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Drug therapies for pre-existing endocrine disorders should not be ceased when pregnancy is confirmed. Specialist review is recommended. During pregnancy, the recommended daily intake of calcium is raised from 800 to 1200 mg per da...
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Drug therapies for pre-existing endocrine disorders should not be ceased when pregnancy is confirmed. Specialist review is recommended. During pregnancy, the recommended daily intake of calcium is raised from 800 to 1200 mg per day. Calcium supplementation is not routinely recommended during lactation, but could be considered for women who are nursing more than one infant or have had closely spaced pregnancies, and for lactating adolescents. Women with mild asymptomatic primary hyperparathyroidism may be monitored without treatment throughout pregnancy with a good outcome. However, surgical parathyroid-ectomy is recommended for more severe disease, preferably in the second trimester. Patients with prolactinomas and other pituitary tumours should be reviewed regularly throughout pregnancy and questioned about symptoms of tumour enlargement and pituitary dysfunction. Patients taking corticosteroids during pregnancy for Addison's disease or for other reasons will need to increase their dosage at times of stress. Breastfeeding is generally not contraindicated in women with endocrine disorders.
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Endocrine-disrupting chemicals (EDCs) have significant impacts on biological systems, and have been shown to interfere with physiological systems, especially by disrupting the hormone balance. During the last few decades, EDCs hav...
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Endocrine-disrupting chemicals (EDCs) have significant impacts on biological systems, and have been shown to interfere with physiological systems, especially by disrupting the hormone balance. During the last few decades, EDCs have been shown to affect reproductive, neurological, and metabolic development and function and even stimulate tumor growth. EDC exposure during development can disrupt normal development patterns and alter susceptibility to disease. Many chemicals have endocrine-disrupting properties, including bisphenol A, organochlorines, polybrominated flame retardants, alkylphenols, and phthalates. These compounds have gradually been elucidated as risk factors for many diseases, such as reproductive, neural, and metabolic diseases and cancers. Endocrine disruption has been spread to wildlife and species that are connected to the food chains. Dietary uptake represents an important source of EDC exposure. Although EDCs represent a significant public health concern, the relationship and specific mechanism between EDCs and diseases remain unclear. This review focuses on the disease-EDC relationship and the disease endpoints associated with endocrine disruption for a better understanding of the relationship between EDCs-disease and elucidates the development of new prevention/treatment opportunities and screening methods.
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ImportanceAs survival rates from cancer have improved dramatically over the last decades, there is a need to explore the long-term consequences. Adolescents and young adults with cancer are at risk for several therapy-related late...
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ImportanceAs survival rates from cancer have improved dramatically over the last decades, there is a need to explore the long-term consequences. Adolescents and young adults with cancer are at risk for several therapy-related late effects; however, these have not been studied extensively.ObjectiveTo investigate the lifetime risks of endocrine late effects of cancer and cancer treatment in adolescent and young adult cancer survivors.Design, Setting, and ParticipantsThis Danish, nationwide, population-based cohort study was conducted from January 1, 1976, through December 31, 2009, and included follow-up from January 1, 1977, through December 31, 2010. A total of 32?548 one-year cancer survivors diagnosed at ages 15 to 39 years were identified using the Danish Cancer Registry and 188?728 cancer-free comparison participants matched by year of birth and sex were randomly chosen from the Danish Civil Registration system. Analyses were performed from July 3, 2015, to February 27, 2018.ExposuresIndividuals in the survivor cohort were diagnosed with a first primary cancer at ages 15 to 39 years and received treatment according to recommendations and guidelines at time of diagnosis.Main Outcomes and MeasuresBy linkage to the National Patient Register, all hospital contacts for endocrine diseases were identified, and standardized hospitalization rate ratios (RRs) and absolute excess risks (AERs) were calculated.ResultsA total of 32?548 adolescent and young adult 1-year cancer survivors (14?021 [43.1%] male) in the Danish Patient Registry were followed up for 379?157 person-years (median [range]: 10 [0-34] years) and 188?728 cancer-free participants (82?669 [43.8%] male) for comparison were followed up for 2?958?994 person-years (median [range]: 15 [0-34] years). A total of 2129 survivors (6.5%) had at least 1 hospital contact for an endocrine disease, while 1232.0 (3.8%) were expected, yielding a statistically significant increased RR of 1.73 (95% CI, 1.65-1.81). The RRs were highest for testicular hypofunction (75.12; 95% CI, 45.99-122.70), ovarian hypofunction (14.65; 95% CI, 8.29-25.86), and pituitary hypofunction (11.14; 95% CI, 8.09-15.34). The leading reasons for hospital contacts were thyroid disease (38.0% of total AER), testicular dysfunction (17.1% of total AER), and diabetes (14.4% of total AER). Leukemia survivors were at a high risk for any endocrine disease (RR, 3.97; 95% CI, 3.10-5.09), while Hodgkin lymphoma survivors (RR, 3.06; 95% CI, 2.62-3.57) had the highest disease-specific excess risk for hypothyroidism (AER, 362 per 100?000 person-years; 95% CI, 280-443 per 100?000 person-years).Conclusions and RelevanceThe increased risk for endocrine diseases in adolescent and young adult cancer survivors indicates the need for counseling and follow-up, and could guide future preventive measures and surveillance strategies. Additional studies are required to determine exact associations between treatment regimens and endocrine diseases.
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Although the possibility of an endocrine emergency occurring in a primary care setting may seem remote, awareness of such emergencies is crucial for appropriate management. While some symptoms are specific to classic endocrine dis...
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Although the possibility of an endocrine emergency occurring in a primary care setting may seem remote, awareness of such emergencies is crucial for appropriate management. While some symptoms are specific to classic endocrine disorders, other symptoms, such as nausea, vomiting, and diarrhea, are so general that the diagnosis may not be considered initially. In these situations, careful and thoughtful diagnostic studies can be lifesaving.
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Purpose The management of endocrine therapy resistance is one of the most challenging facets of advanced breast cancer treatment. Palbociclib is an inhibitor of cyclin-dependent kinases 4 and 6 approved for the treatment of hormon...
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Purpose The management of endocrine therapy resistance is one of the most challenging facets of advanced breast cancer treatment. Palbociclib is an inhibitor of cyclin-dependent kinases 4 and 6 approved for the treatment of hormone receptor-positive, human epidermal growth factor receptor 2-negative advanced or metastatic breast cancer in combination with fulvestrant in postmenopausal women with disease progression following endocrine therapy. However, treatment responsiveness of tumors to palbociclib after multiple lines of endocrine therapy is not clearly established. The purpose of this study was to determine the efficacy of palbociclib and letrozole in patients pretreated with one or more lines of endocrine therapy. Methods This was a single-center, retrospective cohort study of all postmenopausal hormone receptor-positive, human epidermal growth factor receptor 2-negative metastatic breast cancer patients who received palbociclib and letrozole as a second-line endocrine therapy or beyond (and no prior cyclin-dependent kinases 4 and 6 inhibitor therapy) between February 1, 2015, and July 31, 2016. The primary objective was to evaluate time to treatment failure of palbociclib in combination with letrozole as a second-line of therapy or beyond. Results Fifty-three patients meeting eligibility criteria were included in the analysis. For the primary outcome, the median time to treatment failure of palbociclib and letrozole was 6.3 months (95% CI 3.1-7.4 months). Progression-free survival of palbociclib and letrozole therapy was 6.4 months (95% CI 4.9-8.3 months). Conclusions Palbociclib and letrozole therapy is a viable, effective treatment option for metastatic breast cancer patients who were not exposed to cyclin-dependent kinases 4 and 6 inhibitors as a first-line endocrine therapy. The benefits of palbociclib and letrozole therapy were seen without excessive toxicity, and although neutropenia was common, it may be managed with dose reduction.
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Congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency is a disorder characterized by impaired cortisol synthesis leading to excessive production of adrenal androgens. Prenatal and postnatal exposure to excess andro...
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Congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency is a disorder characterized by impaired cortisol synthesis leading to excessive production of adrenal androgens. Prenatal and postnatal exposure to excess androgens may increase neural vulnerability to insult and affect cognitive functions, particularly dopamine-dependent neural circuits responsible for executive functioning (EF). Our study aimed to investigate relationship between more pronounced androgen exposure and EF-related behaviors in children with CAH, as well as sex differences in these associations. Parents of patients with CAH (n=41, boys=17, girls=24; age: M=8.41, SD=4.43) completed the Behavior Rating Inventory of Executive Function (BRIEF), a measure assessing behavioral manifestations of EF. Assessments of bone age advancement, a proxy of cumulative androgen exposure, were analyzed. Advanced bone age predicted more inhibition difficulties in boys but not in girls, and more difficulties in all other BRIEF domains in the total sample. Excessive androgen production affected EF such that more advanced bone age led to more EF-related difficulties. Sex differences in inhibition may result from estrogen exposure moderating the impact of androgens in girls but not in boys. Future interventions may include targeting EF in patients with CAH to enhance quality of life and reduce cognitive consequences associated with this disease.
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In the 2006 endocrinology and metabolism section, Dr A. Poulton reviews the relationship between attention deficit hyperactivity disorder (ADHD) and linear growth, weight gain and pubertal development; Drs C. Fluck and W. Miller d...
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In the 2006 endocrinology and metabolism section, Dr A. Poulton reviews the relationship between attention deficit hyperactivity disorder (ADHD) and linear growth, weight gain and pubertal development; Drs C. Fluck and W. Miller describe the clinical, biochemical, and genetic aspects of P450 oxidoreductase deficiency; Dr M. Tena-Sempere examines the roles of kisspeptin and its G-protein coupled receptor (GPR54) in the regulation of pubertal development; Drs M. Langer, B. Modi, and M. Agus describe the concept of 'relative' adrenal insufficiency in critically ill neonates and children, and review its evaluation, identification and management.
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Controversy persists regarding who should be tested and who should be treated for vitamin D deficiency. Controversy continues to surround vitamin D testing, the diagnosis and clinical significance of vitamin D deficiency, and the ...
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Controversy persists regarding who should be tested and who should be treated for vitamin D deficiency. Controversy continues to surround vitamin D testing, the diagnosis and clinical significance of vitamin D deficiency, and the benefits — or lack thereof — of vitamin D supplementation. Over 2000 peer‐reviewed articles have been published on these topics within the past 12 months, generating much debate and discussion in the scientific literature and lay media.
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Hypothyroidism is caused by a deficiency in the synthesis of thyroid hormone. Dwarfism is the most obvious skeletal manifestation, but most people with hypothyroidism do not have any skeletal evidence of the disease. When the skel...
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Hypothyroidism is caused by a deficiency in the synthesis of thyroid hormone. Dwarfism is the most obvious skeletal manifestation, but most people with hypothyroidism do not have any skeletal evidence of the disease. When the skeleton is affected, the severity of this manifestation depends on the degree of the deficiency and age of onset. Endemic hypothyroidism typically is linked to specific ecological settings such as the high mountains where iodine is absent, or else it occurs with very low concentrations in water and soil. In these areas, the prevalence may be as high as 8%. The disease can be expected to occur in archaeological human skeletal samples from endemic regions. Sporadic hypothyroidism is caused by a deficiency in the thyroid gland itself, and is not linked to any specific environmental context. The disease may be the result of a genetic defect, but can also be caused by other pathological conditions that may affect the thyroid gland, including infection and cancer. The skeletal abnormalities of the two variants will be indistinguishable in archaeological human remains. In order to identify hypothyroidism in archaeological skeletal samples, one must be aware of the differences in pathological skeletal changes seen in hypothyroidism in comparison with other diseases, such as achondroplasia, that can cause similar abnormalities. Twelve clinically documented cases of hypothyroidism provide data for understanding the skeletal abnormalities associated with this disease. All 12 are modern documented cases from Switzerland, where endemic hypothyroidism occurred in the iodine-deficient Alpine regions. However, at least one case in the sample was caused by a defect in the thyroid gland itself. Am J Phys Anthropol 127:1-6, 2005. Published 2004 Wiley-Liss, Inc.
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