Clinical Endocrinology最新文献

{"title":"The Spectrum of Congenital Hypogonadotropic Hypogonadism: A 30-Year Experience at a Tertiary Paediatric Centre","authors":"Minha Kook,&nbsp;Richard G. McGee,&nbsp;Geoffrey Ambler,&nbsp;Yoon Hi Cho","doi":"10.1111/cen.70177","DOIUrl":"10.1111/cen.70177","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 <p>Congenital hypogonadotropic hypogonadism (CHH) is a rare group of disorders of gonadotropin deficiency, either isolated or as a part of multiple pituitary hormone deficiencies (MPHD).</p>\u0000 \u0000 <p>We aimed to describe the spectrum of presentation, diagnosis, and management practices of CHH spanning 30 years at an Australian tertiary paediatric centre.</p>\u0000 \u0000 <p>This is a retrospective cohort study of patients with CHH seen at the Children's Hospital at Westmead between January 1994 and December 2024 (<i>n</i> = 96, 66% male), categorised by diagnostic subtypes: Kallmann Syndrome (KS), normosmic HH, MPHD and other syndromes (including CHARGE).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In patients with KS (<i>n</i> = 31, 87% male), the most common presenting features were micropenis and/or cryptorchidism (45%) or pubertal delay (45%), with two peak ages of presentation: 0.6 [IQR 0.3–0.8] and 14.6 [11.5–15.7] years. Patients with MPHD (<i>n</i> = 23, 52% male) presented with neonatal hypoglycaemia in 52%. Comorbidities stratified by diagnostic subtypes (KS, MPHD, and other syndromes) included hearing impairment (10%, 4%, 100%), visual impairment (7%, 17%, 77%), cardiac anomalies (3%, 9%, 77%), and intellectual disability (13%, 26%, 46%). Genetic testing was performed in 32% in 1995–2009 vs 66% in 2010–2024. Pathogenic gene variants associated with HH were found in 61% of those tested, including <i>CHD7</i> (<i>n</i> = 10), <i>ANOS1</i> (n = 4), and <i>FGFR1</i> (<i>n</i> = 3). Pubertal induction was commenced in males at a mean age of 14.1 ± 1.6 years using testosterone (<i>n</i> = 27 oral; 14 intramuscular; 1 subcutaneous) or gonadotropins (<i>n</i> = 5), and in females, at a mean age of 14.6 ± 1.8 years using oestradiol (<i>n</i> = 21 oral; 8 transdermal) ± progesterone.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>CHH is a heterogeneous group of disorders, with varying prevalence of associated comorbidities according to diagnostic subtypes. Our data highlight the paediatric-specific modes of presentation of CHH, and in KS, the bimodal distribution of age at presentation in males and the under-representation and delayed diagnoses in females. Despite advances in genetics in the past three decades, there remain areas for further research in the diagnostics and therapeutics of CHH in the paediatric age group.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10346,"journal":{"name":"Clinical Endocrinology","volume":"105 4","pages":"464-473"},"PeriodicalIF":2.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cen.70177","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148560982","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":"Referral to Definitive Surgical Treatment in Cushing's Syndrome – An Odyssey That Requires Attention","authors":"Amy Coulden,&nbsp;Amynta Arshad,&nbsp;Shani Mathara,&nbsp;Simon Aylwin,&nbsp;Yasir Mamoojee,&nbsp;Daniel Flanagan,&nbsp;Aparna Pal,&nbsp;Neil Gittoes,&nbsp;Helena Gleeson","doi":"10.1111/cen.70175","DOIUrl":"10.1111/cen.70175","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Cushing's syndrome (CS) requires prompt recognition and referral to explore definitive intervention. Delays can lead to increased mortality and death. This service evaluation aimed to distinguish time from initial referral to definitive surgical management in CS.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Context</h3>\u0000 \u0000 <p>Clinical standards for appropriate timelines for referral are undefined.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Design</h3>\u0000 \u0000 <p>A retrospective service evaluation across five specialised endocrine surgical centres reviewing the timeline from initial referral to definitive surgical treatment.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Patients</h3>\u0000 \u0000 <p>All adult patients diagnosed with CS who underwent definitive surgery between January 2018 and December 2019.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Measurements</h3>\u0000 \u0000 <p>Data were collected on initial referrer, time to first clinical review, tests performed within non-surgical endocrinology centres, timing of referral to specialised endocrine surgical centre, clinical review (if applicable), multi-disciplinary meeting and definitive surgery.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>71 patients received definitive surgical treatment for CS (37 pituitary CS and 34 adrenal CS). Median time from initial primary care referral to a specialised endocrine surgical centre was quicker if referred directly (56 days) than if initially referred to a non-surgical endocrinology hospital (159 days). The overall median time from all initial referrals to definitive surgical treatment was 211 days for pituitary CS and 253 days for adrenal CS. Patients referred directly to the specialised endocrine surgical centre had surgery in a median of 196 days (187 days and 252 days for pituitary and adrenal CS respectively) compared with 253 days in patients that were referred via a non-surgical endocrinology centre (249 days and 346 days for pituitary and adrenal CS respectively).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>There were delays from initial referral to definitive surgical treatment of CS. Clearer, clinically focussed pathways and (inter)national standards on early management of Cushing's syndrome should be considered to more address unwarranted delays in treating Cushing's syndrome.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10346,"journal":{"name":"Clinical Endocrinology","volume":"105 4","pages":"380-385"},"PeriodicalIF":2.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148419242","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serum Copeptin Rises After Tolvaptan for Hyponatraemia, but Does Not Predict Risk of Rapid Sodium Rise: Pre-Specified Secondary Analysis of the TVFR Trial","authors":"Annabelle M. Warren,&nbsp;Kay Weng Choy,&nbsp;Rudolf Hoermann,&nbsp;Nicholas Russell,&nbsp;Mathis Grossmann","doi":"10.1111/cen.70184","DOIUrl":"10.1111/cen.70184","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Hyponatraemia is a common electrolyte disorder often driven by excess arginine vasopressin (AVP). Copeptin is a stable surrogate marker co-secreted with AVP. It is unclear whether treatment of hyponatraemia with tolvaptan, an AVP-V2 receptor antagonist, impacts copeptin. We aimed to assess the effects of tolvaptan on serum copeptin, compared to fluid restriction.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Design</h3>\u0000 \u0000 <p>Pre-specified secondary analysis of an open-label randomised trial comparing tolvaptan or fluid restriction for 3 days.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Patients</h3>\u0000 \u0000 <p>Hospitalised patients with plasma sodium (pNa) 115–130 mmol/L at a single-centre tertiary hospital in Melbourne, Australia.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Measurements</h3>\u0000 \u0000 <p>Copeptin measured at baseline and completion (Day 4, or discharge if sooner).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Copeptin results were available in 45/54 participants, randomised to tolvaptan (<i>n</i> = 25) or FR (<i>n</i> = 20). Mean baseline copeptin was 10.4 pmol/L. pNa increased in both groups, significantly more with tolvaptan as previously reported. Copeptin remained stable after FR, but significantly increased after tolvaptan (mean adjusted difference between groups over 3 days 8.4 pmol/L, 95% CI 2.1–14.6, <i>p</i> = 0.01). Baseline copeptin did not predict rapid sodium rise.</p>\u0000 \u0000 <p>The rise in copeptin after tolvaptan may represent an exaggerated response to osmolality rise in these patients (‘reset osmostat’), or feedback mechanisms from AVP blockade.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Tolvaptan increased serum copeptin compared to fluid restriction. Further research is required to determine if there is clinical utility for measuring copeptin in hyponatraemia before it is adopted into practice.</p>\u0000 \u0000 <p><b>Trial Registration:</b> ACTRN12619001683123.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10346,"journal":{"name":"Clinical Endocrinology","volume":"105 4","pages":"514-518"},"PeriodicalIF":2.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cen.70184","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148663538","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":"Flushing: Neuroendocrine Mechanisms and a Structured Diagnostic Approach","authors":"Manuel Ramón García-Sáenz,&nbsp;Ernesto Sosa-Eroza,&nbsp;Aldo Ferreira-Hermosillo,&nbsp;Claudia Ramírez-Rentería,&nbsp;Nitzia López-Juárez,&nbsp;Etual Espinosa-Cárdenas","doi":"10.1111/cen.70157","DOIUrl":"10.1111/cen.70157","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction</h3>\u0000 \u0000 <p>Flushing is a common clinical symptom characterised by transient cutaneous vasodilation and erythema, frequently accompanied by a sensation of heat. Although often benign, it may signal endocrine, neuroendocrine, autonomic, inflammatory, pharmacologic, or neoplastic disorders.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>To provide an integrated review of the neuroendocrine and vascular mechanisms underlying flushing and to propose a structured, clinically applicable diagnostic approach based on symptom patterns and pathophysiological pathways.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A narrative review of the literature was conducted, focusing on thermoregulatory physiology, neuroendocrine signalling, vascular control, and clinical conditions associated with flushing. Evidence from experimental, observational, and clinical studies was synthesised to develop a mechanistic framework and a stepwise diagnostic algorithm integrating clinical features and targeted laboratory evaluation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Flushing arises from disruption of central thermoregulatory integration involving hypothalamic nuclei, peripheral sensory pathways, and vasoactive mediators, including oestrogens, serotonin, catecholamines, vasoactive intestinal peptide, prostaglandins, substance P, and histamine. Neurotransmitters help modulate the vascular response, which is further influenced by endothelial function and autonomic tone.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Flushing is a multifactorial symptom reflecting integrated neuroendocrine and vascular dysregulation rather than an isolated cutaneous phenomenon. Recognising the distinction between wet and dry flushing and applying a mechanism-based diagnostic framework may improve diagnostic accuracy and facilitate earlier identification of clinically important underlying disorders.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10346,"journal":{"name":"Clinical Endocrinology","volume":"105 4","pages":"367-377"},"PeriodicalIF":2.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cen.70157","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147873781","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":"ThyroidPrint: Thyroid Genetic Classifier Long-Term Follow-Up of Benign Called Lesions","authors":"Nicole Lustig,&nbsp;José Miguel Domínguez,&nbsp;Sergio Vargas-Salas,&nbsp;María Paz Hernandez,&nbsp;Lorena Mosso,&nbsp;Marlín Solorzano,&nbsp;Ignacio Fuentes,&nbsp;Annette Madison,&nbsp;Francisco Cruz,&nbsp;Soledad Loyola,&nbsp;Augusto León,&nbsp;Pablo H. Montero,&nbsp;Francisco Domínguez,&nbsp;Mauricio Camus,&nbsp;Antonieta Solar,&nbsp;Pablo Zoroquiain,&nbsp;Juan Carlos Roa,&nbsp;Hernán E. González","doi":"10.1111/cen.70161","DOIUrl":"10.1111/cen.70161","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The management of indeterminate thyroid nodules (ITNs) remains challenging, with molecular classifiers emerging as valuable tools for risk stratification. ThyroidPrint is a novel quantitative PCR-based 10-gene classifier designed to predict benignity in ITNs, enabling more informed clinical decision-making.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>To evaluate the long-term follow-up (≥ 5 years) of patients with a benign ThyroidPrint result managed via active surveillance, assessing the safety, durability and clinical utility of the test in a real-world setting.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This prospective, single-centre study included 104 patients with indeterminate cytology (Bethesda III/IV) and a previous benign ThyroidPrint result, followed for a median of 5.3 years. Ultrasound monitoring and clinical assessments guided management, with surgery reserved for significant nodule growth or patient preference. Outcomes included the proportion of patients remaining under surveillance, nodule growth and surgical pathology.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Of the 104 patients with benign ThyroidPrint results, 94.2% remained under active surveillance at 5 years, with only 5.8% undergoing surgery, all of which confirmed benign or low-risk histology. The false-negative rate was minimal among resected nodules supports the test's safety as a rule-out tool. Ultrasonographic monitoring proved effective for early detection of changes in warranting intervention.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Long-term follow-up demonstrates that ThyroidPrint provides a reliable, safe and durable approach to managing ITN, significantly reducing unnecessary surgeries while maintaining a low rate of missed malignancies. These findings reinforce its role in personalised patient management and support structured surveillance protocols for selected patients.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10346,"journal":{"name":"Clinical Endocrinology","volume":"105 4","pages":"486-492"},"PeriodicalIF":2.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147986960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endocrine Phenotypes and Hormonal Treatment in Meier-Gorlin Syndrome: Report of Two Cases and a Systematic Review of Literature","authors":"Kumar Swapnil,&nbsp;Rajdeep Basu,&nbsp;Roohi Nanda,&nbsp;Sunetra Mondal,&nbsp;Soumita Mandal,&nbsp;Soumik Goswami,&nbsp;Arjun Baidya,&nbsp;Nilanjan Sengupta","doi":"10.1111/cen.70183","DOIUrl":"10.1111/cen.70183","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Meier-Gorlin-syndrome (MGORS) is a rare cause of primordial dwarfism stemming from pathogenic variants in genes involved in DNA replication. The classic clinical triad is microtia, absent patella and short stature. MGORS can mimic endocrine causes of short stature or delayed/atypical pubertal development.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We report two new cases of MGORS. A systematic literature search of all cases published up to 31 March 2026 was done to identify the cases reporting any endocrinopathy or hormonal therapy, focussing on growth-hormone-deficiency (GHD) and response to growth hormone (GH).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We describe a 14 year-old girl, the first MGORS case with <i>CDC6</i> variant and mammary hypoplasia. Another 11-year old boy with <i>GMNN</i> variant had severe short-stature with GHD and had significant height improvement with GH. Among 29 cases (out of ~150 published), the classic triad was absent in 18.5%. Short stature was almost universal (median height-<i>Z</i>-score −4.4), with 70% exhibiting delayed bone age, 42.9% low IGF-1 and 35.3% GHD. Among 10 GH-treated cases with response data, 6 had reported improvement in height-SDS/growth-velocity. Those with GHD and delayed bone age were more likely to benefit from GH. Among females, all post-pubertal cases had mammary hypoplasia, while 23.5% had clitoromegaly with hypoplastic labia. Among males, cryptorchidism, hypoplastic scrotum and micropenis were common. However, gonadal hormones and gonadotrophins were normal. Data on the effect of estrogen on hypoplastic mammary glands or labia was variable.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>MGORS should be kept in mind as a differential of multiple endocrinopathies. Cases of MGORS should undergo screening for GHD. Available data, mostly from case-reports or small series, suggest that response to GH has been reported in some individuals, particularly where GHD or delayed bone age was present, but evidence remains very limited.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10346,"journal":{"name":"Clinical Endocrinology","volume":"105 4","pages":"416-431"},"PeriodicalIF":2.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148577275","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Revisiting Pre-RAI MLR, PNI, and NRI Estimating Early and Higher Recurrence in Intermediate-Risk DTC in Thyroidology","authors":"Ilker Sengul,&nbsp;Demet Sengul","doi":"10.1111/cen.70187","DOIUrl":"10.1111/cen.70187","url":null,"abstract":"","PeriodicalId":10346,"journal":{"name":"Clinical Endocrinology","volume":"105 4","pages":"378-379"},"PeriodicalIF":2.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148590787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serum Lipid Profile in Patients With Primary Adrenal Insufficiency Receiving Glucocorticoid Replacement.","authors":"Marta Fichna, Piotr Fichna, Marta Sumińska, Bolesław Gębarski, Marek Ruchała","doi":"10.1111/cen.70203","DOIUrl":"https://doi.org/10.1111/cen.70203","url":null,"abstract":"<p><strong>Objective: </strong>Glucocorticoid (GC) replacement in Addison's disease (AD) usually fails to mimic physiological circadian cortisol rhythm. Recurrent hypercortisolemia may contribute to central obesity, hyperglycemia and dyslipidemia, which could explain cardiovascular mortality in AD. Steroid excess alters lipid profile, while effects of the replacement doses remain inconsistent, which led us to evaluate serum lipids in AD.</p><p><strong>Design: </strong>A cross-sectional study in patients treated for autoimmune AD.</p><p><strong>Patients: </strong>The study comprised 66 patients diagnosed <1 year (AD1), 97 diagnosed >1 year (AD2) before the study and 96 matched controls (CON), excluding individuals with diabetes, thyroid dysfunction and lipid-lowering treatment.</p><p><strong>Measurements: </strong>Investigations included physical examination and biochemical analyses.</p><p><strong>Results: </strong>All patients were on immediate-release hydrocortisone (HC), mean ± SD 22.7 ± 6.6 mg/day. AD1 presented significantly lower HC dosage (p ≤ 0.001), higher TSH (p ≤ 0.046) and lower fasting glucose (p ≤ 0.005) versus AD2 and CON. Recently treated patients demonstrated significantly lower total cholesterol (TC), LDL-C and triglyceride (TG) levels versus both AD2 and CON, who displayed similar lipid profile. Only HDL-C was significantly higher in AD2 (p = 0.009). Hyperlipidemia was found in 62.5% CON subjects, 45.5% AD1 (p = 0.032), and 60.8% AD2 patients (p = 0.811). Age was strongly correlated with TC and LDL-C in AD and CON. Daily HC dose correlated with TC and LDL-C in both AD1 and AD2, and with HDL-C in AD1, and multivariable regression confirmed its predictive value with regard to TC and LDL-C.</p><p><strong>Conclusions: </strong>The risk of hyperlipidemia in patients receiving GC replacement does not seem elevated. Nonetheless, metabolic complications should be screened to improve long-term outcomes.</p>","PeriodicalId":10346,"journal":{"name":"Clinical Endocrinology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148817639","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Incidence, Patterns and Predictors of Alemtuzumab-Induced Thyroid Dysfunction in Patients With Multiple Sclerosis: A Northern Ireland Cohort Study.","authors":"Dillon O Flynn, Fiona Kennedy, Stella Hughes, Fiona Magill, Gavin V Mc Donnell, Neil Black, Milad Darrat, Ger Mullan, Robert Darcy, David R McCance, Kirsty Spence, Philip C Johnston","doi":"10.1111/cen.70201","DOIUrl":"10.1111/cen.70201","url":null,"abstract":"<p><strong>Background: </strong>Alemtuzumab (Lemtrada) is highly effective for selected relapsing multiple sclerosis (MS) but can cause autoimmune thyroid dysfunction (AITD). Our aim was to retrospectively review patients and the monitoring of their thyroid function tests (TFTs) during and after treatment with alemtuzumab. We wanted to summarise the incidence and characterise the nature of TD in our Northern Ireland (NI) cohort.</p><p><strong>Methods: </strong>Data was obtained from the NI Disease Modifying Treatment (NIDMT) database for all patients with relapsing remitting MS receiving alemtuzumab in the period between 2015 and 2024. Patients were identified and data collected retrospectively from clinical records. Data collected included dates of alemtuzumab treatment, TFT monitoring results, subsequent follow up and any thyroid treatment required. Demographic and clinical data were obtained from the Northern Ireland Electronic Care Record (NIECR)-an electronic healthcare record.</p><p><strong>Results: </strong>168 patients (female n = 114, male n = 54) received alemtuzumab between 2015 and 2024 in Northern Ireland, with a follow-up period of approximately 60 months. On most recent follow up, TD occurred in 45.8% (n = 77) patients. The spectrum of thyroid disorders observed post-alemtuzumab was diverse; Graves' disease and thyroiditis were the most common thyroid disorders, each affecting 10.7% (n = 18) of patients. Thyroiditis with positive thyroid stimulating receptor antibodies (TRAb) occurred in 7.7% (n = 13), followed by Hashimoto's disease 7.1% (n = 13), with both ab-negative hypothyroidism 6.0% (n = 10) and hyperthyroidism 3.0% (n = 5). Two patients had pre-existing thyroid dysfunction hypothyroidism n = 1 and hyperthyroidism n = 1. Baseline thyroid autoantibody status showed a strong association with TD. Women were twice as likely as men to develop TD following Alemtuzumab treatment. Neither age nor MS duration significantly influenced the risk of TD. TD was diagnosed as early as 12 months after initiating treatment, with the latest diagnosis being made 56 months after.</p><p><strong>Conclusion: </strong>The frequency of Alemtuzumab-induced TD in our cohort was similar to that reported in other literature and the nature of TD varied with a number of patients fluctuating between dysthyroid states. This data highlights the importance of close surveillance for TD due to the risk of complex, late-onset autoimmunity.</p>","PeriodicalId":10346,"journal":{"name":"Clinical Endocrinology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148722130","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigating a Mineralocorticoid Receptor Mediation of an Ultra-Short Feedback Loop Regulating Aldosterone Production in Humans.","authors":"Yan Emily Yuan, Gail K Adler, Bernard Rosner, Annie Altman Merino, Ezgi Caliskan Guzelce, Gordon H Williams, Jonathan S Williams, Andrea V Haas","doi":"10.1111/cen.70189","DOIUrl":"10.1111/cen.70189","url":null,"abstract":"<p><strong>Background: </strong>Preclinical studies suggest a novel aldosterone regulation pathway: the mineralocorticoid receptor (MR) on the adrenal cortex is a part of an MR-mediated ultra-short feedback loop regulating aldosterone production. Activation of MR on the adrenal decreases aldosterone; blockade of the MR increases aldosterone. Whether this regulatory pathway exists in humans is unknown.</p><p><strong>Methods: </strong>This was a double-blinded, 3-way crossover study of 23 healthy participants on a low sodium diet (10 mEq/day). Participants received three study drugs in random order: MR antagonist (eplerenone), MR agonist (fludrocortisone), and placebo. Study drugs were administered at 6:30AM on three separate days with 48 h between each administration. After 90 min, participants received sequential infusions of angiotensin-II (ANGII) for 45 min followed 60 min later by cosyntropin for 45 min. Aldosterone was measured before and after each infusion. Multi-level mixed effects linear regression was used to analyze the data.</p><p><strong>Results: </strong>The change in aldosterone between baseline and post-cosyntropin infusion was greater after treatment with eplerenone as compared to placebo (5.16 ± 2.01 ng/dL, p = 0.01). There were no differences with fludrocortisone as compared to placebo. With ANGII stimulation, there were no differences in the change in aldosterone with either eplerenone or fludrocortisone versus placebo.</p><p><strong>Conclusions: </strong>In humans, MR antagonist treatment led to a greater increase in aldosterone in response to cosyntropin stimulation as compared to placebo, but not after ANGII stimulation. Future studies are needed to investigate the presence of a MR-mediated ultra-short feedback loop at the level of the adrenal gland regulating aldosterone production in humans.</p><p><strong>Clinical trial registration number: </strong>NCT02871648.</p>","PeriodicalId":10346,"journal":{"name":"Clinical Endocrinology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13536288/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148711496","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}