The Diagnostic Challenges of Acute Myocarditis in a Patient with Fulminant Type 1 Diabetes and Transient Elevation of Anti-GAD Antibodies—A Case Report

TL;DR

A 33-year-old woman with sudden type 1 diabetes and heart issues was diagnosed with fulminant type 1 diabetes and acute myocarditis, highlighting the importance of timely diagnosis and treatment.

Contribution

This case report highlights the rare co-occurrence of fulminant type 1 diabetes and acute myocarditis, emphasizing diagnostic challenges and management strategies.

Findings

The patient exhibited abrupt onset of hyperglycemia, ketoacidosis, and elevated cardiac biomarkers consistent with fulminant type 1 diabetes.

Cardiac MRI and ECG findings supported a diagnosis of acute myocarditis despite normal coronary angiography.

The patient showed rapid recovery with insulin therapy and supportive care, maintaining insulin dependence at follow-up.

Abstract

Background: Fulminant type 1 diabetes (FT1D) is a rare but life-threatening subtype of type 1 diabetes. The concurrence of FT1D with myocarditis is uncommon and attracts further clinical attention. Case Presentation: A 33-year-old female was transferred by a local hospital to West China Hospital because of altered consciousness, abrupt onset of hyperglycemia with ketoacidosis, significantly increased cardiac biomarkers, and ST segment elevations. Her random blood glucose at the local hospital was 50.19 mmol/L. Insulin infusion and fluid resuscitation were started immediately before referral. On admission, her random blood glucose was 14.17 mmol/L. HbA1C and glycosylated albumin (GA) were 6.3% and 21.45%, respectively. Her fasting C-peptide level was 0.022 nmol/L. Anti-Glutamic Acid Decarboxylase (anti-GAD) antibody was 25.06 IU/mL. FT1D was diagnosed based on the 2012 New Diagnosis Criteria of FT1D. Electrocardiogram showed significant ST segment elevation in leads II, III, aVF, and V3-V6. Echocardiography revealed a mildly reduced left ventricular ejection fraction (LVEF) of 46%. Coronary angiography displayed no abnormality. Cardiac magnetic resonance imaging revealed areas of increased signal intensity in the interventricular septum, basal and mid inferolateral walls, and apical inferior wall and subepicardial late gadolinium enhancement (LGE), particularly in the lateral aspects of the left ventricle on T2-weighted imaging (T2WI). Acute myocarditis was diagnosed based on the European Society of Cardiology 2013 Task Force Criteria. She was treated with insulin, fluid resuscitation, and supportive care, leading to rapid recovery of ketoacidosis and cardiac function. At the four-month follow-up, she remained on insulin therapy with good glycemic control but persistent low C-peptide levels. Conclusion: This case report raises awareness about FT1D, determines the differential diagnosis of acute cardiac presentations in an FT1D patient, and highlights clinical reasoning so that clinicians can recognize and manage similar presentations on time.

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