Pub Date : 2023-01-01DOI: 10.1177/20420188231199359
Jing Zhu, Yier Zhou, Bihui Jin, Jing Shu
Estrogen plays a prominent role in regulating and coordinating energy homeostasis throughout the growth, development, reproduction, and aging of women. Estrogen receptors (ERs) are widely expressed in the brain and nearly all tissues of the body. Within the brain, central estrogen via ER regulates appetite and energy expenditure and maintains cell glucose metabolism, including glucose transport, aerobic glycolysis, and mitochondrial function. In the whole body, estrogen has shown beneficial effects on weight control, fat distribution, glucose and insulin resistance, and adipokine secretion. As demonstrated by multiple in vitro and in vivo studies, menopause-related decline of circulating estrogen may induce the disturbance of metabolic signals and a significant decrease in bioenergetics, which could trigger an increased incidence of late-onset Alzheimer's disease, type 2 diabetes mellitus, hypertension, and cardiovascular diseases in postmenopausal women. In this article, we have systematically reviewed the role of estrogen and ERs in body composition and lipid/glucose profile variation occurring with menopause, which may provide a better insight into the efficacy of hormone therapy in maintaining energy metabolic homeostasis and hold a clue for development of novel therapeutic approaches for target tissue diseases.
{"title":"Role of estrogen in the regulation of central and peripheral energy homeostasis: from a menopausal perspective.","authors":"Jing Zhu, Yier Zhou, Bihui Jin, Jing Shu","doi":"10.1177/20420188231199359","DOIUrl":"https://doi.org/10.1177/20420188231199359","url":null,"abstract":"<p><p>Estrogen plays a prominent role in regulating and coordinating energy homeostasis throughout the growth, development, reproduction, and aging of women. Estrogen receptors (ERs) are widely expressed in the brain and nearly all tissues of the body. Within the brain, central estrogen <i>via</i> ER regulates appetite and energy expenditure and maintains cell glucose metabolism, including glucose transport, aerobic glycolysis, and mitochondrial function. In the whole body, estrogen has shown beneficial effects on weight control, fat distribution, glucose and insulin resistance, and adipokine secretion. As demonstrated by multiple <i>in vitro</i> and <i>in vivo</i> studies, menopause-related decline of circulating estrogen may induce the disturbance of metabolic signals and a significant decrease in bioenergetics, which could trigger an increased incidence of late-onset Alzheimer's disease, type 2 diabetes mellitus, hypertension, and cardiovascular diseases in postmenopausal women. In this article, we have systematically reviewed the role of estrogen and ERs in body composition and lipid/glucose profile variation occurring with menopause, which may provide a better insight into the efficacy of hormone therapy in maintaining energy metabolic homeostasis and hold a clue for development of novel therapeutic approaches for target tissue diseases.</p>","PeriodicalId":22998,"journal":{"name":"Therapeutic Advances in Endocrinology and Metabolism","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/b2/5d/10.1177_20420188231199359.PMC10504839.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10672034","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.1177/20420188221145549
Rosaria Maria Pipitone, Carlo Ciccioli, Giuseppe Infantino, Claudia La Mantia, Stefanie Parisi, Adele Tulone, Grazia Pennisi, Stefania Grimaudo, Salvatore Petta
Nonalcoholic fatty liver disease (NAFLD), affecting about 25% of general population and more than 50% of dysmetabolic patients, is an emerging cause of chronic liver disease and its complications. Recently, an international consensus of experts proposed to rename this disease as 'Metabolic dysfunction-Associated Fatty Liver Disease' (MAFLD) to focus on the bidirectional interplay between fatty liver and metabolic alterations and to stress the need of assessing fatty liver independently from alcohol consumption and other coexisting causes of liver disease. The peculiarity of NAFLD/MAFLD lies in the presence of a higher risk of not only - as expected - liver-related events but also of extrahepatic events, mostly cardiovascular and cancers. Available evidence suggests that these associations are not only the expression of sharing the same risk factors but shed light about the ability of NAFLD/MAFLD and particularly of its progressive form - nonalcoholic/metabolic dysfunction-associated steatohepatitis - to act as an independent risk factor via promotion of atherogenic dyslipidemia and a proinflammatory, profibrogenic, and procoagulant systemic environment. The present review summarizes available epidemiological and clinical evidence supporting the concept of NAFLD/MAFLD as a multisystemic disease, and highlights potential explanatory mechanisms underlying the association between NAFLD/MAFLD and extrahepatic disorders.
{"title":"MAFLD: a multisystem disease.","authors":"Rosaria Maria Pipitone, Carlo Ciccioli, Giuseppe Infantino, Claudia La Mantia, Stefanie Parisi, Adele Tulone, Grazia Pennisi, Stefania Grimaudo, Salvatore Petta","doi":"10.1177/20420188221145549","DOIUrl":"https://doi.org/10.1177/20420188221145549","url":null,"abstract":"<p><p>Nonalcoholic fatty liver disease (NAFLD), affecting about 25% of general population and more than 50% of dysmetabolic patients, is an emerging cause of chronic liver disease and its complications. Recently, an international consensus of experts proposed to rename this disease as 'Metabolic dysfunction-Associated Fatty Liver Disease' (MAFLD) to focus on the bidirectional interplay between fatty liver and metabolic alterations and to stress the need of assessing fatty liver independently from alcohol consumption and other coexisting causes of liver disease. The peculiarity of NAFLD/MAFLD lies in the presence of a higher risk of not only - as expected - liver-related events but also of extrahepatic events, mostly cardiovascular and cancers. Available evidence suggests that these associations are not only the expression of sharing the same risk factors but shed light about the ability of NAFLD/MAFLD and particularly of its progressive form - nonalcoholic/metabolic dysfunction-associated steatohepatitis - to act as an independent risk factor <i>via</i> promotion of atherogenic dyslipidemia and a proinflammatory, profibrogenic, and procoagulant systemic environment. The present review summarizes available epidemiological and clinical evidence supporting the concept of NAFLD/MAFLD as a multisystemic disease, and highlights potential explanatory mechanisms underlying the association between NAFLD/MAFLD and extrahepatic disorders.</p>","PeriodicalId":22998,"journal":{"name":"Therapeutic Advances in Endocrinology and Metabolism","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/72/85/10.1177_20420188221145549.PMC9885036.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9194249","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.1177/20420188231157194
Jun Tang
maturation are favored over osteoblastogenesis, resulting in bone loss and fracture risks
{"title":"Immune checkpoint inhibitors: friend or foe for osteoporosis.","authors":"Jun Tang","doi":"10.1177/20420188231157194","DOIUrl":"https://doi.org/10.1177/20420188231157194","url":null,"abstract":"maturation are favored over osteoblastogenesis, resulting in bone loss and fracture risks","PeriodicalId":22998,"journal":{"name":"Therapeutic Advances in Endocrinology and Metabolism","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/ac/f2/10.1177_20420188231157194.PMC9983083.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10838776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.1177/20420188231170754
Baodi Xing, Jie Yu, Huabing Zhang, Yuxiu Li
Accumulating evidence demonstrates the link between glucose and bone metabolism. The receptor activator of nuclear factor-kB ligand (RANKL)/the receptor activator of NF-κB (RANK)/osteoprotegerin (OPG) axis is an essential signaling axis maintaining the balance between bone resorption and bone formation. In recent years, it has been found that RANKL and RANK are distributed not only in bone but also in the liver, muscle, adipose tissue, pancreas, and other tissues that may influence glucose metabolism. Some scholars have suggested that the blockage of the RANKL signaling may protect islet β-cell function and prevent diabetes; simultaneously, there also exist different views that RANKL can improve insulin resistance through inducing the beige adipocyte differentiation and increase energy expenditure. Currently, the results of the regulatory effect on glucose metabolism of RANKL remain conflicting. Denosumab (Dmab), a fully human monoclonal antibody that can bind to RANKL and prevent osteoclast formation, is a commonly used antiosteoporosis drug. Recent basic studies have found that Dmab seems to regulate glucose homeostasis and β-cell function in humanized mice or in vitro human β-cell models. Besides, some clinical data have also reported the glucometabolic effects of Dmab, however, with limited and inconsistent results. This review mainly describes the impact of the RANKL signaling pathway on glucose metabolism and summarizes clinical evidence that links Dmab and DM to seek a new therapeutic strategy for diabetes.
{"title":"RANKL inhibition: a new target of treating diabetes mellitus?","authors":"Baodi Xing, Jie Yu, Huabing Zhang, Yuxiu Li","doi":"10.1177/20420188231170754","DOIUrl":"https://doi.org/10.1177/20420188231170754","url":null,"abstract":"<p><p>Accumulating evidence demonstrates the link between glucose and bone metabolism. The receptor activator of nuclear factor-kB ligand (RANKL)/the receptor activator of NF-κB (RANK)/osteoprotegerin (OPG) axis is an essential signaling axis maintaining the balance between bone resorption and bone formation. In recent years, it has been found that RANKL and RANK are distributed not only in bone but also in the liver, muscle, adipose tissue, pancreas, and other tissues that may influence glucose metabolism. Some scholars have suggested that the blockage of the RANKL signaling may protect islet β-cell function and prevent diabetes; simultaneously, there also exist different views that RANKL can improve insulin resistance through inducing the beige adipocyte differentiation and increase energy expenditure. Currently, the results of the regulatory effect on glucose metabolism of RANKL remain conflicting. Denosumab (Dmab), a fully human monoclonal antibody that can bind to RANKL and prevent osteoclast formation, is a commonly used antiosteoporosis drug. Recent basic studies have found that Dmab seems to regulate glucose homeostasis and β-cell function in humanized mice or <i>in vitro</i> human β-cell models. Besides, some clinical data have also reported the glucometabolic effects of Dmab, however, with limited and inconsistent results. This review mainly describes the impact of the RANKL signaling pathway on glucose metabolism and summarizes clinical evidence that links Dmab and DM to seek a new therapeutic strategy for diabetes.</p>","PeriodicalId":22998,"journal":{"name":"Therapeutic Advances in Endocrinology and Metabolism","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/b7/34/10.1177_20420188231170754.PMC10201162.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10300121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.1177/20420188231173327
Ploutarchos Tzoulis, Gregory Kaltsas, Stephanie E Baldeweg, Pierre-Marc Bouloux, Ashley B Grossman
The syndrome of inappropriate antidiuresis (SIAD), the commonest cause of hyponatraemia, is associated with significant morbidity and mortality. Tolvaptan, an oral vasopressin V2-receptor antagonist, leads through aquaresis to an increase in serum sodium concentration and is the only medication licenced in Europe for the treatment of euvolaemic hyponatraemia. Randomised controlled trials have shown that tolvaptan is highly efficacious in correcting SIAD-related hyponatraemia. Real-world data have confirmed the marked efficacy of tolvaptan, but they have also reported a high risk of overly rapid sodium increase in patients with a very low baseline serum sodium. The lower the baseline serum sodium, the higher the tolvaptan-induced correction rate occurs. Therefore, a lower starting tolvaptan dose of 7.5 mg has been evaluated in small cohort studies, demonstrating its efficacy, but it still remains unclear as to whether it can reduce the risk of overcorrection. Most international guidelines, except for the European ones, recommend tolvaptan as second-line treatment for SIAD after fluid restriction. However, the risk of unduly rapid sodium correction in combination with its high cost have limited its routine use. Prospective controlled studies are warranted to evaluate whether tolvaptan-related sodium increase can improve patient-related clinical outcomes, such as mortality and length of hospital stay in the acute setting or neurocognitive symptoms and quality of life in the chronic setting. In addition, the potential role of a low tolvaptan starting dose needs to be further explored. Until then, tolvaptan should mainly be used as second-line treatment for SIAD, especially when there is a clinical need for prompt restoration of normonatraemia. Tolvaptan should be used with specialist input according to a structured clinical pathway, including rigorous monitoring of electrolyte and fluid balance and, if needed, implementation of appropriate measures to prevent, or when necessary reverse, overly rapid hyponatraemia correction.
{"title":"Tolvaptan for the treatment of the syndrome of inappropriate antidiuresis (SIAD).","authors":"Ploutarchos Tzoulis, Gregory Kaltsas, Stephanie E Baldeweg, Pierre-Marc Bouloux, Ashley B Grossman","doi":"10.1177/20420188231173327","DOIUrl":"https://doi.org/10.1177/20420188231173327","url":null,"abstract":"<p><p>The syndrome of inappropriate antidiuresis (SIAD), the commonest cause of hyponatraemia, is associated with significant morbidity and mortality. Tolvaptan, an oral vasopressin V2-receptor antagonist, leads through aquaresis to an increase in serum sodium concentration and is the only medication licenced in Europe for the treatment of euvolaemic hyponatraemia. Randomised controlled trials have shown that tolvaptan is highly efficacious in correcting SIAD-related hyponatraemia. Real-world data have confirmed the marked efficacy of tolvaptan, but they have also reported a high risk of overly rapid sodium increase in patients with a very low baseline serum sodium. The lower the baseline serum sodium, the higher the tolvaptan-induced correction rate occurs. Therefore, a lower starting tolvaptan dose of 7.5 mg has been evaluated in small cohort studies, demonstrating its efficacy, but it still remains unclear as to whether it can reduce the risk of overcorrection. Most international guidelines, except for the European ones, recommend tolvaptan as second-line treatment for SIAD after fluid restriction. However, the risk of unduly rapid sodium correction in combination with its high cost have limited its routine use. Prospective controlled studies are warranted to evaluate whether tolvaptan-related sodium increase can improve patient-related clinical outcomes, such as mortality and length of hospital stay in the acute setting or neurocognitive symptoms and quality of life in the chronic setting. In addition, the potential role of a low tolvaptan starting dose needs to be further explored. Until then, tolvaptan should mainly be used as second-line treatment for SIAD, especially when there is a clinical need for prompt restoration of normonatraemia. Tolvaptan should be used with specialist input according to a structured clinical pathway, including rigorous monitoring of electrolyte and fluid balance and, if needed, implementation of appropriate measures to prevent, or when necessary reverse, overly rapid hyponatraemia correction.</p>","PeriodicalId":22998,"journal":{"name":"Therapeutic Advances in Endocrinology and Metabolism","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/c5/c1/10.1177_20420188231173327.PMC10192810.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9496947","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.1177/20420188231180983
Julie Chen
Hyponatremia is one of the most common lab abnormalities seen in clinical practice. It has become widely accepted that hypothyroidism is a cause of euvolemic hyponatremia. The primary mechanism is thought to be due to impaired free water excretion and changes in sodium handling in the kidney. However, the clinical studies are conflicting and do not definitively confirm the association between hypothyroidism and hyponatremia. Therefore, if severe hyponatremia occurs in a patient without myxedema coma, other potential etiologies should be sought.
{"title":"Is there a causal relationship between hypothyroidism and hyponatremia?","authors":"Julie Chen","doi":"10.1177/20420188231180983","DOIUrl":"https://doi.org/10.1177/20420188231180983","url":null,"abstract":"<p><p>Hyponatremia is one of the most common lab abnormalities seen in clinical practice. It has become widely accepted that hypothyroidism is a cause of euvolemic hyponatremia. The primary mechanism is thought to be due to impaired free water excretion and changes in sodium handling in the kidney. However, the clinical studies are conflicting and do not definitively confirm the association between hypothyroidism and hyponatremia. Therefore, if severe hyponatremia occurs in a patient without myxedema coma, other potential etiologies should be sought.</p>","PeriodicalId":22998,"journal":{"name":"Therapeutic Advances in Endocrinology and Metabolism","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/97/30/10.1177_20420188231180983.PMC10331073.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9805312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.1177/20420188231178371
Jensen Reckhow, Hakan Kula, Samir Babayev
Transgender and nonbinary individuals are historically underserved by healthcare systems. A crucial area for improvement is fertility preservation counseling and service delivery, as gender-affirming hormone therapy and gender-affirming surgery may negatively affect future fertility. The methods available for fertility preservation depend on the patient's pubertal status and utilization of gender-affirming therapies, and counseling and delivery of these services are complex and require a multidisciplinary approach. Further research is needed to identify pertinent stakeholders in managing the care of these patients, as well as to better understand the optimal frameworks for delivering integrated and comprehensive care to this patient population. Fertility preservation is an active and exciting area of scientific discovery and offers a wealth of opportunities to improve the care of transgender and nonbinary individuals.
{"title":"Fertility preservation options for transgender and nonbinary individuals.","authors":"Jensen Reckhow, Hakan Kula, Samir Babayev","doi":"10.1177/20420188231178371","DOIUrl":"https://doi.org/10.1177/20420188231178371","url":null,"abstract":"<p><p>Transgender and nonbinary individuals are historically underserved by healthcare systems. A crucial area for improvement is fertility preservation counseling and service delivery, as gender-affirming hormone therapy and gender-affirming surgery may negatively affect future fertility. The methods available for fertility preservation depend on the patient's pubertal status and utilization of gender-affirming therapies, and counseling and delivery of these services are complex and require a multidisciplinary approach. Further research is needed to identify pertinent stakeholders in managing the care of these patients, as well as to better understand the optimal frameworks for delivering integrated and comprehensive care to this patient population. Fertility preservation is an active and exciting area of scientific discovery and offers a wealth of opportunities to improve the care of transgender and nonbinary individuals.</p>","PeriodicalId":22998,"journal":{"name":"Therapeutic Advances in Endocrinology and Metabolism","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/06/fc/10.1177_20420188231178371.PMC10265329.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9708989","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.1177/20420188231185958
Nicole Kattner
The different types of diabetes differ in disease pathogenesis but share the impairment or loss of β-cell function leading to chronic hyperglycaemia. While immune cells are present throughout the whole pancreas in normality, their number and activation is increased in diabetes. Different patterns and composition of inflammation could be observed in type 1, type 2 and type 3c diabetes. Immune cells, pancreatic stellate cells and fibrosis were present in the islet microenvironment and could add to β-cell dysfunction and therefore development and progression of diabetes. First studies investigating the use of anti-inflammatory drugs demonstrate their ability to rescue remaining β-cell function and their potential benefit in diabetes treatment. This article provides an overview of immune cell infiltrates in different types of diabetes, highlights the knowledge of their impact on β-cell function and introduces the potential of immunomodulatory strategies.
{"title":"Immune cell infiltration in the pancreas of type 1, type 2 and type 3c diabetes.","authors":"Nicole Kattner","doi":"10.1177/20420188231185958","DOIUrl":"https://doi.org/10.1177/20420188231185958","url":null,"abstract":"<p><p>The different types of diabetes differ in disease pathogenesis but share the impairment or loss of β-cell function leading to chronic hyperglycaemia. While immune cells are present throughout the whole pancreas in normality, their number and activation is increased in diabetes. Different patterns and composition of inflammation could be observed in type 1, type 2 and type 3c diabetes. Immune cells, pancreatic stellate cells and fibrosis were present in the islet microenvironment and could add to β-cell dysfunction and therefore development and progression of diabetes. First studies investigating the use of anti-inflammatory drugs demonstrate their ability to rescue remaining β-cell function and their potential benefit in diabetes treatment. This article provides an overview of immune cell infiltrates in different types of diabetes, highlights the knowledge of their impact on β-cell function and introduces the potential of immunomodulatory strategies.</p>","PeriodicalId":22998,"journal":{"name":"Therapeutic Advances in Endocrinology and Metabolism","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/e7/f1/10.1177_20420188231185958.PMC10387691.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10649802","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.1177/20420188221145550
Laure Boutsen, Elise Costenoble, Olivier Pollé, Kezban Erdem, Céline Bugli, Philippe A Lysy
Objective: To evaluate the residual effect of partial remission (PR) on immediate post-PR glycemic control according to its occurrence and duration in a cohort of children with type 1 diabetes mellitus (T1DM).
Patients and methods: Values of glycemic control parameters [i.e. HbA1C, insulin dose-adjusted hemoglobin A1C (IDAA1C), glycemic target-adjusted HbA1C (GTAA1C)] and data from glucose monitoring devices from 189 pediatric patients with new-onset type 1 diabetes were collected retrospectively from 24 months. Patients were characterized according to their remission status (PR+ and PR-). PR+ patients were subdivided into three subgroups regarding PR duration [i.e. short (⩾3-⩽6 months), intermediate (>6-⩽12 months), and long PR (>12-⩽14 months)]. We compared glycemic control data from each PR+ subgroup at +6 and +12 months post-PR with PR- patients at the same postdiagnosis time. Second, PR+ subgroups were compared with each other.
Results: PR+ patients showed improved glycemic control (i.e. HbA1C, IDAA1C, and GTAA1C) at + 6 months post-PR when compared with nonremitters (PR-), independently of the PR duration subgroups (p < 0.05). Interestingly, patients in long PR+ subgroup exhibited higher positive residual effect than short PR+ subgroup with lower GTAA1C scores (p = 0.02), better time in range (TIR) (p = 0.003), less time in hypoglycemia (10.45 versus 16.13%, p = 0.03) and less glycemic variability (83.1 mg/dl versus 98.84 mg/dl, p = 0.03). No significant differences were found for glucose control between PR+ and PR- patients at +12 months post-PR.
Conclusion: This study supports the positive impact of PR occurrence and duration on short-term metabolic control (better HbA1C levels, IDAA1C and GTAA1C scores, TIR, and less glycemic variability) with the residual effect increasing according to PR duration.
{"title":"Influence of the occurrence and duration of partial remission on short-term metabolic control in type 1 diabetes: the DIABHONEY pediatric study.","authors":"Laure Boutsen, Elise Costenoble, Olivier Pollé, Kezban Erdem, Céline Bugli, Philippe A Lysy","doi":"10.1177/20420188221145550","DOIUrl":"https://doi.org/10.1177/20420188221145550","url":null,"abstract":"<p><strong>Objective: </strong>To evaluate the residual effect of partial remission (PR) on immediate post-PR glycemic control according to its occurrence and duration in a cohort of children with type 1 diabetes mellitus (T1DM).</p><p><strong>Patients and methods: </strong>Values of glycemic control parameters [i.e. HbA<sub>1C</sub>, insulin dose-adjusted hemoglobin A<sub>1C</sub> (IDAA<sub>1C</sub>), glycemic target-adjusted HbA<sub>1C</sub> (GTAA<sub>1C</sub>)] and data from glucose monitoring devices from 189 pediatric patients with new-onset type 1 diabetes were collected retrospectively from 24 months. Patients were characterized according to their remission status (PR<sup>+</sup> and PR<sup>-</sup>). PR<sup>+</sup> patients were subdivided into three subgroups regarding PR duration [i.e. short (⩾3-⩽6 months), intermediate (>6-⩽12 months), and long PR (>12-⩽14 months)]. We compared glycemic control data from each PR<sup>+</sup> subgroup at +6 and +12 months post-PR with PR<sup>-</sup> patients at the same postdiagnosis time. Second, PR<sup>+</sup> subgroups were compared with each other.</p><p><strong>Results: </strong>PR<sup>+</sup> patients showed improved glycemic control (i.e. HbA<sub>1C</sub>, IDAA<sub>1C</sub>, and GTAA<sub>1C</sub>) at + 6 months post-PR when compared with nonremitters (PR<sup>-</sup>), independently of the PR duration subgroups (p < 0.05). Interestingly, patients in long PR<sup>+</sup> subgroup exhibited higher positive residual effect than short PR<sup>+</sup> subgroup with lower GTAA<sub>1C</sub> scores (p = 0.02), better time in range (TIR) (p = 0.003), less time in hypoglycemia (10.45 <i>versus</i> 16.13%, p = 0.03) and less glycemic variability (83.1 mg/dl <i>versus</i> 98.84 mg/dl, p = 0.03). No significant differences were found for glucose control between PR<sup>+</sup> and PR<sup>-</sup> patients at +12 months post-PR.</p><p><strong>Conclusion: </strong>This study supports the positive impact of PR occurrence and duration on short-term metabolic control (better HbA<sub>1C</sub> levels, IDAA<sub>1C</sub> and GTAA<sub>1C</sub> scores, TIR, and less glycemic variability) with the residual effect increasing according to PR duration.</p>","PeriodicalId":22998,"journal":{"name":"Therapeutic Advances in Endocrinology and Metabolism","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/e8/a6/10.1177_20420188221145550.PMC9869204.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10624430","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.1177/20420188231173325
Kevin K W Kuan, Sean Omoseni, Javier A Tello
Background: Endometriosis is an oestrogen-dependent disease that can cause subfertility in women who may require assisted reproductive technology (ART) to achieve their pregnancy goals.
Objectives: The aim of this study was to compare ART outcomes in women with endometriosis following the long GnRH-agonist controlled ovarian stimulation (COS) protocol with those taking the GnRH-antagonist COS protocol.
Data sources and methods: MEDLINE, Embase and Web of Science were systematically searched in June 2022. Randomized controlled trials (RCTs) and observational studies comparing the long GnRH-agonist COS protocol and the GnRH-antagonist COS protocol in women with all stages/subtypes of endometriosis were included. Data were synthesized into comprehensive tables for systematic review. The Scottish Intercollegiate Guidelines Network (SIGN) checklists were used for the risk of bias assessment of non-randomized studies and randomized studies, and all the included studies were deemed to have acceptable quality.
Main results: Eight studies (one RCT and seven observational) with 2695 patients (2761 cycles) were included. Most studies generally reported non-significant differences in clinical pregnancy or live birth rates regardless of the COS protocol used. However, the GnRH-agonist protocol may yield a higher total number of oocytes retrieved, especially mature oocytes. Conversely, the GnRH-antagonist protocol required a shorter COS duration and lower gonadotrophin dose. Adverse outcomes, such as rates of cycle cancellation and miscarriage, were similar between both COS protocols.
Conclusion: Both the long GnRH-agonist and GnRH-antagonist COS protocols generally yield similar pregnancy outcomes. However, the long GnRH-agonist protocol may be associated with a higher cumulative pregnancy rate due to the higher number of retrieved oocytes available for cryopreservation. The underlying mechanisms of the two COS protocols on the female reproductive tract remain unclear. Clinicians should consider treatment costs, stage/subtype of endometriosis and pregnancy goals of their patients when selecting a GnRH analogue for COS. A well-powered RCT is needed to minimize the risk of bias and compare the risk for ovarian hyperstimulation syndrome.
Registration: This review was prospectively registered at PROSPERO under Registration No. CRD42022327604.
背景:子宫内膜异位症是一种雌激素依赖性疾病,可导致需要辅助生殖技术(ART)来实现妊娠目标的妇女生育能力低下。目的:本研究的目的是比较长期使用gnrh激动剂控制卵巢刺激(COS)方案和使用gnrh拮抗剂控制卵巢刺激(COS)方案的子宫内膜异位症妇女的ART结果。数据来源和方法:2022年6月系统检索MEDLINE、Embase和Web of Science。随机对照试验(RCTs)和观察性研究比较了长gnrh激动剂COS方案和gnrh拮抗剂COS方案在所有阶段/亚型子宫内膜异位症妇女中的应用。将数据合成综合表进行系统评价。苏格兰校际指南网络(SIGN)检查表用于非随机研究和随机研究的偏倚风险评估,所有纳入的研究都被认为具有可接受的质量。主要结果:纳入8项研究(1项RCT和7项观察性研究),共2695例患者(2761个周期)。大多数研究普遍报道,无论使用何种COS方案,临床妊娠率或活产率均无显著差异。然而,gnrh激动剂方案可能产生更高的卵母细胞总数,特别是成熟卵母细胞。相反,gnrh拮抗剂方案需要更短的COS持续时间和更低的促性腺激素剂量。不良结果,如周期取消率和流产率,在两种COS方案之间相似。结论:长gnrh激动剂和gnrh拮抗剂COS方案通常产生相似的妊娠结局。然而,长gnrh激动剂方案可能与较高的累积妊娠率相关,因为可用于冷冻保存的卵母细胞数量较多。两种COS方案对女性生殖道的潜在机制尚不清楚。临床医生在选择GnRH类似物治疗COS时应考虑治疗费用、子宫内膜异位症的分期/亚型和患者的妊娠目标。需要一项功能完善的随机对照试验来降低偏倚风险,并比较卵巢过度刺激综合征的风险。注册:本综述在普洛斯彼罗前瞻性注册,注册号为。CRD42022327604。
{"title":"Comparing ART outcomes in women with endometriosis after GnRH agonist <i>versus</i> GnRH antagonist ovarian stimulation: a systematic review.","authors":"Kevin K W Kuan, Sean Omoseni, Javier A Tello","doi":"10.1177/20420188231173325","DOIUrl":"https://doi.org/10.1177/20420188231173325","url":null,"abstract":"<p><strong>Background: </strong>Endometriosis is an oestrogen-dependent disease that can cause subfertility in women who may require assisted reproductive technology (ART) to achieve their pregnancy goals.</p><p><strong>Objectives: </strong>The aim of this study was to compare ART outcomes in women with endometriosis following the long GnRH-agonist controlled ovarian stimulation (COS) protocol with those taking the GnRH-antagonist COS protocol.</p><p><strong>Data sources and methods: </strong>MEDLINE, Embase and Web of Science were systematically searched in June 2022. Randomized controlled trials (RCTs) and observational studies comparing the long GnRH-agonist COS protocol and the GnRH-antagonist COS protocol in women with all stages/subtypes of endometriosis were included. Data were synthesized into comprehensive tables for systematic review. The Scottish Intercollegiate Guidelines Network (SIGN) checklists were used for the risk of bias assessment of non-randomized studies and randomized studies, and all the included studies were deemed to have acceptable quality.</p><p><strong>Main results: </strong>Eight studies (one RCT and seven observational) with 2695 patients (2761 cycles) were included. Most studies generally reported non-significant differences in clinical pregnancy or live birth rates regardless of the COS protocol used. However, the GnRH-agonist protocol may yield a higher total number of oocytes retrieved, especially mature oocytes. Conversely, the GnRH-antagonist protocol required a shorter COS duration and lower gonadotrophin dose. Adverse outcomes, such as rates of cycle cancellation and miscarriage, were similar between both COS protocols.</p><p><strong>Conclusion: </strong>Both the long GnRH-agonist and GnRH-antagonist COS protocols generally yield similar pregnancy outcomes. However, the long GnRH-agonist protocol may be associated with a higher cumulative pregnancy rate due to the higher number of retrieved oocytes available for cryopreservation. The underlying mechanisms of the two COS protocols on the female reproductive tract remain unclear. Clinicians should consider treatment costs, stage/subtype of endometriosis and pregnancy goals of their patients when selecting a GnRH analogue for COS. A well-powered RCT is needed to minimize the risk of bias and compare the risk for ovarian hyperstimulation syndrome.</p><p><strong>Registration: </strong>This review was prospectively registered at PROSPERO under Registration No. CRD42022327604.</p>","PeriodicalId":22998,"journal":{"name":"Therapeutic Advances in Endocrinology and Metabolism","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10331103/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10302217","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}