1,720,974 research outputs found
Metabolic effects of prolactin
No full textOver the last years, the metabolic role of PRL has emerged. PRL excess is known to promote weight gain, obesity, metabolic syndrome, and impairment in gluco-insulinemic and lipid profiles, likely due to the suppression of physiologic dopaminergic tone. Prolactin receptors and dopamine receptors type 2 have been demonstrated to be expressed on both human pancreatic β- cell and adipocytes, supporting a key role of prolactin and dopamine in peripheral metabolic regulation. Medical treatment with the dopamine agonists bromocriptine and cabergoline has been demonstrated to decrease the prevalence of metabolic syndrome and obesity, and significantly improve gluco-insulinemic and lipid profiles. In hyperprolactinemic men with concomitant hypogonadism, correction of hyperprolactinaemia and testosterone replacement has been proven to restore metabolic impairment. In turn, low prolactin levels have also been demonstrated to exert a detrimental effect on weight gain, glucose and lipid metabolism, thus leading to an increased prevalence of metabolic syndrome. Therefore, PRL values ranging from 25 to 100 mg/L, in absence of other recognizable pathological causes, have been proposed to represent a physiological response to the request for an increase in metabolic activity, and nowadays classify the so-called HomeoFIT- PRL as a promoter of metabolic homeostasis. The current review focuses mainly on the effects of hyperprolactinemia and its control by medical treatment with DAs on the modulation of food intake, body weight, gluco-insulinemic and lipid profile. Furthermore, it provides the latest knowledge about the metabolic impact of hypoprolactinemia
Editorial: Resistance to Medical Therapy in Pituitary Tumors.
No full textPituitary tumors may exhibit resistance to conventional medical treatments, including somatostatin receptor (SST) ligands (SRLs) and dopamine agonists (DAs) (1, 2). Resistance to medical treatment leads to multi-modal therapies, including surgery and radiotherapy. However, treatment-resistant tumors frequently relapse after radical surgical excision. This is of crucial interest as it occurs in a considerable proportion of patients with pituitary tumors (3). Indeed, resistance to conventional treatments is nowadays considered a predictive factor of the aggressive behavior of the pituitary tumor, being associated with poor prognosis and increased mortality. Predictors of responsiveness to medical treatments are still under investigation, and there is no clear evidence for the best individualized medical therapy in patients with aggressive pituitary lesionsS
Cushing, acromegaly, GH deficiency and tendons
Full text linkCushing’s syndrome, induced by an endogenous or exogenous cortisol excess, and acromegaly, the clinical syndrome caused by growth hormone (GH) excess in adulthood, as well as the disease induced by GH deficiency (GHD), represent perfect models for the evaluation of the effects induced by chronic exposure in vivo, respectively, to cortisol and GH/IGF-1 excess or deficiency on the complex structure of the tendons as well as on the related post-traumatic repair mechanism. Although the literature is still scant, here in main scientific evidence on this topic is summarized in order to provide suggestions about the management of the above mentioned illnesses, to translate such information in the field of sports medicine and/or traumatology, and to increase and to disseminate knowledge on this misunderstood theme
Resistance to somatostatin analogs in acromegaly
No full textSomatostatin analogs (SA) are widely used in acromegaly, either as first-line or adjuvant treatment after surgery. First-line treatment with these drugs is generally used in the patients with macroadenomas or in those with clinical conditions so severe as to prevent unsafe reactions during anesthesia. Generally, the response to SA takes into account both control of GH and IGF-I excess, with consequent improvement of clinical symptoms directly related to GH and IGF-I excess, and tumor shrinkage. This latter effect is more prominent in the patients treated first-line and bearing large macroadenomas, but it is also observed in patients with microadenomas, even with little clinical implication. Predictors of response are patients' gender, age, initial GH and IGF-I levels, and tumor mass, as well as adequate expression of somatostatin receptor types 2 and 5, those with the highest affinity for octreotide and lanreotide. Only sporadic cases of somatostatin receptor gene mutation or impaired signaling pathways have been described in GH-secreting tumors so far. The response to SA also depends on treatment duration and dosage of the drug used, so that a definition of resistance based on short-term treatments using low doses of long-acting SA is limited. Current data suggest that response to these drugs is better analyzed taking together biochemical and tumoral effects because only the absence of both responses might be considered as a poor response or resistance. This latter evidence seems to occur in 25% of treated patients after 12 months of currently available long-acting SA
Investigational drugs for the treatment of acromegaly: new agents to transform therapy
No full textIntroduction: Disease control is essential to decrease morbidity burden and mortality in acromegaly patients. In the last decades, the availability of new drugs increased the rate of disease control. However, up to 55% of patients remain uncontrolled despite available treatment strategies in real-world data. The reasons for this finding may include poor adherence, inadequate tolerability, therapeutic inertia, and high costs. Since acromegaly is a chronic disease and medical therapy is usually life-long, patient's adherence to treatment is fundamental in both achieving and maintaining disease control. Less invasive routes of administration could improve adherence and concur to increase disease control rate. Areas covered: The aim of current review is to provide a detailed update about investigational drugs for acromegaly treatment currently under investigation as paltusotine, ONO-5788, AP102, GT-02037, ISIS 766720, CAM2024, Lanreotide PRF, DP1038, MTD201, solid dose injection of octreotide. Expert opinion: Medical therapy of acromegaly is an evolving field. Current studies are addressing patient's need for both new molecules and less invasive routes of administration for already existing drugs. It cannot be ruled out that drugs currently used for other diseases such as cancer could be considered in the future for the treatment of acromegaly
Diurnal cortisol profiles across pregnancy: challenges in the current state of knowledge
No full textSomatostatin analogs, cabergoline and pegvisomant: comparing the efficacy of medical treatment for acromegaly
No full textCardiometabolic effects of hypoprolactinemia
No full text: The fall of PRL levels below the lower limit of the normal range configures the condition of hypoprolactinemia. Unlike PRL excess, whose clinical features and treatments are well established, hypoprolactinemia has been only recently described as a morbid entity requiring prompt identification and proper therapeutic approach. Particularly, hypoprolactinemia has been reported to be associated with the development of metabolic syndrome and impaired cardiometabolic health, as visceral obesity, insulin-resistance, diabetes mellitus, dyslipidaemia, chronic inflammation, and sexual dysfunction have been found more prevalent in patients with hypoprolactinemia as compared to those with normoprolactinemia. This evidence has been collected mainly in patients on chronic treatment with dopamine agonists for PRL excess due to a PRL-secreting pituitary tumour, and less frequently in those receiving the atypical antipsychotic aripiprazole. Nowadays, hypoprolactinemia appears to represent a novel and unexpected risk factor for cardiovascular diseases, as is the case for hyperprolactinemia. Nevertheless, current knowledge still lacks an accurate biochemical definition of hypoprolactinemia, since no clear PRL threshold has been established to rule in the diagnosis of PRL deficiency enabling early identification of those individual subjects with increased cardiovascular risk directly ascribable to the hormonal imbalance. The current review article focuses on the effects of hypoprolactinemia on the modulation of body weight, gluco-insulinemic and lipid profile, and provides latest knowledge about potential cardiovascular outcomes of hypoprolactinemia
Le forme familiari di adenoma ipofisario
No full textGli adenomi ipofisari insorgono nel 5–6% dei
casi in un contesto familiare, nell’ambito di sindromi come
le Neoplasia Endocrine Multiple (MEN1, MEN4) o in
forma isolata (Familial Isolated Pituitary Adenomas, FIPA).
Negli ultimi anni sono state riconosciute nuove entità e nuovi
geni di predisposizione tra cui, in particolare, il gene Aryl
hydrocarbon receptor Interacting Protein (AIP). Il riconoscere
una predisposizione genetica, anche in forme apparentemente
sporadiche, è essenziale non solo per il caso indice
ma anche per la sua famiglia
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