy is characterized by systolic and diastolic dysfunction, increased myocardial mass, ventricular cavity dilatation, hiperpfolactinemia increased systemic vascular resistance.
[Current diagnosis and treatment of hyperprolactinemia].
Up to two thirds of patients with acromegaly meet echocardiographic criteria for left ventricular hypertrophy LVHincluding about half of all normotensive acromegalics.
Cardiac valve disease aortic and mitral regurgitation is frequent in acromegaly. The risk of valve disease increases significantly with the duration of GH excess. Aortic and mitral valve dysfunction often persist despite treatment of hormonal excess.
Electrocardiogram ECG and Holter studies have documented cardiac rhythm abnormalities in acromegaly. The frequency of ventricular premature complexes increases with the duration of acromegaly.
The severity of ventricular arrhythmias correlates with increases in LV mass. Adrenocorticotropic hormone is synthesized and secreted by corticotroph cells of the anterior pituitary gland. The primary role of ACTH is to regulate adrenal cortisol secretion. Excess ACTH can be produced by pituitary corticotroph adenoma or, rarely, by an extrapituitary tumor ectopic ACTH syndrome such as small cell lung cancer, carcinoid tumor, or medullary thyroid cancer.
The diagnosis of Cushing’s syndrome requires demonstration of elevated cortisol levels with at least two confirmatory tests, including hour urinary-free cortisol, late-night salivary free cortisol, or overnight dexamethasone suppression test. Treatment options include transsphenoidal surgery, unilateral or bilateral adrenalectomy, radiotherapy and medical therapy.
The selection and efficacy of any given treatment modality depends on the underlying cause of hypercortisolism. Hypercortisolism is associated with hypertension, central obesity, insulin resistance, dyslipidemia, and alterations in clotting and platelet function 51 Figure 2.
Cortisol also increases the synthesis of several coagulation factors, stimulating endothelial production of von Willebrand factor and concomitantly increasing factor VIII. Mechanisms of increased cardiovascular risk mediated by hypercortisolism. Reprinted with permission from Fallo et al.
Cushing’s syndrome has been associated with LVH, concentric remodeling, diastolic dysfunction, and subclinical LV systolic dysfunction.
Diastolic dysfunction has been demonstrated, with impaired early LV relaxation, longer isovolumetric relaxation times, and evidence of global myocardial relaxation impairment.
The abnormalities of LV structure and function may be reversible with normalization of hypercortisolism. However, patients may continue to exhibit exercise intolerance due to steroid-induced myopathy and resultant muscle weakness.
Thyroid dysfunction is common. Hyperthyroidism is present in 1. Thyrotoxicosis may result from autoimmune disease, thyroid nodule autonomy, or exogenous thyroid hormone ingestion. Hyperthyroid patients often present with signs and symptoms related to the cardiovascular system including palpitations, sinus tachycardia, atrial fibrillation, systolic hypertension, widened pulse pressure, exercise intolerance, and exertional dyspnea.
Other symptoms include fatigue, weight loss, heat intolerance, and diarrhea. Treatments for hyperthyroidism include antithyroid medications methimazole, carbimazole, and propylthiouracilbeta-blockers, radioactive iodine ablation, and thyroid surgery.
Subclinical hyperthyroidism is defined by low or undetectable serum TSH and normal peripheral free thyroid hormone levels. Patients are usually asymptomatic, but remain at risk for some cardiovascular changes associated with hyperthyroidism. Genomic and nongenomic actions of thyroid hormone result in cardiovascular hemodynamic changes in overt hyperthyroidism that include decreased systemic vascular resistance SVRincreased heart rate, increased cardiac preload, and increased cardiac output.
Thyroid hormone also promotes hiperprolwctinemia increase in blood volume via up-regulation of erythropoietin secretion, further enhancing cardiac preload.
LVH has been associated with hyperthyroidism. In the short term, hyperthyroidism may be associated with improved diastolic function.
However, in the long term, chronic thyrotoxicosis may induce LVH and diastolic dysfunction. Exercise intolerance and dyspnea on exertion in overt hyperthyroidism may result from an inability to further increase heart rate and ejection fraction, or to further decrease SVR in the setting of exercise.
Patients with subclinical hyperthyroidism may also artculo decreased exercise tolerance. Hypothyroid patients may present with fatigue, weight gain, cold intolerance, constipation, mild diastolic hypertension, narrowed pulse pressure, and bradycardia.
Overt hypothyroidism is characterized by elevated serum TSH and decreased peripheral thyroid hormone levels, with etiologies including autoimmune thyroid gland failure, iatrogenic failure radioactive iodine, external beam radiation hiprrprolactinemia, and thyroidectomy.
The treatment of hypothyroidism consists of thyroxine T 4 replacement. Subclinical hypothyroidism is defined by elevated serum TSH with normal peripheral free thyroid hormone levels. Patients with subclinical hypothyroidism are generally asymptomatic or mildly symptomatic.
The hemodynamic changes in hypothyroidism are the opposite of those seen in hyperthyroidism. Overt hypothyroidism is associated with increased SVR, normal or decreased resting heart rate, decreased contractility, and decreased cardiac output.
In addition, diastolic pressure is increased and pulse pressure is narrowed. Overt hypothyroidism is associated with accelerated atherosclerosis and coronary artery disease that hiperprlactinemia be attributable to diastolic hypertension, impaired endothelial function, and hypercholesterolemia.
This hiiperprolactinemia in diastolic pressure is the result of increased systemic vascular resistance and increased arterial stiffness, and resolves with T 4 replacement therapy. Apolipoprotein B and the atherogenic LDL variant, lipoprotein aare also increased in hypothyroidism. Triglyceride and very low density lipoprotein levels are normal to increased, whereas changes in HDL are variable. Subclinical hypothyroidism has been associated with increased LDL and total cholesterol levels in several cross-sectional studies, but the effects of treatment in small trials have been inconsi stent.
In hypothyroidism there is resting LV diastolic dysfunction, and both systolic and diastolic dysfunction with exertion. In overt hypothyroidism, impaired LV diastolic function has been demonstrated by slowed myocardial relaxation and impaired early ventricular filling. T 4 replacement resolves these functional abnormalities, improving both diastolic and systolic function. Alterations in resting LV diastolic dysfunction have also been demonstrated in patients with subclinical hypothyroidism, with improvements seen in response to T 4 replacement.
Amiodarone-induced hypothyroidism AIH results from persi stent iodine-induced inhibition of thyroid gland function, and is more prevalent in patients with preexisting thyroid autoimmunity. High T 4 doses are often required because amiodarone decreases deiodinase activity, resulting in decreased conversion of T 4 to the active form, T 3. Amiodarone-induced thyrotoxicosis AIT is present in two forms: Type 1 AIT results in the synthesis and release of excess thyroid hormone, whereas Type 2 AIT results in the release of preformed thyroid hormone from the inflamed thyroid gland.
Differentiating between the two forms can be difficult, and management of AIT can be challenging. Type 1 AIT is managed with hiperprolactinejia drugs and possibly potassium perchlorate.