The lancet. Diabetes & endocrinology最新文献

{"title":"Diagnosis of thyroid nodules.","authors":"Erik K Alexander,&nbsp;Edmund S Cibas","doi":"10.1016/S2213-8587(22)00101-2","DOIUrl":"https://doi.org/10.1016/S2213-8587(22)00101-2","url":null,"abstract":"<p><p>Thyroid nodules are common, usually asymptomatic, and often pose minimal risk to the affected patient. However, 10-15% prove malignant and serve as the rationale for diagnostic assessment. Safely identifying and treating a relevant thyroid cancer through a cost-effective process is the primary goal of the treating practitioner. Ultrasound is the principal means of initial nodule assessment and should be performed when any thyroid nodule is suspected. Fine-needle aspiration provides further cytological determination of benign or malignant disease and is generally applied to nodules larger than 1-2 cm in diameter, on the basis of holistic risk assessment. The Bethesda System for Reporting Thyroid Cytopathology provides standardised terminology, which enhances communication among health-care providers and patients. Benign cytology is highly accurate, whereas indeterminate cytology could benefit from further application of molecular testing. The ultimate goal of diagnostic assessment of thyroid nodules is to accurately identify malignancy while avoiding overtreatment. Low-risk thyroid nodules can be safely monitored in many patients with minimal diagnostic intervention.</p>","PeriodicalId":519532,"journal":{"name":"The lancet. Diabetes & endocrinology","volume":" ","pages":"533-539"},"PeriodicalIF":44.5,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40398711","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}

{"title":"A global view of the interplay between non-alcoholic fatty liver disease and diabetes.","authors":"Norbert Stefan,&nbsp;Kenneth Cusi","doi":"10.1016/S2213-8587(22)00003-1","DOIUrl":"https://doi.org/10.1016/S2213-8587(22)00003-1","url":null,"abstract":"<p><p>Non-alcoholic fatty liver disease (NAFLD) has become an epidemic, much like other non-communicable diseases (NCDs), such as cancer, obesity, diabetes, and cardiovascular disease. The pathophysiology of NAFLD, particularly involving insulin resistance and subclinical inflammation, is not only closely linked to that of those NCDs but also to a severe course of the communicable disease COVID-19. Genetics alone cannot explain the large increase in the prevalence of NAFLD during the past 2 decades and the increase that is projected for the next decades. Impairment of glucose and lipid metabolic pathways, which has been propelled by the worldwide increase in the prevalence of obesity and type 2 diabetes, is most likely behind the increase in people with NAFLD. As the prevalence of NAFLD varies among subgroups of patients with diabetes and prediabetes identified by cluster analyses, stratification of people with diabetes and prediabetes by major pathological mechanistic pathways might improve the diagnosis of NAFLD and prediction of its progression. In this Review, we aim to understand how diabetes can affect the development of hepatic steatosis and its progression to advanced liver damage. First, we emphasise the extent to which NAFLD and diabetes jointly occur worldwide. Second, we address the major mechanisms that are involved in the pathogenesis of NAFLD and type 2 diabetes, and we discuss whether these mechanisms place NAFLD in an important position to better understand the pathogenesis of NCDs and communicable diseases, such as COVID-19. Third, we address whether this knowledge can be used for personalised treatment of NAFLD in the future. Finally, we discuss the current treatment strategies for people with type 2 diabetes and their effectiveness in treating the spectrum of hepatic diseases from simple steatosis to non-alcoholic steatohepatitis and hepatic fibrosis.</p>","PeriodicalId":519532,"journal":{"name":"The lancet. Diabetes & endocrinology","volume":" ","pages":"284-296"},"PeriodicalIF":44.5,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39634439","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}

{"title":"Corrections to Lancet Diabetes Endocrinol 2022; 10: 120-28.","authors":"","doi":"10.1016/S2213-8587(22)00083-3","DOIUrl":"https://doi.org/10.1016/S2213-8587(22)00083-3","url":null,"abstract":"","PeriodicalId":519532,"journal":{"name":"The lancet. Diabetes & endocrinology","volume":" ","pages":"e7"},"PeriodicalIF":44.5,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40319666","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}

{"title":"Correction to Lancet Diabetes Endocrinol 2020; 8: 594-605.","authors":"","doi":"10.1016/S2213-8587(22)00082-1","DOIUrl":"https://doi.org/10.1016/S2213-8587(22)00082-1","url":null,"abstract":"","PeriodicalId":519532,"journal":{"name":"The lancet. Diabetes & endocrinology","volume":" ","pages":"e7"},"PeriodicalIF":44.5,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40319667","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}

{"title":"Semaglutide once a week in adults with overweight or obesity, with or without type 2 diabetes in an east Asian population (STEP 6): a randomised, double-blind, double-dummy, placebo-controlled, phase 3a trial.","authors":"Takashi Kadowaki,&nbsp;Joakim Isendahl,&nbsp;Usman Khalid,&nbsp;Sang Yeoup Lee,&nbsp;Tomoyuki Nishida,&nbsp;Wataru Ogawa,&nbsp;Kazuyuki Tobe,&nbsp;Toshimasa Yamauchi,&nbsp;Soo Lim","doi":"10.1016/S2213-8587(22)00008-0","DOIUrl":"https://doi.org/10.1016/S2213-8587(22)00008-0","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Semaglutide 2·4 mg once weekly has been investigated for weight management in global populations. Differences exist between Asian and non-Asian populations in terms of body composition and definitions of obesity. In the Semaglutide Treatment Effect in People with obesity (STEP) 6 trial, we assessed the effect of semaglutide versus placebo for weight management in adults from east Asia with obesity, with or without type 2 diabetes.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;This randomised, double-blind, double-dummy, placebo-controlled, phase 3a superiority trial was done at 28 outpatient clinics in Japan and South Korea. Eligible participants were adults (aged ≥18 years in South Korea; ≥20 years in Japan) with a BMI of at least 27·0 kg/m&lt;sup&gt;2&lt;/sup&gt; with two or more weight-related comorbidities or a BMI of 35·0 kg/m&lt;sup&gt;2&lt;/sup&gt; or more with one or more weight-related comorbidity (one comorbidity had to be either hypertension, dyslipidaemia, or, in Japan only, type 2 diabetes) who had at least one self-reported unsuccessful dietary attempt to lose bodyweight. Participants were randomly assigned (4:1:2:1) to once-weekly subcutaneous semaglutide 2·4 mg or matching placebo, or semaglutide 1·7 mg or matching placebo, plus lifestyle recommendations for 68 weeks. Data for the placebo groups were pooled in statistical analyses. The primary endpoints were percentage change in bodyweight from baseline at week 68 and the proportion of participants who had achieved a reduction of at least 5% of baseline bodyweight at week 68. Change in abdominal visceral fat area was assessed as a supportive secondary endpoint using computed tomography scanning in a subset of participants. Efficacy outcomes were assessed in the full analysis set, which included all randomly assigned participants according to the intention-to-treat principle. Safety was assessed in all participants who received at least one dose of the study drug. This trial was registered with ClinicalTrials.gov, NCT03811574.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Findings: &lt;/strong&gt;Between Jan 21, 2019 and June 4, 2019, 437 participants were screened, of whom 401 were randomly assigned to semaglutide 2·4 mg (n=199), semaglutide 1·7 mg (n=101), or placebo (n=101) and included in the intention-to-treat analysis. Estimated mean change in bodyweight from baseline to week 68 was -13·2% (SEM 0·5) in the semaglutide 2·4 mg group and -9·6% (0·8) in the semaglutide 1·7 mg group versus -2·1% (0·8) in the placebo group (estimated treatment difference [ETD] -11·1 percentage points [95% CI -12·9 to -9·2] for semaglutide 2·4 mg vs placebo; -7·5 percentage points [95% CI -9·6 to -5·4] for semaglutide 1·7 mg vs placebo; both p&lt;0·0001). At week 68, a larger proportion of participants had achieved a 5% or higher reduction in baseline bodyweight in the semaglutide 2·4 mg group (160 [83%] of 193 participants) and semaglutide 1·7 mg group (71 [72%] of 98 participants) than in the placebo group (21 [21%] of 100 participants); odds ","PeriodicalId":519532,"journal":{"name":"The lancet. Diabetes & endocrinology","volume":" ","pages":"193-206"},"PeriodicalIF":44.5,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39594612","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}

{"title":"Managing Diabetes and Homelessness.","authors":"Talha Burki","doi":"10.1016/S2213-8587(22)00039-0","DOIUrl":"https://doi.org/10.1016/S2213-8587(22)00039-0","url":null,"abstract":"","PeriodicalId":519532,"journal":{"name":"The lancet. Diabetes & endocrinology","volume":" ","pages":"164-165"},"PeriodicalIF":44.5,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39889554","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}

{"title":"Correction to Lancet Diabetes Endocrinol 2022; 10: 102-11.","authors":"","doi":"10.1016/S2213-8587(22)00051-1","DOIUrl":"https://doi.org/10.1016/S2213-8587(22)00051-1","url":null,"abstract":"","PeriodicalId":519532,"journal":{"name":"The lancet. Diabetes & endocrinology","volume":" ","pages":"e3"},"PeriodicalIF":44.5,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39813155","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}

{"title":"Childhood cancer survival: a gap in need of closing.","authors":"The Lancet Diabetes Endocrinology","doi":"10.1016/S2213-8587(22)00050-X","DOIUrl":"https://doi.org/10.1016/S2213-8587(22)00050-X","url":null,"abstract":"","PeriodicalId":519532,"journal":{"name":"The lancet. Diabetes & endocrinology","volume":" ","pages":"149"},"PeriodicalIF":44.5,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39916906","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}

{"title":"Data-driven type 2 diabetes patient clusters predict metabolic surgery outcomes.","authors":"Jason Flannick","doi":"10.1016/S2213-8587(22)00034-1","DOIUrl":"https://doi.org/10.1016/S2213-8587(22)00034-1","url":null,"abstract":"","PeriodicalId":519532,"journal":{"name":"The lancet. Diabetes & endocrinology","volume":" ","pages":"150-151"},"PeriodicalIF":44.5,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9173087/pdf/nihms-1807460.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39910681","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bone fragility in diabetes: novel concepts and clinical implications.","authors":"Lorenz C Hofbauer,&nbsp;Björn Busse,&nbsp;Richard Eastell,&nbsp;Serge Ferrari,&nbsp;Morten Frost,&nbsp;Ralph Müller,&nbsp;Andrea M Burden,&nbsp;Fernando Rivadeneira,&nbsp;Nicola Napoli,&nbsp;Martina Rauner","doi":"10.1016/S2213-8587(21)00347-8","DOIUrl":"https://doi.org/10.1016/S2213-8587(21)00347-8","url":null,"abstract":"<p><p>Increased fracture risk represents an emerging and severe complication of diabetes. The resulting prolonged immobility and hospitalisations can lead to substantial morbidity and mortality. In type 1 diabetes, bone mass and bone strength are reduced, resulting in up to a five-times greater risk of fractures throughout life. In type 2 diabetes, fracture risk is increased despite a normal bone mass. Conventional dual-energy x-ray absorptiometry might underestimate fracture risk, but can be improved by applying specific adjustments. Bone fragility in diabetes can result from cellular abnormalities, matrix interactions, immune and vascular changes, and musculoskeletal maladaptation to chronic hyperglycaemia. This Review summarises how the bone microenvironment responds to type 1 and type 2 diabetes, and the mechanisms underlying fragility fractures. We describe the value of novel imaging technologies and the clinical utility of biomarkers, and discuss current and future therapeutic approaches that protect bone health in people with diabetes.</p>","PeriodicalId":519532,"journal":{"name":"The lancet. Diabetes & endocrinology","volume":" ","pages":"207-220"},"PeriodicalIF":44.5,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39738095","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}