Reviews in Endocrine & Metabolic Disorders最新文献

Osteosarcopenia is an emerging clinical condition highly prevalent in the older people. Affected subjects due to their intrinsic skeletal fragility and propensity to falls are at elevated risk of hip fractures which can increase morbidity and mortality. Strategies for attenuating the impact of predisposing factors on hip fractures are not yet well defined and should derive from multidisciplinary care and collaborations. Our aim was to narratively review available data on the preventive role of vitamin D and hip protectors on hip fractures in older patients with sarcopenia. Older subjects are at high risk of vitamin D deficiency and of falls due to several concomitant factors besides osteosarcopenia. Vitamin D protective actions against hip fractures may be mediated by both skeletal (increased mineralization) and extra-skeletal (reduced risk of falls) actions. Hip protectors may act downstream attenuating the effects of falls although their use is still not yet enough widespread due to the suboptimal compliance obtained by traditional hard devices. Concomitant use of vitamin D and hip protectors may represent an effective strategy in the prevention of hip fractures which need to be tested in ad hoc designed clinical trials.

Hypopituitarism is a heterogenous disorder characterised by a deficiency in one or more anterior pituitary hormones. There are marked sex disparities in the morbidity and mortality experienced by patients with hypopituitarism. In women with hypopituitarism, the prevalence of many cardiovascular risk factors, myocardial infarction, stroke and mortality are significantly elevated compared to the general population, however in men, they approach that of the general population. The hypothalamic-pituitary-gonadal axis (HPG) is the most sexually dimorphic pituitary hormone axis. Gonadotropin deficiency is caused by a deficiency of either hypothalamic gonadotropin-releasing hormone (GnRH) or pituitary gonadotropins, namely follicle-stimulating hormone (FSH) and luteinising hormone (LH). HPG axis dysfunction results in oestrogen and testosterone deficiency in women and men, respectively. Replacement of deficient sex hormones is the mainstay of treatment in individuals not seeking fertility. Oestrogen and testosterone replacement in women and men, respectively, have numerous beneficial health impacts. These benefits include improved body composition, enhanced insulin sensitivity, improved atherogenic lipid profiles and increased bone mineral density. Oestrogen replacement in women also reduces the risk of developing type 2 diabetes mellitus. When women and men are considered together, untreated gonadotropin deficiency is independently associated with an increased mortality risk. However, treatment with sex hormone replacement reduces the mortality risk comparable to those with an intact gonadal axis. The reasons for the sex disparities in mortality remain poorly understood. Potential explanations include the reversal of women's natural survival advantage over men, premature loss of oestrogen's cardioprotective effect, less aggressive cardiovascular risk factor modification and inadequate oestrogen replacement in women with gonadotropin deficiency. Regrettably, historical inertia and unfounded concerns about the safety of oestrogen replacement in women of reproductive age have impeded the treatment of gonadotropin deficiency.

Prolactin levels can be influenced by multiple medications primarily through the interaction with dopamine receptors which regulate its secretion. Unlike hyperprolactinemia which has a well-defined clinical phenotype, the effects of hypoprolactinemia beyond inability to lactate are incompletely understood. Recent studies have raised concerns regarding detrimental changes in glucose metabolism, sexual function and psychological profile in patients with low prolactin levels. In contrast with anatomic and genetic etiologies, drug-induced hypoprolactinemia is usually reversible after dose reduction of the offending medication. The most common clinical scenario of drug-induced hypoprolactinemia in the endocrine clinic pertains to patients treated with cabergoline or bromocriptine for prolactin-secreting or other types of pituitary adenomas. Also, data has accumulated regarding hypoprolactinemia in patients receiving aripiprazole for schizophrenia and other psychiatric disorders. These patients warrant careful evaluation for comorbidities. This review aims to increase awareness about the potentially detrimental effects of drug-induced hypoprolactinemia, which should be considered in clinical practice decisions.

Traumatic brain injury (TBI) is a well-known etiologic factor for pituitary dysfunctions, with a prevalence of 15% during long-term follow-up. The most common hormonal disruption is growth hormone deficiency, followed by central adrenal insufficiency, central hypogonadism, and central hypothyroidism in varying order across studies. The prevalence of serum prolactin disturbances ranged widely from 0 to 85%. Prolactin release is mainly regulated by hypothalamic dopamine inhibition, and mediators such as TRH, serotonin, cytokines, and neurotransmitters have modulatory effects. Many factors, such as hypothalamic and/or pituitary gland injuries, as well as fluctuations in dopaminergic activity and other mediators and stress response, may cause derangements in serum prolactin levels after TBI. Although it is challenging to investigate the direct effects of TBI on serum prolactin levels due to many confounders, basal prolactin measurements and stimulation tests provide insight into the functionality of the hypothalamus and pituitary gland after TBI. Moreover, during the acute phase of TBI, prolactin levels appear to correlate with TBI severity. In contrast, in the chronic phase, hypoprolactinemia may function as an indirect indicator of pituitary dysfunction and reduced pituitary volume. Further investigations are needed to elucidate the pathophysiologic mechanisms underlying the prolactin trend following TBI, its significance, and its associations with other pituitary hormone dysfunctions. In this article, we re-evaluated our patients' TBI data regarding prolactin levels during prospective long-term follow-up, and reviewed the literature regarding the prevalence, pathophysiology, and clinical implications of serum prolactin disturbances during acute and chronic phases following TBI.

Both local and external cranial radiotherapy (RT) can induce neurotoxicity and vascular damage of the hypothalamic-pituitary area, which can promote neuroendocrine alterations. While anterior pituitary insufficiency after RT has been extensively characterized, data on the effect of RT on prolactin (PRL) secretion are limited and heterogeneous, with different patterns of PRL behavior described in the literature. A progressive decline in PRL levels, reflecting a time-dependent, slowly evolving radiation-induced damage to the pituitary lactotroph cells has been reported. To date, the association between hypopituitarism and hypoprolactinemia in patients undergoing RT has not yet been fully investigated. The few available data suggest that lower PRL levels can predict an extent damage of the pituitary tissue and a higher degree of hypothalamic dysfunction. However, most studies on the effect of RT on pituitary function do not properly assess PRL secretion, as PRL deficiency is usually detected as part of hypopituitarism and not systematically investigated as an isolated disorder, which may lead to an underestimation of hypoprolactinemia after RT. In addition, the often-inadequate follow-up over a long period of time may contribute to the non-recognition of PRL deficiency after RT. Considering that hypoprolactinemia is associated with various metabolic complications, there is a need to define appropriate diagnostic and management criteria. Therefore, hypoprolactinemia should enter in the clinical investigation of patients at risk for hypopituitarism, mainly in those patients who underwent RT.

Acromegaly is a rare disease and thus challenging to accurately quantify epidemiologically. In this comprehensive literature review, we compare different approaches to studying acromegaly from an epidemiological perspective and describe the temporal evolution of the disease pertaining to epidemiological variables, clinical presentation and mortality. We present updated epidemiological data from the population-based Danish cohort of patients with acromegaly (Acro_DEN), along with meta-analyses of existing estimates from around the world.Based on this, we conclude that the incidence, prevalence and age at acromegaly diagnosis are all steadily increasing, but with considerable variation between studies. An increased number of incidental cases may contribute to the increase in incidence and age at diagnosis, respectively. The clinical features at presentation are trending toward a milder disease phenotype at diagnosis, and advances in therapeutic options have reduced the mortality of patients with acromegaly to a level similar to that of the general population. Moreover, the underlying cause of death has shifted from cardiovascular to malignant neoplastic diseases.

Bariatric surgery is widely recognized as the most effective intervention for obesity and offers benefits beyond weight loss. However, not all patients achieve satisfactory weight loss, balanced changes in body composition, and resolution of comorbidities. Therefore, thorough pre- and postoperative evaluations are important to predict success and minimize adverse effects. More comprehensive assessments require broadening the focus beyond body weight and fat measurements to consider quantitative and qualitative evaluations of muscles. Introducing the concept of sarcopenia is useful for assessing the degradative and pathological changes in muscles associated with cardiometabolic function, physical performance, and other obesity-related comorbidities in patients undergoing bariatric surgery. However, there is currently no consensus or definition regarding the research and clinical use of sarcopenia in patients undergoing bariatric surgery. Therefore, this review aimed to define the concept of sarcopenia applicable to patients undergoing bariatric surgery, based on the consensus reached for sarcopenia in the general population. We also discuss the methods and significance of measuring muscle mass, quality, and strength, which are key variables requiring a comprehensive assessment.

A minority of children born small for gestational age (SGA) may experience catch-up growth failure and remain short in adulthood. However, the underlying causes and mechanisms of this phenomenon are not yet fully comprehended. We reviewed the present state of research concerning the growth hormone-insulin-like growth factor axis and growth plate in SGA children who fail to achieve catch-up growth. Additionally, we explored the factors influencing catch-up growth in SGA children and potential molecular mechanisms involved. Furthermore, we considered the potential benefits of supplementary nutrition, specific dietary patterns, probiotics and drug therapy in facilitating catch-up growth.

Hepatic glycogen storage diseases constitute a group of disorders due to defects in the enzymes and transporters involved in glycogen breakdown and synthesis in the liver. Although hypoglycemia and hepatomegaly are the primary manifestations of (most of) hepatic GSDs, involvement of the endocrine system has been reported at multiple levels in individuals with hepatic GSDs. While some endocrine abnormalities (e.g., hypothalamic‑pituitary axis dysfunction in GSD I) can be direct consequence of the genetic defect itself, others (e.g., osteopenia in GSD Ib, insulin-resistance in GSD I and GSD III) may be triggered by the (dietary/medical) treatment. Being aware of the endocrine abnormalities occurring in hepatic GSDs is essential (1) to provide optimized medical care to this group of individuals and (2) to drive research aiming at understanding the disease pathophysiology. In this review, a thorough description of the endocrine manifestations in individuals with hepatic GSDs is presented, including pathophysiological and clinical implications.

Childhood obesity is a chronic inflammatory epidemic that affects children worldwide. Obesity affects approximately 1 in 5 children worldwide. Obesity in children can worsen weight gain and raise the risk of obesity-related comorbidities like diabetes and non-alcoholic fatty liver disease (NAFLD). It can also negatively impact the quality of life for these children. Obesity disrupts immune system function, influencing cytokine (interleukins) balance and expression levels, adipokines, and innate and adaptive immune cells. The altered expression of immune system mediators, including interleukin-1 (IL-1), interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin-17 (IL-17), interleukin-18 (IL-18), transforming growth factor (TGF), tumor necrosis factor (TNF), and others, caused inflammation, progression, and the development of pediatric obesity and linked illnesses such as diabetes and NAFLD. Furthermore, anti-inflammatory cytokines, including interleukin-2 (IL-2), have been shown to have anti-diabetes and IL-1 receptor antagonist (IL-1Ra) anti-diabetic and pro-NAFLFD properties, and interleukin-10 (IL-10) has been shown to have a dual role in managing diabetes and anti-NAFLD. In light of the substantial increase in childhood obesity-associated disorders such as diabetes and NAFLD and the absence of an effective pharmaceutical intervention to inhibit immune modulation factors, it is critical to consider the alteration of immune system components as a preventive and therapeutic approach. Thus, the current review focuses on the most recent information regarding the influence of pro- and anti-inflammatory cytokines (interleukins) and their molecular mechanisms on pediatric obesity-associated disorders (diabetes and NAFLD). Furthermore, we discussed the current therapeutic clinical trials in childhood obesity-associated diseases, diabetes, and NAFLD.