Therapeutic Advances in Endocrinology and Metabolism最新文献

{"title":"MAFLD: a multisystem disease.","authors":"Rosaria Maria Pipitone,&nbsp;Carlo Ciccioli,&nbsp;Giuseppe Infantino,&nbsp;Claudia La Mantia,&nbsp;Stefanie Parisi,&nbsp;Adele Tulone,&nbsp;Grazia Pennisi,&nbsp;Stefania Grimaudo,&nbsp;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}

{"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}

{"title":"RANKL inhibition: a new target of treating diabetes mellitus?","authors":"Baodi Xing,&nbsp;Jie Yu,&nbsp;Huabing Zhang,&nbsp;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}

{"title":"Tolvaptan for the treatment of the syndrome of inappropriate antidiuresis (SIAD).","authors":"Ploutarchos Tzoulis,&nbsp;Gregory Kaltsas,&nbsp;Stephanie E Baldeweg,&nbsp;Pierre-Marc Bouloux,&nbsp;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}

{"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}

{"title":"Fertility preservation options for transgender and nonbinary individuals.","authors":"Jensen Reckhow,&nbsp;Hakan Kula,&nbsp;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}

{"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}

{"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,&nbsp;Elise Costenoble,&nbsp;Olivier Pollé,&nbsp;Kezban Erdem,&nbsp;Céline Bugli,&nbsp;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_1C, insulin dose-adjusted hemoglobin A_1C (IDAA_1C), glycemic target-adjusted HbA_1C (GTAA_1C)] 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.</p><p><strong>Results: </strong>PR⁺ patients showed improved glycemic control (i.e. HbA_1C, IDAA_1C, and GTAA_1C) 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 GTAA_1C 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⁺ and PR^- 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_1C levels, IDAA_1C and GTAA_1C 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}

{"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,&nbsp;Sean Omoseni,&nbsp;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}

{"title":"Prevalence and associated factors of hyperuricemia among Chinese patients with diabetes: a cross-sectional study.","authors":"Shiyi Sun,&nbsp;Lihong Chen,&nbsp;Dawei Chen,&nbsp;Yan Li,&nbsp;Guanjian Liu,&nbsp;Lin Ma,&nbsp;Jun Li,&nbsp;Fangwei Cao,&nbsp;Xingwu Ran","doi":"10.1177/20420188231198620","DOIUrl":"https://doi.org/10.1177/20420188231198620","url":null,"abstract":"<p><strong>Background: </strong>As a part of metabolic syndrome, hyperuricemia has a higher incidence in patients with diabetes than in the general population owing to various underlying factors.</p><p><strong>Objectives: </strong>The objective of the present study was to investigate the prevalence of hyperuricemia among patients with diabetes and identify associated factors.</p><p><strong>Design: </strong>A cross-sectional study.</p><p><strong>Methods: </strong>Herein, we included patients with diabetes managed at nine healthcare centers in Chenghua District, Chengdu, from February 2021 to November 2021. Clinical data, lifestyle habits, and laboratory data were collected to determine the prevalence and factors associated with hyperuricemia.</p><p><strong>Results: </strong>In total, we included 1577 patients with diabetes (males, 50.35%; females, 49.65%). The median serum uric acid level was 337.9 μmol/L, and the prevalence of hyperuricemia in patients with diabetes was 21.24%. The prevalence of hyperuricemia in male patients was significantly higher than in females (29.35% in males <i>versus</i> 13.03% in females, <i>p</i> < 0.001). Male patients with obesity (<i>p</i> = 0.006) or triglyceride (TG) ⩾ 1.7 mmol/L (<i>p</i> < 0.001) had a high risk of developing hyperuricemia, and hyperuricemia was negatively associated with estimated glomerular filtration rate (eGFR) ⩾ 60 mL/min/1.73 m² (<i>p</i> < 0.001), glycosylated hemoglobin (HbA1c) ⩾ 7% (<i>p</i> < 0.001), fenofibrate (<i>p</i> = 0.010), and sodium-glucose cotransporter 2 (SGLT-2) inhibitors (<i>p</i> = 0.035). Considering females, overweight (<i>p</i> = 0.004), alanine transaminase (ALT) > 40 U/L (<i>p</i> < 0.001), and TG ⩾ 1.7 mmol/L (<i>p</i> = 0.015) showed a significant positive correlation with hyperuricemia, while eGFR ⩾ 60 mL/min/1.73 m² (<i>p</i> < 0.001) was negatively associated with the risk of hyperuricemia.</p><p><strong>Conclusion: </strong>Hyperuricemia is highly prevalent in patients with diabetes, especially in males. In addition to traditionally associated factors, fenofibrate and SGLT-2 inhibitors were also associated with the risk of hyperuricemia.</p><p><strong>Registration: </strong>The study protocol was registered in the Chinese Clinical Trial Registry (http://www.chictr.org.cn/), and the registration number was ChiCTR 2100042742.</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/cb/dc/10.1177_20420188231198620.PMC10501065.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10299942","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}