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Clinicians should treat unexplained illness in patients taking SGLT2 inhibitors as potentially metabolic acidosis, independent of blood glucose levels. The case highlights a non-diabetic elderly man with transthyretin cardiac amyloidosis who developed severe ketosis and high anion-gap acidosis while presenting with confusion, dehydration, and gastrointestinal symptoms on background SGLT2 inhibitor use.",{"@graph":69,"@context":123},[70,84,106],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":35,"@type":76,"position":81},"https://docshare.wps.com/document/healthcare/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/euglycemic-ketoacidosis-induced-by-dapagliflozin-in-a-non-diabetic-patient-with-cardiac-amyloidosis/455187/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/euglycemic-ketoacidosis-induced-by-dapagliflozin-in-a-non-diabetic-patient-with-cardiac-amyloidosis/455187.png","ImageObject",300,407,{"name":92,"@type":93},"SANS","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-31","2026-09-30",true,{"@type":102,"interactionType":103,"userInteractionCount":105},"InteractionCounter",{"@type":104},"ViewAction",12,{"@type":107,"mainEntity":108},"FAQPage",[109,115,119],{"name":110,"@type":111,"acceptedAnswer":112},"Why can dapagliflozin cause euglycemic ketoacidosis in non-diabetic patients?","Question",{"text":113,"@type":114},"SGLT2 inhibitors can induce euglycemic ketoacidosis by causing significant ketosis and metabolic acidosis without marked hyperglycemia. Reports in non-diabetics are scarce, but the risk still exists.","Answer",{"name":116,"@type":111,"acceptedAnswer":117},"What symptoms and exam findings occurred in the reported patient?",{"text":118,"@type":114},"The patient presented with generalized weakness and confusion, along with progressive fatigue and reduced oral intake followed by diarrhea and vomiting. Examination showed dehydration and an irregular rhythm due to new-onset atrial fibrillation, with abdominal epigastric tenderness.",{"name":120,"@type":111,"acceptedAnswer":121},"How was the diagnosis of euglycemic ketoacidosis established?",{"text":122,"@type":114},"Diagnosis relied on metabolic acidosis with a high anion gap and low bicarbonate plus significant ketonemia, alongside euglycemia in a patient taking an SGLT2 inhibitor. Differential causes included starvation ketosis, lactic acidosis, sepsis-related acidosis, and mixed causes.","https://schema.org",{"og:url":83,"og:type":125,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":127,"canonical":83},"index,follow",{"doc_id":129,"site_id":62},455187,1790813107,{"code":4,"msg":5,"data":132},{"doc_id":129,"user_id":133,"nickname":92,"user_avatar":134,"doc_module":4,"category_id":34,"category_name":35,"doc_title":65,"doc_description":67,"doc_content":135,"file_id":136,"file_url":137,"file_type":138,"file_size":139,"view_count":105,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":19,"language":140,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":141,"faqs":142,"seo_title":143,"seo_description":67,"update_tm":144,"read_time":52,"preview_page_count":4},962090760505,"https://ap-avatar.wpscdn.com/davatar_155a257f0dc6eb9ab79c44ca47cae57d","Clinical Case Reports  \nCASE REPORT  OPEN ACCESS   \nEuglycemic Ketoacidosis Induced by Dapagliflozin ina Non-Diabetic Patient With Cardiac Amyloidosis  \nSalhamoud Abdelfatah Saleh Hamoud | Ellie Harding  \nDepartment of Medicine, University Hospitals Plymouth NHS Trust, Plymouth, UK Correspondence: Salhamoud Abdelfatah Saleh Hamoud ([salhamoud@hotmail.com](salhamoud@hotmail.com))  \nReceived: 29 October 2025 | Revised: 23 December 2025 | Accepted: 28 December 2025  \nKeywords: cardiac amyloidosis | dapagliflozin | euglycemic ketoacidosis | non-diabetic patient | SGLT2 inhibitors  \nABSTRACT  \nDapagliflozin, though beneficial in heart failure, can rarely cause euglycemic ketoacidosis even in non-diabetic patients. Clinicians should maintain a high index of suspicion for metabolic acidosis in patients on SGLT2 inhibitors presenting with unexplained illness, regardless of blood glucose level.  \n1 | Introduction  \nSodium–glucose co-transporter 2 (SGLT2) inhibitors, including dapagliflozin, canagliflozin, and empagliflozin, have proven benefits in reducing morbidity and mortality in heart failure, regardless of diabetes status [1, 2]. However, their use carries a risk of euglycemic ketoacidosis (eKA), characterized by significant ketosis and metabolic acidosis without marked hyperglycemia [3–5] . Although well described in diabetic populations, reports in non-diabetics remain scarce [6, 7] .  \nCardiac amyloidosis is a restrictive cardiomyopathy caused by extracellular amyloid fibril deposition, often involving multiple organ systems including the gastrointestinal tract and kidneys [8, 9]. These effects may predispose to dehydration, reduced oral intake, and autonomic dysfunction, potentially increasing the risk of metabolic complications related to SGLT2 inhibitors.  \n2 | Case History and Examination  \nAn 88-year-old man with ischaemic heart disease, chronic heart failure (LVEF 45%), moderate mitral regurgitation, pulmonary artery systolic pressure 58 mmHg, and transthyretin cardiac amyloidosis treated with tafamidis (61 mg daily) presented with generalized weakness and confusion.  \nHis daughter reported progressive fatigue and reduced oral intake over several weeks, followed by 4 days of diarrhea and vomiting. On the day of admission, he developed upper abdominal discomfort and acute confusion. Due to his confusion, a reliable history regarding alcohol consumption could not be obtained.  \nHe had no history of diabetes. His current medications included dapagliflozin 10 mg daily (for 5 months), bumetanide, nicorandil, bisoprolol, apixaban, ranolazine, and tafamidis.  \nOn examination, he was afebrile, with a blood pressure of 106/60 mmHg, a heart rate of 105 bpm (irregularly irregular), and a respiratory rate of 22 breaths per minute. Oxygen saturation was 96% on room air. He appeared dehydrated with dry mucous membranes and reduced skin turgor. Jugular venous pressure was not elevated. Cardiovascular examination revealed an irregular rhythm with a soft systolic murmur at the apex. Abdominal examination was soft with mild epigastric tenderness. No focal neurological deficit was found. ECG revealed new-onset atrial fibrillation without ST-T changes.  \nUrine culture grew Enterococcus faecalis sensitive to coamoxiclav. HbA1c was 43 mmol/mol (normal range \u003C 42 mmol/ mol) . Echocardiography showed concentric LV hypertrophy with apical trabeculations consistent with cardiac amyloidosis. His blood tests on admission are summarized in Table 1.  \nThis is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.  \n© 2026 The Author(s). Clinical Case Reports published by John Wiley & Sons Ltd.  \nClinical Case Reports, 2026; 14:e71818 1 of 4  \n[https://doi.org/10.1002/ccr3.71818](https://doi.org/10.1002/ccr3.71818)  \n3 | Differential Diagnosis, Investigations, and Treatment  \nDifferential diagnoses included the foll","cbCaiqc5PySFGbJ7","https://ap.wps.com/l/cbCaiqc5PySFGbJ7","pdf",165825,"English","# Introduction\n# Case History and Examination\n# Differential Diagnosis, Investigations, and Treatment","[{\"question\":\"Why can dapagliflozin cause euglycemic ketoacidosis in non-diabetic patients?\",\"answer\":\"SGLT2 inhibitors can induce euglycemic ketoacidosis by causing significant ketosis and metabolic acidosis without marked hyperglycemia. Reports in non-diabetics are scarce, but the risk still exists.\"},{\"question\":\"What symptoms and exam findings occurred in the reported patient?\",\"answer\":\"The patient presented with generalized weakness and confusion, along with progressive fatigue and reduced oral intake followed by diarrhea and vomiting. Examination showed dehydration and an irregular rhythm due to new-onset atrial fibrillation, with abdominal epigastric tenderness.\"},{\"question\":\"How was the diagnosis of euglycemic ketoacidosis established?\",\"answer\":\"Diagnosis relied on metabolic acidosis with a high anion gap and low bicarbonate plus significant ketonemia, alongside euglycemia in a patient taking an SGLT2 inhibitor. Differential causes included starvation ketosis, lactic acidosis, sepsis-related acidosis, and mixed causes.\"}]","Euglycemic Ketoacidosis Induced by Dapagliflozin in a Non-Diabetic Patient With Cardiac Amyloidosis | PDF",1790742291]