Pub Date : 2021-07-01DOI: 10.1093/med/9780198870197.003.0283
B. Williams
High blood pressure (hypertension) is very common in people with diabetes. There is moreover an association between hypertension and diabetes that tracks through life, while the blood glucose concentration of young non-diabetic individuals has been shown to predict risk of future hypertension. Conversely, people with hypertension are twice as likely to develop type 2 diabetes over their lifetime. High blood pressure (hypertension) is arguably the most important preventable cause of premature microvascular and macrovascular disease and their associated morbidity and mortality in people with diabetes. This chapter will review key aspects of the epidemiology and pathophysiology of hypertension in people with diabetes, as well as recommended approaches to its clinical evaluation and treatment.
{"title":"Hypertension in Diabetes Mellitus","authors":"B. Williams","doi":"10.1093/med/9780198870197.003.0283","DOIUrl":"https://doi.org/10.1093/med/9780198870197.003.0283","url":null,"abstract":"High blood pressure (hypertension) is very common in people with diabetes. There is moreover an association between hypertension and diabetes that tracks through life, while the blood glucose concentration of young non-diabetic individuals has been shown to predict risk of future hypertension. Conversely, people with hypertension are twice as likely to develop type 2 diabetes over their lifetime. High blood pressure (hypertension) is arguably the most important preventable cause of premature microvascular and macrovascular disease and their associated morbidity and mortality in people with diabetes. This chapter will review key aspects of the epidemiology and pathophysiology of hypertension in people with diabetes, as well as recommended approaches to its clinical evaluation and treatment.","PeriodicalId":130301,"journal":{"name":"Oxford Textbook of Endocrinology and Diabetes 3e","volume":"138 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"133172393","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-07-01DOI: 10.1093/med/9780198870197.003.0071
C. Moran, M. Gurnell, K. Chatterjee
Disorders of cellular uptake, metabolism, or action of thyroid hormones comprise syndromes of resistance to thyroid hormone. Reduced entry of thyroid hormones into the central nervous system via a membrane transporter mediates severe mental and psychomotor retardation associated with peripheral hyperthyroidism. Failure of selenocysteine incorporation into 25 different proteins results in a multisystem, selenoprotein deficiency, disorder associated with abnormal thyroid function due to impaired activity of deiodinase selenoenzymes. Resistance to Thyroid Hormone β, due to thyroid hormone β receptor mutations, is characterized by elevated circulating thyroid hormones, impaired feedback inhibition of thyroid-stimulating hormone (TSH) secretion and variable hormone resistance in peripheral tissues. Thyroid hormone receptor α defects cause resistance to thyroid hormone α, characterized by features of hypothyroidism in specific tissues but paradoxically associated with near-normal thyroid hormone levels. We describe the genetic basis, clinical features, pathogenesis, and management of these disorders.
{"title":"Syndromes of Resistance to Thyroid Hormone","authors":"C. Moran, M. Gurnell, K. Chatterjee","doi":"10.1093/med/9780198870197.003.0071","DOIUrl":"https://doi.org/10.1093/med/9780198870197.003.0071","url":null,"abstract":"Disorders of cellular uptake, metabolism, or action of thyroid hormones comprise syndromes of resistance to thyroid hormone. Reduced entry of thyroid hormones into the central nervous system via a membrane transporter mediates severe mental and psychomotor retardation associated with peripheral hyperthyroidism. Failure of selenocysteine incorporation into 25 different proteins results in a multisystem, selenoprotein deficiency, disorder associated with abnormal thyroid function due to impaired activity of deiodinase selenoenzymes. Resistance to Thyroid Hormone β, due to thyroid hormone β receptor mutations, is characterized by elevated circulating thyroid hormones, impaired feedback inhibition of thyroid-stimulating hormone (TSH) secretion and variable hormone resistance in peripheral tissues. Thyroid hormone receptor α defects cause resistance to thyroid hormone α, characterized by features of hypothyroidism in specific tissues but paradoxically associated with near-normal thyroid hormone levels. We describe the genetic basis, clinical features, pathogenesis, and management of these disorders.","PeriodicalId":130301,"journal":{"name":"Oxford Textbook of Endocrinology and Diabetes 3e","volume":"20 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"133751199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-07-01DOI: 10.1093/med/9780198870197.003.0061
N. Perrier, O. Clark, S. Fisher
Antithyroid medications, radioactive iodine, or thyroidectomy are viable therapeutic options for the patient with thyrotoxicosis, with relative pros and cons for each modality varying with patient comorbidities and preferences, and the expertise of the treating physicians. Of the three modalities, surgery is the most invasive but also the most definitive, and is favoured for patients with symptomatic compression, concomitant documented/suspected malignancy, or coexisting hyperparathyroidism requiring surgical intervention. Thyroidectomy for treatment of thyrotoxicosis is also advantageous for women who are pregnant, lactating, or planning pregnancy, for patients with moderate to severe Graves’ orbitopathy, or when immediate control of symptoms is necessary. In experienced hands, thyroidectomy is performed with minimal morbidity and should be considered in the patient who places more relative emphasis on prompt and definitive control of symptoms with avoidance of radioactive therapy and/or medications, with less concerns regarding operative risks and/or need for lifelong thyroid hormone replacement.
{"title":"Surgery for Thyrotoxicosis","authors":"N. Perrier, O. Clark, S. Fisher","doi":"10.1093/med/9780198870197.003.0061","DOIUrl":"https://doi.org/10.1093/med/9780198870197.003.0061","url":null,"abstract":"Antithyroid medications, radioactive iodine, or thyroidectomy are viable therapeutic options for the patient with thyrotoxicosis, with relative pros and cons for each modality varying with patient comorbidities and preferences, and the expertise of the treating physicians. Of the three modalities, surgery is the most invasive but also the most definitive, and is favoured for patients with symptomatic compression, concomitant documented/suspected malignancy, or coexisting hyperparathyroidism requiring surgical intervention. Thyroidectomy for treatment of thyrotoxicosis is also advantageous for women who are pregnant, lactating, or planning pregnancy, for patients with moderate to severe Graves’ orbitopathy, or when immediate control of symptoms is necessary. In experienced hands, thyroidectomy is performed with minimal morbidity and should be considered in the patient who places more relative emphasis on prompt and definitive control of symptoms with avoidance of radioactive therapy and/or medications, with less concerns regarding operative risks and/or need for lifelong thyroid hormone replacement.","PeriodicalId":130301,"journal":{"name":"Oxford Textbook of Endocrinology and Diabetes 3e","volume":"7 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"122477238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-07-01DOI: 10.1093/med/9780198870197.003.0167
A. Gambineri, D. Ibarra-Gasparini
Female infertility affects 8–15% of reproductive-aged couples worldwide and ovulatory disorders account of more than a quarter of cases. It is defined as the failure to establish a clinical pregnancy after 12 months of regular and unprotected sexual intercourse in women younger than 35 and after six months in women over the age of 35. The ovaries and the uterus are under the control of many hormones such as LH, FSH, thyroid hormones, GH, prolactin, glucocorticoids, and sex steroids. Thus, an excess or defect of these hormones may account for female infertility. This chapter explains in detail the mechanisms by which each hormone regulates folliculogenesis, uterus decidualization, and embryo implantation in order to understand the complex regulation of female reproduction and of its alteration.
{"title":"Exogenous Factors and Female Reproductive Health","authors":"A. Gambineri, D. Ibarra-Gasparini","doi":"10.1093/med/9780198870197.003.0167","DOIUrl":"https://doi.org/10.1093/med/9780198870197.003.0167","url":null,"abstract":"Female infertility affects 8–15% of reproductive-aged couples worldwide and ovulatory disorders account of more than a quarter of cases. It is defined as the failure to establish a clinical pregnancy after 12 months of regular and unprotected sexual intercourse in women younger than 35 and after six months in women over the age of 35. The ovaries and the uterus are under the control of many hormones such as LH, FSH, thyroid hormones, GH, prolactin, glucocorticoids, and sex steroids. Thus, an excess or defect of these hormones may account for female infertility. This chapter explains in detail the mechanisms by which each hormone regulates folliculogenesis, uterus decidualization, and embryo implantation in order to understand the complex regulation of female reproduction and of its alteration.","PeriodicalId":130301,"journal":{"name":"Oxford Textbook of Endocrinology and Diabetes 3e","volume":"46 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"117065146","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-07-01DOI: 10.1093/med/9780198870197.003.0103
W. Arlt
In 1855, Thomas Addison identified a clinical syndrome characterized by wasting and hyperpigmentation as the result of adrenal gland destruction. This landmark observation paved the way for progress in understanding and treating adrenal insufficiency, with the introduction of adrenal extracts for treatment of Addison’s disease by the groups of Hartman and Pfiffner in 1929. However, long-term survival of patients with adrenal insufficiency only became possible after the seminal work of Edward Kendall, Philip Hench, and Tadeus Reichstein on the characterization and therapeutic use of cortisone. In 1946, Lewis Sarrett, a Merck scientist, achieved a partial synthesis of cortisone, which marked the beginning of industrial-scale production of cortisone. In 1948, in a fundamental clinical experiment at the Mayo Clinic, the first patient with Addison’s received intravenous injections of Kendall’s Compound E, cortisone, resulting in ‘notable improvement of his condition’. This was followed by ground-breaking trials on the use of cortisone in rheumatoid arthritis. In November 1950, cortisone was made available to all physicians in the United States, which culminated in the award of the 1950 Nobel Prize in Medicine to Kendall, Hench, and Reichstein. This progress reached other countries and widespread availability of cortisone in the United Kingdom was achieved by joint efforts of Glaxo and the Medical Research Council. Though almost 150 years have passed since Addison’s landmark observations and 60 years since the introduction of life-saving cortisone, there are still advances and challensges in the management of adrenal insufficiency, summarized in this chapter.
1855年，托马斯·艾迪生(Thomas Addison)发现了一种临床综合征，其特征是肾上腺破坏导致的消耗和色素沉着。这一具有里程碑意义的观察为理解和治疗肾上腺功能不全铺平了道路，并在1929年由Hartman和pffner小组引入肾上腺提取物治疗Addison病。然而，只有在Edward Kendall, Philip Hench和Tadeus Reichstein对可的松的特性和治疗使用的开创性工作之后，肾上腺功能不全患者的长期生存才成为可能。1946年，默克公司的科学家Lewis Sarrett实现了可的松的部分合成，这标志着可的松工业规模生产的开始。1948年，在梅奥诊所进行的一项基础临床实验中，第一位艾迪生患者接受了肯德尔化合物E可的松的静脉注射，结果“他的病情有了显著改善”。随后是可的松治疗类风湿性关节炎的开创性试验。1950年11月，可的松被提供给美国所有的医生，并最终将1950年诺贝尔医学奖授予肯德尔、亨奇和赖希斯坦。这一进展传到了其他国家，可的松在联合王国的广泛供应是由葛兰素史克和医学研究委员会共同努力实现的。尽管距Addison里程碑式的观察已近150年，距救命的可的松问世已近60年，但肾上腺功能不全的治疗仍有进展和挑战，本章将对此进行总结。
{"title":"Management of Adrenal Insufficiency","authors":"W. Arlt","doi":"10.1093/med/9780198870197.003.0103","DOIUrl":"https://doi.org/10.1093/med/9780198870197.003.0103","url":null,"abstract":"In 1855, Thomas Addison identified a clinical syndrome characterized by wasting and hyperpigmentation as the result of adrenal gland destruction. This landmark observation paved the way for progress in understanding and treating adrenal insufficiency, with the introduction of adrenal extracts for treatment of Addison’s disease by the groups of Hartman and Pfiffner in 1929. However, long-term survival of patients with adrenal insufficiency only became possible after the seminal work of Edward Kendall, Philip Hench, and Tadeus Reichstein on the characterization and therapeutic use of cortisone. In 1946, Lewis Sarrett, a Merck scientist, achieved a partial synthesis of cortisone, which marked the beginning of industrial-scale production of cortisone. In 1948, in a fundamental clinical experiment at the Mayo Clinic, the first patient with Addison’s received intravenous injections of Kendall’s Compound E, cortisone, resulting in ‘notable improvement of his condition’. This was followed by ground-breaking trials on the use of cortisone in rheumatoid arthritis. In November 1950, cortisone was made available to all physicians in the United States, which culminated in the award of the 1950 Nobel Prize in Medicine to Kendall, Hench, and Reichstein. This progress reached other countries and widespread availability of cortisone in the United Kingdom was achieved by joint efforts of Glaxo and the Medical Research Council. Though almost 150 years have passed since Addison’s landmark observations and 60 years since the introduction of life-saving cortisone, there are still advances and challensges in the management of adrenal insufficiency, summarized in this chapter.","PeriodicalId":130301,"journal":{"name":"Oxford Textbook of Endocrinology and Diabetes 3e","volume":"37 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"114950085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-07-01DOI: 10.1093/med/9780198870197.003.0241
S. Persaud, P. Jones
This chapter provides an overview of the physiological mechanisms underlying appropriate control of blood glucose levels. In particular, it focuses on the anatomy and cellular composition of islets of Langerhans; regulation of synthesis and storage of the anabolic hormone insulin in secretory granules of islet beta-cells; cellular mechanisms by which elevations in blood glucose levels stimulate insulin release from beta-cells by a process known as exocytosis; modulation of glucose-stimulated insulin secretion by hormones and neurotransmitters; and the physiological signal transduction pathways used by insulin to stimulate storage of fuels in adipose tissue, liver, and skeletal muscle. It also reviews the deleterious effects of chronic hyperglycaemia that are responsible for diabetic complications.
{"title":"Physiology of Glucose Homeostasis","authors":"S. Persaud, P. Jones","doi":"10.1093/med/9780198870197.003.0241","DOIUrl":"https://doi.org/10.1093/med/9780198870197.003.0241","url":null,"abstract":"This chapter provides an overview of the physiological mechanisms underlying appropriate control of blood glucose levels. In particular, it focuses on the anatomy and cellular composition of islets of Langerhans; regulation of synthesis and storage of the anabolic hormone insulin in secretory granules of islet beta-cells; cellular mechanisms by which elevations in blood glucose levels stimulate insulin release from beta-cells by a process known as exocytosis; modulation of glucose-stimulated insulin secretion by hormones and neurotransmitters; and the physiological signal transduction pathways used by insulin to stimulate storage of fuels in adipose tissue, liver, and skeletal muscle. It also reviews the deleterious effects of chronic hyperglycaemia that are responsible for diabetic complications.","PeriodicalId":130301,"journal":{"name":"Oxford Textbook of Endocrinology and Diabetes 3e","volume":"6 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"115364756","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-07-01DOI: 10.1093/med/9780198870197.003.0271
J. Tomlinson
Diabetes mellitus is associated with a variety of endocrine conditions affecting the pituitary, adrenal, and thyroid glands. It may occur as a consequence of hormonal excess (or less commonly deficiency) which interferes with either the secretion and/or the action of insulin. Diabetes is often diagnosed as part of the diagnostic work-up during an oral glucose tolerance test when glucose excursions can be measured alongside assessing the ability of a glucose load to suppress growth hormone levels. These associated conditions can include acromegaly, Cushing’s disease, hypo- and hyperthyroid, hyperaldosteronism, phaeochromocytoma, somatostatinoma, and glucagonoma. While the principles of management may not differ (and include treating the underling endocrine disease), the fundamental importance lies in making the diagnosis so that appropriate treatment can be instigated without delay.
{"title":"Diabetes Secondary to Endocrine Disorders","authors":"J. Tomlinson","doi":"10.1093/med/9780198870197.003.0271","DOIUrl":"https://doi.org/10.1093/med/9780198870197.003.0271","url":null,"abstract":"Diabetes mellitus is associated with a variety of endocrine conditions affecting the pituitary, adrenal, and thyroid glands. It may occur as a consequence of hormonal excess (or less commonly deficiency) which interferes with either the secretion and/or the action of insulin. Diabetes is often diagnosed as part of the diagnostic work-up during an oral glucose tolerance test when glucose excursions can be measured alongside assessing the ability of a glucose load to suppress growth hormone levels. These associated conditions can include acromegaly, Cushing’s disease, hypo- and hyperthyroid, hyperaldosteronism, phaeochromocytoma, somatostatinoma, and glucagonoma.\u0000 While the principles of management may not differ (and include treating the underling endocrine disease), the fundamental importance lies in making the diagnosis so that appropriate treatment can be instigated without delay.","PeriodicalId":130301,"journal":{"name":"Oxford Textbook of Endocrinology and Diabetes 3e","volume":"67 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"115678207","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-07-01DOI: 10.1093/med/9780198870197.003.0097
E. Maher, R. Casey
Phaeochromocytomas, paragangliomas, and neuroblastomas are the main primary tumours that arise from the autonomic nervous system. The autonomic nervous system is subdivided into the sympathetic and parasympathetic systems. Phaeochromocytomas arise from sympathetic nervous system (chromaffin) cells in the adrenal medulla. Paragangliomas may arise from the sympathetic or parasympathetic system. The former, previously known as extra-adrenal phaeochromocytomas but referred herein as paragangliomas, typically occur along the sympathetic chain and, like phaeochromocytomas, are usually secretory and most commonly present with symptoms of excess catecholamine secretion. Parasympathetic ganglia-derived paragangliomas (herein referred to as head and neck paraganglioma, HNPGL) develop along branches of the vagal and glossopharyngeal nerves (e.g. carotid body tumours, glomus jugulare) and are only rarely secretory. Phaeochromocytoma, paraganglioma, and HNPGL are rare in childhood but neuroblastomas, which are derived from neuroblasts in the developing sympathetic nervous system and are most common in children under the age of 5 years. Familial forms of neuroblastoma are rare but a major feature of phaeochromocytoma and paraganglioma (PPGL) and HNPGL is the high frequency of inherited cases and the major inherited syndromic and non-syndromic disorders that predispose to these tumours are described in Chapter 6.13.
{"title":"Genetics of Phaeochromocytomas, Paragangliomas, and Neuroblastoma","authors":"E. Maher, R. Casey","doi":"10.1093/med/9780198870197.003.0097","DOIUrl":"https://doi.org/10.1093/med/9780198870197.003.0097","url":null,"abstract":"Phaeochromocytomas, paragangliomas, and neuroblastomas are the main primary tumours that arise from the autonomic nervous system. The autonomic nervous system is subdivided into the sympathetic and parasympathetic systems. Phaeochromocytomas arise from sympathetic nervous system (chromaffin) cells in the adrenal medulla. Paragangliomas may arise from the sympathetic or parasympathetic system. The former, previously known as extra-adrenal phaeochromocytomas but referred herein as paragangliomas, typically occur along the sympathetic chain and, like phaeochromocytomas, are usually secretory and most commonly present with symptoms of excess catecholamine secretion. Parasympathetic ganglia-derived paragangliomas (herein referred to as head and neck paraganglioma, HNPGL) develop along branches of the vagal and glossopharyngeal nerves (e.g. carotid body tumours, glomus jugulare) and are only rarely secretory. Phaeochromocytoma, paraganglioma, and HNPGL are rare in childhood but neuroblastomas, which are derived from neuroblasts in the developing sympathetic nervous system and are most common in children under the age of 5 years. Familial forms of neuroblastoma are rare but a major feature of phaeochromocytoma and paraganglioma (PPGL) and HNPGL is the high frequency of inherited cases and the major inherited syndromic and non-syndromic disorders that predispose to these tumours are described in Chapter 6.13.","PeriodicalId":130301,"journal":{"name":"Oxford Textbook of Endocrinology and Diabetes 3e","volume":"17 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"123352245","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-07-01DOI: 10.1093/med/9780198870197.003.0012
R. Ross
The aim of hormone replacement is to replace the missing physiological effects of a deficient hormone. The last century identified most of the endocrine hormones, which can now be replaced when deficient; however, the challenge of the twenty-first century is to optimize replacement. The guiding principle in hormone replacement is replicating the natural levels and rhythms of hormones at different ages but this requires a good understanding of physiology. There is a need for better biomarkers of hormone actions and using these to develop new ways to deliver hormone replacement tailored to the individual. This chapter discusses current approaches to this problem.
{"title":"Principles of Hormone Replacement","authors":"R. Ross","doi":"10.1093/med/9780198870197.003.0012","DOIUrl":"https://doi.org/10.1093/med/9780198870197.003.0012","url":null,"abstract":"The aim of hormone replacement is to replace the missing physiological effects of a deficient hormone. The last century identified most of the endocrine hormones, which can now be replaced when deficient; however, the challenge of the twenty-first century is to optimize replacement. The guiding principle in hormone replacement is replicating the natural levels and rhythms of hormones at different ages but this requires a good understanding of physiology. There is a need for better biomarkers of hormone actions and using these to develop new ways to deliver hormone replacement tailored to the individual. This chapter discusses current approaches to this problem.","PeriodicalId":130301,"journal":{"name":"Oxford Textbook of Endocrinology and Diabetes 3e","volume":"32 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"121337434","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-07-01DOI: 10.1093/med/9780198870197.003.0182
A. Hokken-Koelega
Small-for-gestational-age (SGA) is defined as a birth weight and/or length <–2 SDS. As the aetiology of SGA is multifactorial and includes maternal lifestyle and obstetric factors, placental dysfunction, and numerous (epi)genetic abnormalities, SGA-born children comprise a heterogeneous group. The majority of SGA-born infants show catch-up growth to a normal stature, but 10% remains short. For more than 30 years, studies have been performed in short children after SGA birth, including children with Silver–Russell syndrome (SRS). Studies have generally excluded short SGA children with major dysmorphic features or a (suspected) syndrome, primordial dwarfism, or DNA repair disorder. Thus present knowledge and management, particularly on GH treatment, are based on the results in non-syndromic short SGA/SRS children. This chapter presents our current knowledge of the (epi)genetic causes of short stature for those born SGA, the health consequences of SGA, and the diagnostic approach and management of short SGA-born children, including the efficacy and safety of GH treatment.
{"title":"Short Stature in Children Born Small for Gestational Age","authors":"A. Hokken-Koelega","doi":"10.1093/med/9780198870197.003.0182","DOIUrl":"https://doi.org/10.1093/med/9780198870197.003.0182","url":null,"abstract":"Small-for-gestational-age (SGA) is defined as a birth weight and/or length <–2 SDS. As the aetiology of SGA is multifactorial and includes maternal lifestyle and obstetric factors, placental dysfunction, and numerous (epi)genetic abnormalities, SGA-born children comprise a heterogeneous group. The majority of SGA-born infants show catch-up growth to a normal stature, but 10% remains short. For more than 30 years, studies have been performed in short children after SGA birth, including children with Silver–Russell syndrome (SRS). Studies have generally excluded short SGA children with major dysmorphic features or a (suspected) syndrome, primordial dwarfism, or DNA repair disorder. Thus present knowledge and management, particularly on GH treatment, are based on the results in non-syndromic short SGA/SRS children. This chapter presents our current knowledge of the (epi)genetic causes of short stature for those born SGA, the health consequences of SGA, and the diagnostic approach and management of short SGA-born children, including the efficacy and safety of GH treatment.","PeriodicalId":130301,"journal":{"name":"Oxford Textbook of Endocrinology and Diabetes 3e","volume":"5 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"123914059","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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