Case Reports in Endocrinology最新文献

{"title":"Capivasertib-Associated Diabetic Ketoacidosis With Concurrent Myocardial Injury in a Patient With Pre-Existing Coronary Artery Disease.","authors":"Rabih A Noun, Ossama Sajeh Maadarani, Zouheir I Bitar","doi":"10.1155/crie/6940757","DOIUrl":"10.1155/crie/6940757","url":null,"abstract":"<p><p>Capivasertib is a serine/threonine kinase AKT (AKT1-3) inhibitor, disrupting phosphorylation of AKT substrates. When combined with fulvestrant, it is approved for hormone receptor-positive advanced breast cancer. Capivasertib therapy frequently causes hyperglycemia, including diabetic ketoacidosis (DKA). Ensure glycemic control before initiation and maintain ongoing blood glucose monitoring to reduce the risk of this potentially fatal complication. We present a case of metastatic breast cancer with initially controlled blood glucose who developed ketoacidosis and myocardial infarction during capivasertib therapy.</p>","PeriodicalId":9621,"journal":{"name":"Case Reports in Endocrinology","volume":"2026 ","pages":"6940757"},"PeriodicalIF":0.8,"publicationDate":"2026-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13655374/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149166058","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":"Persistent Hyperinsulinemic Hypoglycemia After Insulinoma Surgery: Diagnostic Impact of GLP-1 Receptor PET/CT After Negative Conventional Imaging.","authors":"Lorenzo Taglia, Alessandra Guercio, Silvia Migliari, Angela Vazzana, Riccardo C Bonadonna, Livia Ruffini, Alessandra Dei Cas","doi":"10.1155/crie/7874466","DOIUrl":"10.1155/crie/7874466","url":null,"abstract":"<p><strong>Background: </strong>Localization of recurrent or residual insulinoma may be particularly challenging in postoperative setting, especially in the presence of postoperative anatomical distortion and inconclusive conventional imaging.</p><p><strong>Case presentation: </strong>A 71-year-old man developed recurrent endogenous hyperinsulinemic hypoglycemia following apparently curative surgical enucleation of a pancreatic insulinoma. The postoperative course was complicated by intra-abdominal hemorrhage and pseudocyst formation, resulting in marked anatomical distortion. Despite persistent biochemical evidence of insulinoma recurrence, serial contrast-enhanced computed tomography (CT) and ⁶⁸Ga-DOTATOC PET/CT failed to identify residual disease. Subsequent glucagon-like peptide-1 receptor (GLP-1R) imaging with ⁶⁸Ga-NODAGA-Exendin-4 PET/CT demonstrated focal tracer uptake in the pancreatic head, highly suggestive of recurrent or residual insulinoma. Endoscopic ultrasound (EUS) subsequently confirmed a small lesion in the uncinate process, which was successfully treated with EUS-guided radiofrequency ablation (EUS-RFA). Following the procedure, hypoglycemic episodes resolved, with normalization of glucose, insulin, and C-peptide levels and no signs of recurrence at follow-up.</p><p><strong>Conclusion: </strong>This case highlights the clinical value of GLP-1 receptor PET/CT for localizing insulinoma in the context of negative conventional or somatostatin receptor (SSTR)-based imaging. Accurate functional localization may directly guide minimally invasive therapeutic interventions and help avoid high-risk reoperative pancreatic surgery.</p>","PeriodicalId":9621,"journal":{"name":"Case Reports in Endocrinology","volume":"2026 ","pages":"7874466"},"PeriodicalIF":0.8,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13647209/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149135036","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":"An Infant With Hyponatremia, Hyperkalemia, and Faltering Growth: A Case Report.","authors":"Felicia Cooper, Heather Fagan, Sindy Villacres, Pamela Ellsworth, Shilpa Gurnurkar","doi":"10.1155/crie/1964629","DOIUrl":"10.1155/crie/1964629","url":null,"abstract":"<p><p>Infants presenting with hyponatremia and hyperkalemia routinely engage clinician concern for congenital adrenal hyperplasia (CAH), a set of disorders resulting in difficulty producing glucocorticoids, mineralocorticoids, and sex steroids in the adrenal glands. However, we present the case of an infant with classic CAH-like symptoms, a negative newborn screen, and clinical features inconsistent with the diagnosis of CAH. Ultimately, the patient was diagnosed with pseudohypoaldosteronism (PHA), a condition in which aldosterone is unable to activate its receptor in the kidney. Notably, he also exhibited an uncommon complication of a left external iliac thrombus. Infants with hyponatremia and hyperkalemia without an immediately identifiable cause should be screened for urinary tract infection (UTI) and urinary tract malformations, and infants with severe urinary tract abnormality or malformation should have electrolytes monitored. This recommendation stems from the increased susceptibility of developing PHA in the setting of UTI without genitourinary tract malformation.</p>","PeriodicalId":9621,"journal":{"name":"Case Reports in Endocrinology","volume":"2026 ","pages":"1964629"},"PeriodicalIF":0.8,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13613423/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149058468","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":"Recurrent Euglycemic Diabetic Ketoacidosis Weeks After SGLT2 Inhibitor Cessation: A Case Report.","authors":"Celine Mansour, Emile Katrib, Myriam Mansour, Mirna Fares","doi":"10.1155/crie/9610048","DOIUrl":"10.1155/crie/9610048","url":null,"abstract":"<p><p>Euglycemic diabetic ketoacidosis (EDKA) is a complication of sodium-glucose cotransporter-2 (SGLT2) inhibitors that is being increasingly documented. It is challenging to diagnose, especially in critically ill patients because hyperglycemia is absent or mild. We report the case of a 71-year-old man with type 2 diabetes mellitus previously treated with dapagliflozin, which had been discontinued 2 weeks before presentation, who was admitted for tracheostomy and percutaneous endoscopic gastrostomy (PEG) placement in the context of a neurodegenerative disorder. On postoperative day 2, he was transferred to the intensive care unit (ICU) for aspiration pneumonia complicated by septic shock. He subsequently experienced recurrent episodes of high anion gap metabolic acidosis associated with positive ketonuria and relative euglycemia. The initial episode was interpreted as mixed septic lactic acidosis and SGLT2 inhibitor-associated EDKA, whereas later episodes were more consistent with isolated recurrent EDKA. Management consisted of treatment of the underlying septic shock, and repeated courses of fixed intravenous (IV) insulin infusions to close the anion gap while maintaining euglycemia. This case demonstrates the importance of suspecting EDKA, especially in critically ill patients on SGLT2 inhibitors who present with unexplained high anion gap metabolic acidosis, even when lactic acidosis is present. Early diagnosis and treatment are essential to prevent complications and relapse.</p>","PeriodicalId":9621,"journal":{"name":"Case Reports in Endocrinology","volume":"2026 ","pages":"9610048"},"PeriodicalIF":0.8,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13613943/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149058551","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":"Diazoxide-Responsive Congenital Hyperinsulinism in a Preterm Infant With Homozygous <i>ABCC8</i> Mutation: A Case Report.","authors":"Prerana Kansakar, Grisha Gurung, Sadikshya Bhandari, Kriti Shrestha, Bhumika G C, Shreya Thapa, Rasik Acharya","doi":"10.1155/crie/7968566","DOIUrl":"https://doi.org/10.1155/crie/7968566","url":null,"abstract":"<p><strong>Introduction: </strong>Congenital hyperinsulinism (CHI) is characterized by inappropriate insulin secretion resulting in persistent neonatal hypoglycemia. CHI is often linked to mutations in the <i>ABCC8</i> and <i>KCNJ11</i> genes and can lead to persistent hypoglycemia, seizures, and neurological injury, making early diagnosis and management essential.</p><p><strong>Case report: </strong>We describe a late-preterm Nepalese infant born at 34 weeks and 5 days of gestation, weighing 5.26 kg, to a 32-year-old gravida four nondiabetic mother. The infant developed significant hypoglycemia just 2 h after birth. Despite a glucose infusion rate (GIR) of 12 mg/kg/min, the infant had persistent hypoglycemia. A critical sample confirmed hyperinsulinism, prompting treatment with octreotide, intravenous (IV) GIR of 17 mg/kg/min and later diazoxide. Due to limited IV access, a continuous enteral GIR of 9 mg/kg/min was administered through an orogastric (OG) tube. Genetic testing revealed a homozygous pathogenic p.Arg1214Gln mutation in the <i>ABCC8</i> gene, and ¹⁸F-DOPA PET-CT (2-deoxy-2-[fluorine-18]fluoro-D-glucose positron emission computed tomography) showed diffuse pancreatic uptake. At 5 months, interruption of diazoxide therapy led to a hypoglycemic seizure (blood glucose level: 29 mg/dL), which resolved after the treatment resumed. Despite the typical association of homozygous <i>ABCC8</i> mutations with diazoxide nonresponsiveness, this infant achieved sustained glycemic control on diazoxide. On subsequent follow-ups, the child remains stable and continues to achieve normal developmental milestones.</p><p><strong>Conclusion: </strong>Early recognition and timely management are crucial in effective management of CHI. This case shows rare diazoxide responsiveness in homozygous <i>ABCC8</i> mutation. This case suggests that a carefully monitored therapeutic trial of diazoxide may still be reasonable in selected patients with homozygous <i>ABCC8</i> mutations before concluding complete medical unresponsiveness.</p>","PeriodicalId":9621,"journal":{"name":"Case Reports in Endocrinology","volume":"2026 ","pages":"7968566"},"PeriodicalIF":0.8,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13599591/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149036594","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":"Exploring Thyrotoxic Hypercalcaemia Through Two Cases: A Myriad of Uncertainties.","authors":"Don Asiri Abeysiriwardana, Pahala Gamage Nipuna Jeewantha Dias, Warsha Dilhani De Zoysa, Arosha Sampath Dissanayake","doi":"10.1155/crie/3906797","DOIUrl":"10.1155/crie/3906797","url":null,"abstract":"<p><p>Hypercalcaemia is a recognised complication of thyrotoxicosis usually related to increased bone resorption. However, coexistent hyperphosphataemia is uncommon and may create diagnostic uncertainty. It is postulated that serum calcium and phosphate levels rise due to high bone turnover and increased renal reabsorption of phosphate in response to excess thyroxine. Hypercalcaemia may also alter the clinical presentation of thyrotoxicosis, making both diagnosis and management challenging. We report two patients with this unusual biochemical presentation. The first patient was a 69-year-old woman who presented with body aches, lethargy, low mood, constipation, polyuria, and proximal muscle weakness for 2 months. The second was a 56-year-old woman who presented with palpitations, anxiety, tremulousness, dyspnoea, dysphagia, and headache for 4 months. Both had multinodular goitres (MNGs) without eye disease. Their TSH levels were undetectably low with extremely high free T4 levels. Serum calcium and phosphate levels were high in both patients. ALP levels were mildly elevated, vitamin D levels were deficient or insufficient, and parathyroid hormone (PTH) levels were low-normal. DXA scans revealed severe osteoporosis. Both patients improved clinically and biochemically with adequate intravenous hydration, frusemide, carbimazole, propranolol, and bisphosphonates. The second patient underwent a successful left thyroid lobectomy, while the first patient remained well on medical treatment. Unexplained hypercalcaemia and hyperphosphataemia should alert the clinicians to the possibility of underlying thyrotoxicosis. Prompt recognition and management is essential to prevent bone loss, correct metabolic abnormalities, and avoid complications. Clinicians should also consider the possibility of hypercalcaemia associated with thyroid dysfunction in patients presenting with nonspecific symptoms such as fatigue, constipation, proximal weakness, polyuria, or mood changes.</p>","PeriodicalId":9621,"journal":{"name":"Case Reports in Endocrinology","volume":"2026 ","pages":"3906797"},"PeriodicalIF":0.8,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13591542/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149015603","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":"Ultrasound-Guided Drainage via Thyroid Catheterization for Acute Suppurative Thyroiditis: A Case Report.","authors":"Bao-Dong Zhang, Xue-Meng Guan, Hai-Quan Wang, Feng Zhang, Xiao-Zhi Zhai, Xiao-Sha Pei, Xin Zhao, Xin He","doi":"10.1155/crie/2098333","DOIUrl":"10.1155/crie/2098333","url":null,"abstract":"<p><strong>Background: </strong>Acute suppurative thyroiditis (AST) is a rare but potentially life-threatening infection of the thyroid gland that requires prompt diagnosis and management. While antibiotic therapy remains the cornerstone of treatment, surgical intervention is often necessary in cases complicated by abscess formation. Minimally invasive approaches have emerged as alternative strategies.</p><p><strong>Case presentation: </strong>A 49-year-old woman with no significant past medical history presented with a rapidly enlarging painful neck mass, dysphagia, and radiating pain. Initial laboratory findings demonstrated suppressed thyroid-stimulating hormone (TSH) and elevated free thyroxine (FT4), accompanied by elevated inflammatory markers, leading to an initial misdiagnosis of subacute thyroiditis. However, persistent and worsening symptoms prompted further evaluation. Ultrasonography (USG) and contrast-enhanced computed tomography (CT) revealed a large abscess involving the left thyroid lobe. Fine-needle aspiration confirmed AST. The patient was treated with intravenous antibiotics and underwent ultrasound-guided catheter drainage, with approximately 14 mL of pus initially evacuated. She showed rapid clinical improvement, and follow-up imaging confirmed resolution of the abscess with normalization of thyroid function.</p><p><strong>Conclusion: </strong>This case highlights the importance of distinguishing AST from other causes of thyrotoxicosis. Ultrasound-guided catheter drainage may represent an effective and minimally invasive alternative to conventional surgical management, particularly in patients with large or deep thyroid abscesses.</p>","PeriodicalId":9621,"journal":{"name":"Case Reports in Endocrinology","volume":"2026 ","pages":"2098333"},"PeriodicalIF":0.8,"publicationDate":"2026-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13591121/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149015574","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":"Diagnosis of Antipsychotic Medication-Induced Severe Hypertriglyceridaemia by the Phenomenon of Pseudohyponatraemia and Successful Management With Variable-Rate Intravenous Insulin Infusion: A Case Report.","authors":"Adam Coleman, Grace Kettyle, Monica Monaghan, Edward McKeever","doi":"10.1155/crie/2376136","DOIUrl":"10.1155/crie/2376136","url":null,"abstract":"<p><strong>Background: </strong>Hypertriglyceridaemia (HTG) is a common condition resulting from genetic and environmental factors. Second-generation antipsychotic (SGA) medications are classically associated with the development of metabolic syndrome, of which HTG is a hallmark feature. Severe HTG is the third most common cause of acute pancreatitis, which has significant associated morbidity and mortality risk. It is therefore vital to rapidly and sustainably reduce triglyceride levels in patients presenting with severe HTG.</p><p><strong>Clinical case: </strong>A 35-year-old gentleman with a history of psychiatric illness taking SGA medications (quetiapine and risperidone) presented to our hospital with apparent hyponatraemia. With associated hyperosmolality (302 mOsm/kg), a diagnosis of pseudohyponatraemia was made. Upon further investigation, pseudohyponatraemia was identified to be due to severe HTG (72.8 mmol/L) and hyperglycaemia (26.0 mmol/L). There were no clinical or biochemical features of pancreatitis. A variable-rate infusion of intravenous insulin was commenced. Over the 10-day admission a fall in triglycerides to 10.5 mmol/L was observed without any adverse events. Acute pancreatitis did not develop during the inpatient admission or during outpatient follow-up, and triglyceride levels have fallen substantially (3.2 mmol/L at 5 months) having been switched from quetiapine and risperidone to aripiprazole, an SGA associated with less metabolic disturbance.</p><p><strong>Conclusion: </strong>This case demonstrates the safe and effective management of SGA-associated severe HTG with intravenous insulin infusion to prevent acute pancreatitis. It also highlights the utility of pseudohyponatraemia as a useful way of detecting severe HTG and the impact of SGA medications in the aetiology of severe HTG.</p>","PeriodicalId":9621,"journal":{"name":"Case Reports in Endocrinology","volume":"2026 ","pages":"2376136"},"PeriodicalIF":0.8,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13554722/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148918186","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":"Metyrapone in the Management of Severe Hypercortisolism Secondary to Ectopic Cushing's Syndrome.","authors":"Guy I Sydney, Spyridon Ntelis, Sachin K Majumdar","doi":"10.1155/crie/1796526","DOIUrl":"10.1155/crie/1796526","url":null,"abstract":"<p><p>Ectopic Cushing's syndrome (ECS) is a rare but important cause of ACTH-dependent Cushing's syndrome. Metyrapone, a steroidogenesis inhibitor targeting 11-β hydroxylase, has shown effectiveness in controlling hypercortisolism. However, little is known about the practical aspects of its initiation, use, and effectiveness in ECS. We present three cases of severe hypercortisolism secondary to ECS managed with metyrapone and report our experience. Case 1: a 56-year-old male with high-grade neuroendocrine carcinoma. Case 2: a 67-year-old man with a history of stage IIB non-small cell lung cancer (NSCLC) with metastatic neuroendocrine carcinoma. Case 3: a 64-year-old man with metastatic prostate cancer. Biochemical control was achieved with rapid titration of low doses of daily metyrapone in all three cases. Based on our experience, we recommend an initial dose of 1000-1500 mg of metyrapone daily, in divided doses, with physiologic glucocorticoid replacement to mitigate the risk of adrenal insufficiency. Despite improvements in cortisol levels and stabilization of metabolic derangements, all three patients ultimately transitioned to comfort-focused care. Given the rarity, heterogeneity, and aggressiveness of this condition, rapid diagnosis and standardized pharmacologic approach are difficult to achieve. More data are needed to guide optimal therapy selection, dosing, and titration in ECS.</p>","PeriodicalId":9621,"journal":{"name":"Case Reports in Endocrinology","volume":"2026 ","pages":"1796526"},"PeriodicalIF":0.8,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13535853/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148879222","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":"Unilateral Graves' Disease Developing During Treatment With Tirzepatide in a Patient With Diabetes: A Case Report.","authors":"Yusuke Deto, Ryo Hasegawa, Shoya Ino, Satoru Shibata, Kouhei Ohno, Takahito Itoh, Tomoaki Matsumoto, Takayuki Miki","doi":"10.1155/crie/9628050","DOIUrl":"10.1155/crie/9628050","url":null,"abstract":"<p><strong>Background: </strong>Tirzepatide is a dual agonist of the glucose-dependent insulinotropic polypeptide (GIP) receptor and glucagon-like peptide-1 (GLP-1) receptor, demonstrates significant efficacy in lowering blood glucose levels and reducing body weight. Consequently, its use has increased among patients with type 2 diabetes and obesity. Gastrointestinal symptoms are commonly recognized as adverse effects of tirzepatide, while other adverse effects, such as thyroid abnormalities, are rare. This report describes a rare case of unilateral Graves' disease that developed during treatment with tirzepatide.</p><p><strong>Case presentation: </strong>A 59-year-old woman with type 2 diabetes was treated with tirzepatide resulting in marked glycemic improvement and weight loss. During treatment, she developed fatigue and palpitations, initially attributed to the effects of the drug. Further evaluation revealed thyrotoxicosis with suppressed thyroid-stimulating hormone (TSH), elevated free thyroid hormones, and positive autoantibodies. Imaging revealed increased vascularity and technetium-99 m uptake confined to the right thyroid lobe, consistent with unilateral Graves' disease. The patient's clinical symptoms and thyroid function rapidly improved after initiating antithyroid medications.</p><p><strong>Conclusions: </strong>Although a causal relationship between tirzepatide and the development of Graves' disease cannot be established, this case highlights the difficulty of recognizing hyperthyroidism during potent glucose-lowering therapy. Thus, thyroid function testing should be considered in patients with type 2 diabetes who experience symptoms such as fatigue or palpitations during treatment with tirzepatide.</p>","PeriodicalId":9621,"journal":{"name":"Case Reports in Endocrinology","volume":"2026 ","pages":"9628050"},"PeriodicalIF":0.8,"publicationDate":"2026-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13527387/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863726","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}