Frontiers of Hormone Research最新文献

Long-term childhood adolescent and young adult (CAYA) cancer survivors may develop health conditions that often coexist at young adulthood or middle age and that normally occur in persons aged 65 years and older, including cardiovascular and musculoskeletal diseases, metabolic syndrome, and secondary malignancies, suggesting that a process of accelerated aging occurs. This chapter summarizes epidemiological evidence and physiological mechanisms of accelerated aging, and possible preventive measures to delay the process of accelerated aging in CAYA cancer survivors. Evidence is mounting that in addition to a high prevalence of specific and multiple aging-related chronic diseases (multimorbidity), CAYA cancer survivors seem to also have a higher risk of other aging phenotypes, including frailty, poor physical performance, and changes in body composition (low muscle and high fat mass). Risk factors for these aging phenotypes include treatment-related factors (cranial-spinal radiotherapy, anthracyclines), sociodemographic factors (higher age, female sex, low socioeconomic status), and unhealthy lifestyle factors (i.e., physical inactivity, obesity, smoking, excess alcohol consumption). The process of accelerated aging may be prevented or delayed by adopting and maintaining a healthy lifestyle, so that CAYA cancer survivors may live a life with optimal quality of life after cancer.

Growth hormone deficiency (GHD) is common in childhood cancer survivors (CCS). Major risk factors for GHD include radiation therapy, both cranial and total body irradiation, and tumor location. Some newer anti-cancer therapies may impact growth and the GH-IGF-1 axis as well. While untreated childhood-onset GHD adversely impacts adult height in CCS, longstanding GHD can cause or exacerbate multiple metabolic and skeletal health problems. This chapter discusses considerations in the diagnosis and treatment of GHD in CCS and discusses long-term outcomes in survivors of childhood cancer who have GHD.

Childhood cancer survivors (CCS) are at increased risk of developing thyroid disorders during follow-up. Radiation therapy to a field that includes the thyroid gland and 131I-meta-iodobenzylguanidine (131I-MIBG) treatment are the main risk factors for thyroid sequelae, which include decreased thyroid function, hyperthyroidism, thyroid nodules, and differentiated thyroid cancer, specifically papillary thyroid carcinoma. In addition, treatment with anti-neoplastic drugs or immunotherapy may result in thyroid dysfunction. Central hypothyroidism may be seen in CCS after cranial radiotherapy, after immunotherapy, or secondary to a brain tumor that involves the hypothalamic-pituitary region and will be discussed elsewhere in this series. In this chapter, the prevalence, risk factors, surveillance, and management of primary hypothyroidism, hyperthyroidism, thyroid nodules, and differentiated thyroid carcinoma in CCS are discussed.

Cardiovascular diseases represent one of the most common and serious late complications of anticancer treatments. In the general population, metabolic syndrome is closely related to the risk of cardiovascular events and mortality. In recent years, metabolic syndrome has gained attention as a crucial determinant of long-term cardiovascular risk in cancer survivors. Several risk factors have been associated with metabolic syndrome after cancer treatments, even if the pathophysiological mechanisms of this association are not fully understood. This chapter reviews the clinical features of metabolic syndrome in cancer survivors, analyzing in more detail patients treated with hormonal therapy and survivors of hematopoietic stem cell transplantation, who are burdened with a greater cardiovascular risk. Moreover, the role of lifestyle factors in the development of metabolic syndrome is discussed as well as the screening strategy for the early detection of metabolic alterations in cancer survivors. Finally, we discuss the available recommendations for cardiovascular risk assessment in cancer survivors and treatments for metabolic syndrome in this specific context.

Hyponatremia is a frequent occurrence in patients with neurosurgical disorders. Acute onset hyponatremia is particularly common in patients who have any type of cerebral insult, including traumatic brain injury, subarachnoid hemorrhage, and brain tumors. Furthermore, it is a common complication of intracranial procedures. Acute hyponatremia creates an osmotic gradient between the brain and the plasma, which promotes the movement of water from the plasma into brain cells, causing cerebral edema and neurological compromise. It is therefore far more likely to be symptomatic, and to have adverse outcomes, than chronic hyponatremia. Uncorrected acute hyponatremia with consequent cerebral edema may manifest through impaired consciousness level, seizures, elevated intracranial pressure, and, potentially, death due to cerebral herniation. The majority of cases of hyponatremia due to neurosurgical pathology are caused by the syndrome of inappropriate antidiuresis, but acute glucocorticoid insufficiency is increasingly being recognized as an important contributing factor. In this chapter, we summarize the existing literature on the clinical features and differential diagnosis of hyponatremia in the neurosurgical patient, and briefly discuss the management options.

In clinical practice, several medications such as diuretics, psychotropic drugs, and anticonvulsants have been reported to be a frequent cause of hyponatremia. Drugs may cause hyponatremia either by affecting the homeostasis of sodium and water (e.g., diuretics) or by altering the water homeostasis as a consequence of the syndrome of inappropriate secretion of antidiuretic hormone. On the contrary, drugs commonly prescribed in everyday clinical practice, including proton pump inhibitors, antibiotics, angiotensin-converting enzyme inhibitors, hypoglycemic agents and, amiodarone, have been infrequently 'incriminated' as causes of hyponatremia. Therefore, in the diagnostic approach of patients with low serum [Na+] levels, meticulous history taking and recording of pharmacotherapy is warranted to identify potentially culprit medications. Taking into account the adverse outcomes associated with even mild hyponatremia (i.e., impaired cognition, falls and fractures, mortality), recognition of drug-induced hyponatremia is of vital importance, while responsible agents should be discontinued and "re-challenge" should be avoided by informing the patient and involved caregivers.

Hyponatremia is frequent in cancer patients and potentially deleterious. Cancer patients have specific requirements due to the nature and treatment of their disease, which can directly impact the occurrence and severity of hyponatremia, and limit treatment choices. Although essential for successful hyponatremia management, appropriate diagnostic testing is not routinely performed in the current practice. Despite clear evidence that hyponatremia is associated with poor outcome in oncology patients, most patients are still hyponatremic while under observation. Guidance on specific treatment of cancer patients with hyponatremia is needed to optimize patient care in the face of these challenges.