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Case Report

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

by
Thet Htar Swe
1,†,
Yan Ren
1,†,
Hongping Gong
1,2,
Zhenyi Li
1,
Qingguo Lv
1,
Xingwu Ran
1,
Xin Wei
3,* and
Chun Wang
1,*
1
Department of Endocrinology and Metabolism, West China Hospital, Sichuan University, Chengdu 610041, China
2
International Medical Center Ward, General Practice Medical Center, West China Hospital, Sichuan University, Chengdu 610041, China
3
Department of Cardiology, West China Hospital, Sichuan University, Chengdu 610041, China
*
Authors to whom correspondence should be addressed.
†
These authors contributed equally to this work.
J. Clin. Med. 2026, 15(4), 1553; https://doi.org/10.3390/jcm15041553
Submission received: 20 January 2026 / Revised: 9 February 2026 / Accepted: 12 February 2026 / Published: 15 February 2026
(This article belongs to the Section Endocrinology & Metabolism)
Browse Figures
Versions Notes

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.

1. Introduction

Fulminant type 1 diabetes (FT1D) is an independent subtype of type 1 diabetes which was first reported by Imagawa and colleagues in 2000 [1]. It is characterized by a sudden, rapid onset of hyperglycemia and a marked reduction in endogenous insulin secretion because of almost complete destruction of beta cells within days or weeks [2]. This leads to severe metabolic derangement and diabetic ketoacidosis (DKA), which is often life-threatening. Acute myocarditis, most commonly caused by viral infection, sometimes leads to acute heart failure and sudden death. The concomitant occurrence of FT1D and acute myocarditis is relatively rare, and the presentation is usually severe and potentially life-threatening. Herein, we report an FT1D case complicated with acute myocarditis to raise awareness about this rare diabetic subtype and its potential cardiac involvement, as well as to emphasize differential diagnosis in acute cardiac presentations.

2. Case Report

2.1. Case Presentation and Diagnosis Assessment

A 33-year-old female with no significant past medical history presented with two days of persistent nausea, vomiting, and lethargy at a local hospital. The patient was considered to have acute gastritis and treated, but the symptoms were not relieved. One day later, she was brought to the emergency department of another local hospital because of conscious disturbance, shortness of breath, and chest tightness. Her blood tests showed a random blood glucose level of 50.19 mmol/L, with elevated cardiac markers. The electrocardiogram also showed ST segment elevations. DKA complicated with acute coronary syndrome was suspected, and she was transferred to the emergency department of West China Hospital, Sichuan University, after regular insulin infusion and fluid resuscitation were started immediately.
On examination, the patient was verbally responsive. Initial vital signs revealed T 36.3 °C, P 105/min, R 18/min, and BP 99/52 mmHg. Her oxygen saturation was 97%. Her body mass index (BMI) was 18.6 kg/m2. Her skin, lips, and oral mucosa were dry. Pupils were equal and responsive to light and accommodation. There is no jugular venous distension. No pathological murmurs and abnormal heart sounds were heard. No abnormality was detected in her lungs and abdomen. No pathological reflexes or signs of meningeal irritation were present. Muscle strength of both limbs was Grade 5/5. No peripheral edema was observed.
Laboratory findings are shown in Table 1. Routine blood tests showed WBC of 18.06 × 109/L, neutrophils of 16.63 × 109/L, RBC of 3.8 × 1012/L, and Hb of 118 g/L. Urine analysis showed glucose (+++) and ketone (+++). Arterial blood gas analysis showed metabolic acidosis with pH of 7.284 and HCO3− of 9.2 mmol/L. Her liver and renal functions were normal. Her random blood glucose was 14.7 mmol/L, and 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) antibodies were 25.06 IU/mL, while insulin autoantibody (IAA), insulinoma-associated antigen-2 antibody (IA-2A), islet cell antibody (ICA), and zinc transporter 8 antibody (ZnT8A) were negative. Serological tests for TORCH (toxoplasmosis, rubella, cytomegalovirus, and herpes simplex virus types I/II) and assays for Epstein–Barr virus, coxsackievirus, parainfluenza virus, and SARS-CoV-2 were all negative. The autoimmune and vasculitis screens were negative (Table 1). The detailed methods of measuring laboratory data are described in Appendix A.
Her cardiac biomarkers were myoglobin of 1495 ng/mL, CK-MB > 300.00 ng/mL, troponin-T(TnT) of 3378.0 ng/L, and N-terminal B-type natriuretic peptide (NT-proBNP) of 4278 ng/L (Figure 1).
The electrocardiogram (ECG) showed significant ST segment elevation in leads II, III, aVF, and V3-V6. The serial ECG changes are shown in Figure 2 and Figure 3. ECG changes paralleled troponin kinetics and improved progressively as troponin levels declined.
Echocardiography revealed a mildly reduced left ventricular ejection fraction (LVEF) of 46%. There was diffuse hypokinesis of the posterior–inferior wall, along with global wall motion incoordination, and left ventricular systolic function was mildly impaired. Coronary angiography did not detect any stenosis or obstruction (Figure 4).
Cardiac magnetic resonance imaging showed areas of increased signal intensity in the interventricular septum, basal and mid-inferolateral walls, and apical inferior wall, consistent with myocardial edema and subepicardial late gadolinium enhancement (LGE), particularly in the lateral aspects of the left ventricle, with sparing of the sub-endocardium in T2-weighted imaging (T2WI), consistent with a non-ischemic pattern of myocardial injury. Elevated native T1 of 1316.2 ms (reference range: 1193.2 (1124.9–1265.1) ms at 3 T) and T2 relaxation times of 44.3 ms (reference range: 35.9 (30.9–41.0) ms at 3 T) were observed (Figure 5).

2.2. Diagnosis, Treatment, and Outcomes

The patient was diagnosed with acute myocarditis based on the European Society of Cardiology 2013 Task Force Criteria [3], diabetic ketoacidosis, and fulminant type 1 diabetes according to the 2012 New Diagnosis Criteria of FT1D [4]. She was treated with fluid resuscitation, regular insulin infusion, correcting electrolyte disturbance, and acid–base imbalance. ST segment elevation gradually disappeared on the twelfth day. CK-MB and troponin-T levels gradually decreased and returned to normal on the tenth day. Anti-Glutamic Acid Decarboxylase Antibody (Anti-GAD) was reduced to 19.53 IU/mL on the second day. A cardiac MRI scan on the seventh day revealed a recovered ejection fraction of 51.9%. The 75 g oral glucose tolerance test and C-peptide releasing test showed that plasma glucose (mmol/L) at 0 min, 30 min, 60 min, 120 min, and 180 min was 9.53, 16.52, 22.73, 28.49, and 31.06, and C-peptide (nmol/L) at 0 min, 30 min, 60 min, 120 min, and 180 min was 0.018, 0.030, 0.040, 0.040, and 0.050, respectively. Insulin Aspart before meals and Insulin Glargine at bedtime were started subcutaneous on the fourth day, and blood glucose was controlled. The patient was discharged with multiple daily insulin injections (MDIs).

2.3. Follow-Up

At the four-month follow-up, her self-monitored blood glucose (SMBG) was fasting blood glucose of 4–5 mmol/L and postprandial blood glucose of 6–9 mmol/L. Results of the 75 g OGTT and C-peptide releasing test revealed that plasma glucose (mmol/L) at 0 min, 30 min, 60 min, and 120 min was 4.71, 10.27, 16.39, and 24.39, and C-peptide (nmol/L) at 0 min, 30 min, 60 min, and 120 min was <0.007, <0.007, 0.013, and 0.030, respectively. HbA1C was 6%. Anti-GAD was 1.34 IU/mL (reference range: <10 IU/mL). Later, it transitioned from multiple daily insulin injections (MDIs) to continuous subcutaneous insulin infusion (CSII).

3. Discussion

This is a rare case of acute myocarditis [3] and fulminant type 1 diabetes (FT1D) [4]. FT1D was first identified by Imagawa and colleagues in 2000 [1]. In 2012, the new diagnosis criteria of FT1D were reported by the same authors [4]. FT1D is confirmed when (1) DKA develops within approximately 7 days of hyperglycemic symptom onset, (2) plasma glucose ≥ 16.0 mmol/L (≥288 mg/dL) and HbA1c < 8.5%, and 3) urinary C-peptide excretion < 10 μg/day or fasting serum C-peptide level < 0.3 ng/mL (<0.10 nmol/L) and <0.5 ng/mL (<0.17 nmol/L) after intravenous glucagon (or after meal) load at onset. Our patient’s clinical course and laboratory findings fulfilled all three major criteria for the diagnosis of FT1D.
Islet autoantibodies are generally not detected in FT1D patients. However, a nationwide survey in Japan stated that 4.8% of FT1D patients had anti-GAD antibodies [5]. Oikawa et al. described a significant inverse correlation between islet autoantibody titers and the interval from the onset of prodromal symptoms to diagnosis [6]. Consistent with this finding, our case’s anti-GAD titers declined rapidly from 25.06 IU/mL to 19.53 IU/mL within one day after diagnosis and to 1.34 IU/mL four months later. To our knowledge, this is the first reported case of fulminant type 1 diabetes complicated by acute myocarditis, which documented the transient elevation of anti-GAD antibodies.
Abrupt destruction of beta cells can release autoantigens, and this may trigger the production of autoantibodies, including anti-GAD. However, only a few percent of FT1D patients are anti-GAD-positive. This may be explained by genetic susceptibility. Tsutsumi et al. reported that the most common HLA genotype associated with FT1D is the DRB1*04:05-DQB1*04:01 haplotype (DR4-DQ4), but DRB1*09:01-DQB1*03:03 (DR9-DQ3) was strongly associated with anti-GAD-positive FT1D [7]. We did not perform genetic testing in this patient. But there are some reported cases of FT1D with transient elevation of anti-GAD antibodies with susceptible haplotype DRB1*09: 01-DQB1*03: 03 [8,9]. Recently, Imagawa highlighted that the presence or absence of GAD antibodies is not described in the diagnosis criteria because the clinical characteristics of FT1D patients with or without GAD antibodies are similar. Here, we would like to raise awareness about transient GAD positivity in FT1D to avoid misclassification as classic autoimmune T1D. FT1D progresses more rapidly and causes more severe metabolic derangement. Therefore, it is important to recognize the disease on time and provide more intensive treatment and monitoring for other systemic complications.
Her symptoms of chest tightness, abnormally elevated cardiac biomarkers, and ST segment elevations can be misdiagnosed as acute coronary syndrome (ACS). However, considering her age of onset and absence of risk factors, ST-elevated myocardial infarction (STEMI) was unlikely. We excluded ACS with coronary angiography. Subsequently, based on the patient’s clinical history and presenting symptoms, a high suspicion of viral infection, diffuse hypokinesis on echocardiography, and characteristic late gadolinium enhancement (LGE) on cardiovascular magnetic resonance imaging, acute myocarditis was diagnosed according to the 2013 European Society of Cardiology Task Force criteria [3].
FT1D and myocarditis are frequently associated with preceding viral infection [2,4]. Clinicians have reported the involvement of Coxsackie B4 [10], Parainfluenza-3 [11], cytomegalovirus [12], and Epstein–Barr virus [13] in the pathogenesis of FT1D and acute myocarditis. Notably, our patient exhibited gastrointestinal and flu-like symptoms three days before the onset of the disease. We checked common viral serologies such as TORCH (toxoplasmosis, rubella, cytomegalovirus, and herpes simplex virus types I/II) and performed assays for Epstein–Barr virus, coxsackievirus, parainfluenza virus, and SARS-CoV-2. However, we did not check the viral subtypes. Although the tested viral panel was negative, the possibility of a viral etiology cannot be ruled out. Four main factors that can cause FT1D include viral infection, drug-induced hypersensitivity syndrome (DIHS)/drug reaction with eosinophilia and systemic symptoms (DRESS), pregnancy, and the administration of immune checkpoint inhibitors [2]. Based on the patient’s presentation and clinical course, we suspect the viral infection to be a common cause of both FT1D and acute myocarditis. There are similar reports that cannot definitely detect the virus but cannot rule out viral infection, like our case [14,15].
Makino et al. [10] reported a similar case of myocarditis and FT1D with positive anti-GAD antibodies in a 25-year-old Japanese man. It is unclear whether the elevation was transient. Our case and Makino et al.’s case had preceding flu-like symptoms before the onset of the disease. The level of anti-GAD antibodies in Makino et al.’s case was lower, random blood glucose was similar, acidosis and cardiac dysfunction was more severe. Sub-epicardial late gadolinium enhancement was found in the septal and lateral walls of the left ventricle in both cases. Treatment of both cases was insulin infusion and supportive therapy, and the ejection fraction improved around the 7th and 10th day. Interestingly, in the cases of Makino et al., Ohara et al., Hiramatsu et al., Egashira et al., Qin Jin et al., and Yu Fang et al., acute myocarditis developed one to three days after the onset of hyperglycemia and correction of DKA [10,11,12,13,14,15]. A maladaptive metabolic response under the influence of fluid and electrolyte imbalance due to DKA and DKA correction may also contribute to the development of myocardial injury. In our case, hyperglycemia, DKA, ST elevation, and elevated cardiac enzyme levels occurred together on the same day before DKA correction. Frankly, it is almost impossible to definitely determine the cause of myocarditis in FT1D patients. It can be because of viral infection or metabolic derangement or DKA. In other words, it is challenging to definitely identify whether myocarditis is a bystander complication of infection or caused by metabolic derangement or DKA in FT1D patients. We acknowledge it as a limitation of this case report. It requires further research and larger sample studies to clarify.
Beyond myocarditis, FT1D can be associated with other types of acute myocardial injury, especially those with DKA. Hyperglycemia and metabolic acidosis can lead to volume depletion and electrolyte disturbances. Hadi et al. reported that severe dehydration can cause coronary underfilling, consequently causing coronary spasm, myocardial hypoperfusion, injury, and even myocardial infarction [16]. This may lead to elevated cardiac enzymes and ST segment elevation. However, the coronary angiography of Hadi et al.’s case showed low-caliber, atretic vessels, with multiple stenoses in all major epicardial vessels. Our case’s coronary angiogram on admission revealed no stenosis or occlusion. Moreover, patients with DKA often complicate with moderate-to-severe hypophosphatemia [17], which could result in impairment of myocardial contractility, unexplained ECG changes, and reduced cardiac output [18]. Although our patient had acute hypophosphatemia on admission, this does not explain the ST segment elevation or the cardiac MRI findings.
Another differential diagnosis is stress-induced (Takotsubo) cardiomyopathy triggered by catecholamine surge related to DKA-associated stress and infection. Stress-induced cardiomyopathy shows a similar clinical course to myocarditis. Three cases of FT1D, DKA, and stress-induced cardiomyopathy have been reported [19,20,21]. However, the elevations of cardiac enzymes in stress-induced cardiomyopathy are typically lower compared to myocarditis and myocardial infarction [14,22]. Our case had higher levels of cardiac enzymes. In addition, stress-induced cardiomyopathy affects the apical and midventricular myocardium, often with a characteristic “apical ballooning” pattern rather than diffuse hypokinesis. Our patient’s echocardiogram revealed diffuse hypokinesis of the posterior–inferior wall. Stress-induced cardiomyopathy patients present with diffuse ST elevation or T-wave inversion in the precordial leads, sometimes mimicking anterior STEMI. Our case’s 12-lead ECG showed ST elevation in the lateral and inferior leads. Furthermore, late gadolinium enhancement (LGE), which is typically seen in areas of myocardial scarring, is usually absent in Takotsubo cardiomyopathy [10]. The levels of elevated cardiac enzymes, echocardiogram, ECG, and MRI findings make Takotsubo cardiomyopathy less likely in this case. However, stress-induced cardiomyopathy should be considered in similar DKA-related stressful presentations.
Given the age of onset, myocarditis in the patient can be the first clinical expression of inherited cardiac conditions (ICCs), especially dilated cardiomyopathy (DCM) and arrhythmogenic cardiomyopathy (ACM). A population-based cohort study identified DCM- or ACM-associated genetic variants in 8% of patients with acute myocarditis [23]. Genetic testing was not performed in this case. The patient and her family denied familial history of cardiomyopathy or sudden cardiac death. Her parents, her parents’ siblings, and her siblings are all healthy and alive. Echocardiogram on admission showed normal cardiac chamber sizes, wall thickness, interventricular septum thickness, and no features suggestive of hypertrophic, dilated, or restrictive cardiomyopathy. Cardiac magnetic resonance imaging also showed no features suggestive of structural abnormality. Regular follow-up after discharge was recommended. Genetic sequencing may help predict the prevalence of inherited cardiomyopathy in previously healthy but genotype-positive individuals, in whom myocarditis may trigger the phenotypic expression of ICCs. About 30% of myocarditis cases progress to dilated cardiomyopathy and are associated with poor prognosis [3]. A recent meta-analysis reported that TTN and DSP are the most frequently affected sarcomeric and desmosomal genes in myocarditis patients who were later diagnosed with cardiomyopathy [24]. Therefore, in similar cases, genetic sequencing may be considered, and regular follow-up for cardiac imaging should be recommended.
Cardiac function in FT1D patients complicated by acute myocarditis can recover completely with accurate diagnosis and prompt treatment, with recovered ejection fraction reaching ≥ 60% in reported cases [10,11,12,14]. Our case’s ejection fraction improved to 51.9% by the seventh day. However, a nationwide 5-year study in Japan reported that the 5-year cumulative incidence of microangiopathy in FT1D was approximately 9.4 times higher than in type 1A diabetes [25]. This may reflect the almost complete destruction of beta cells, glycemic instability, and low C-peptide levels in the FT1D patients. To reduce microvascular complications in FT1D patients, effective glycemic control is critical, and new insulin formulations and advanced devices, such as closed-loop systems and sensor-augmented pumps (SAPs), may be beneficial. Our patient was discharged with multiple daily insulin injections (MDIs) and later changed to continuous subcutaneous insulin infusion (CSII). A case series report from Singapore indicated that four out of seven FT1D patients were transitioned from the MDIs to CSII, and their hypoglycemic episodes improved after the transition [26].

4. Conclusions

The simultaneous onset of FT1D and acute myocarditis is rare. FT1D patients usually do not have a history of diabetes, and because of the limited awareness of the new diabetes subtype and non-specific initial presentations due to viral infection, they can easily be misdiagnosed. As the onset is abrupt and metabolic derangement is severe, it is important to recognize this disease and treat it on time. If viral infection is suspected, it is critical to monitor cardiac enzymes, echocardiogram, and cardiac MRI to detect and prevent life-threatening complications. If an FT1D patient presents with chest tightness, palpitations, and dyspnea at the onset of the disease, significantly elevated cardiac enzymes, and abnormal ECG, it is relevant to suspect acute myocarditis, which should be distinguished from acute coronary syndrome, stress-induced cardiomyopathy, and myocardial injury caused by other etiologies. For young patients with myocarditis, regular follow-up should be recommended for early detection of structural or rhythmic complications.

Author Contributions

T.H.S.: writing—full manuscript, review and editing; Y.R.: writing—original draft; H.G.: investigation; Z.L.: investigation; Q.L.: resources; X.R.: supervision and funding acquisition; X.W.: supervision and validation; C.W.: supervision and validation. All authors have read and agreed to the published version of the manuscript.

Funding

This study was financially supported by the Science and Technology Bureau of Sichuan Province (2024YFFK0290), the Health Commission of Sichuan Province (23LCYJ042), the Science and technology cooperation between Sichuan University and Zigong City (2024CDZG-22), the Clinical Collaboration of Traditional Chinese and Western Medicine for Major and Difficult Diseases (No: ZDYN-2024-B-037), and the 1.3.5 Foundation of West China Hospital of Sichuan University (No. ZYGD24005).

Institutional Review Board Statement

The study was conducted in accordance with the Declaration of Helsinki, and, as a single case study, this work did not require ethical approval.

Informed Consent Statement

The patient consented to the use of clinical details for scientific and educational purposes. Verbal informed consent was obtained from the patient for writing and publication of this case report via telephone communication. Verbal consent was obtained rather than written because the patient resides in a different city, and in-person attendance at the hospital is not easily feasible.

Data Availability Statement

The raw data supporting the conclusions of this article will be made available by the authors without undue reservation.

Acknowledgments

We acknowledge the joint efforts of the Emergency Department, Cardiology Department, and Department of Endocrinology and Metabolism from West China Hospital regarding the diagnosis, treatment, and care of this patient. Thanks to the patient for her help and compliance with follow-up.

Conflicts of Interest

The authors declare no conflicts of interest.

Abbreviations

The following abbreviations are used in this manuscript:
FT1DFulminant type 1 diabetes
DKADiabetes ketoacidosis
Anti-GADsAnti-Glutamic Acid Decarboxylate antibodies
LVEFLeft ventricular ejection fraction
MRIMagnetic resonance imaging
LGELate gadolinium enhancement

Appendix A

Methods

Glycosylated hemoglobin (HbA1c) levels were measured in EDTA-anticoagulated whole blood using high-performance liquid chromatography (HPLC) on a Tosoh G8 analyzer. Serum C-peptide levels were measured using an electrochemiluminescence immunoassay (ECLIA) on a Roche Cobas e601 analyzer. Fasting blood glucose (FBG) levels and plasma glucose during a 75 g oral glucose tolerance test (OGTT) were measured using an enzymatic hexokinase method on a Roche Cobas c702 clinical chemistry analyzer. Islet autoantibodies, including anti-Glutamic Acid Decarboxylase (anti-GAD), insulinoma-associated antigen-2 antibody (IA-2A), and zinc transporter 8 antibody (ZnT8A), were measured using chemiluminescence immunoassays (CLIAs). Insulin autoantibodies (IAAs) and islet cell antibodies (ICAs) were detected by indirect immunofluorescence (IIF). All assays were performed according to the manufacturers’ protocols or standardized consensus guidelines, with cut-off values defined based on reference controls.

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Figure 1. Clinical timeline and serial changes in cardiac enzymes, white blood cells, and liver enzymes. CK-MB: Creatine Kinase Myocardial Band, NT-proBNP: N-terminal pro-B-type natriuretic peptide, MYO: Myoglobin, WBC: White Blood Cell Count, ALT: Alanine Aminotransferase, AST: Aspartate Aminotransferase.
Figure 1. Clinical timeline and serial changes in cardiac enzymes, white blood cells, and liver enzymes. CK-MB: Creatine Kinase Myocardial Band, NT-proBNP: N-terminal pro-B-type natriuretic peptide, MYO: Myoglobin, WBC: White Blood Cell Count, ALT: Alanine Aminotransferase, AST: Aspartate Aminotransferase.
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Figure 2. Day 1 (admission) ECG shows widespread, diffuse, and concave (saddle-shaped) ST segment elevation without reciprocal ST depression in lead II, III, aVF, and V3–V6 (red arrows) and Day 3 ECG shows QRS attenuation in all leads, coinciding with peak serum troponin levels, and a decrease in amplitude of ST segment elevation in V2 and V3 leads (red arrows).
Figure 2. Day 1 (admission) ECG shows widespread, diffuse, and concave (saddle-shaped) ST segment elevation without reciprocal ST depression in lead II, III, aVF, and V3–V6 (red arrows) and Day 3 ECG shows QRS attenuation in all leads, coinciding with peak serum troponin levels, and a decrease in amplitude of ST segment elevation in V2 and V3 leads (red arrows).
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Figure 3. Day 4 ECG shows QRS attenuation in inferior leads, and a decrease in amplitude of ST segment elevation in V2 and V3 leads (red arrows), Day 7 ECG shows a decrease in amplitude of ST segment elevation in V2–V6 leads and shallow T-wave inversion in inferior leads (red arrows), Discharge ECG shows normalization of ST segments, with residual, shallow T-wave inversions in previously affected leads (red arrows).
Figure 3. Day 4 ECG shows QRS attenuation in inferior leads, and a decrease in amplitude of ST segment elevation in V2 and V3 leads (red arrows), Day 7 ECG shows a decrease in amplitude of ST segment elevation in V2–V6 leads and shallow T-wave inversion in inferior leads (red arrows), Discharge ECG shows normalization of ST segments, with residual, shallow T-wave inversions in previously affected leads (red arrows).
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Figure 4. No stenotic or obstructive lesions in the left main coronary artery (LMCA), left anterior descending (LAD) artery, left circumflex (LCx) artery, and right coronary artery (RCA): (a) LAO 45°, Caudal 30°; (b) RAO 30°, Cranial 30°; (c) RAO 30°, Cranial 0°; (d) LAO 30°, Cranial 10.
Figure 4. No stenotic or obstructive lesions in the left main coronary artery (LMCA), left anterior descending (LAD) artery, left circumflex (LCx) artery, and right coronary artery (RCA): (a) LAO 45°, Caudal 30°; (b) RAO 30°, Cranial 30°; (c) RAO 30°, Cranial 0°; (d) LAO 30°, Cranial 10.
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Figure 5. High signal intensity (arrows) in the interventricular septum, basal and mid-inferolateral walls, and apical inferior wall (a,b); LGE (arrows) showed subepicardial enhancement in the basal to mid-anterolateral and inferolateral segments and the apical lateral segment, most pronounced along the inferolateral wall, with sparing of the sub-endocardium (c,d).
Figure 5. High signal intensity (arrows) in the interventricular septum, basal and mid-inferolateral walls, and apical inferior wall (a,b); LGE (arrows) showed subepicardial enhancement in the basal to mid-anterolateral and inferolateral segments and the apical lateral segment, most pronounced along the inferolateral wall, with sparing of the sub-endocardium (c,d).
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Table 1. Laboratory findings of patient.
Table 1. Laboratory findings of patient.
Admission
2 April 2022		Discharge
25 April 2022		Reference Range
Blood routine test
Red blood cells (×1012/L)3.84.193.8–5.1
Hemoglobin (g/L)118126115–150
White blood cells (×109/L)18.065.713.5–9.5
Platelets (×109/L)157178100–300
Neutrophils (×109/L)16.639.721.8–6.3
Lymphocytes (×109/L)0.611.831.1–3.2
Eosinophils (×109/L)0.000.020.02–0.52
Monocytes (×109/L)1.070.470.1–0.6
Arterial Blood Gas Analysis
pH7.2847.4627.35–7.45
Partial pressure of oxygen (mmHg)142.4120.480–100
Partial pressure of carbon dioxide (mmHg)22.33135–45
Bicarbonate (mmol/L)9.225.722–27
Anion gap (mmol/L)15.412.212.0–20.0
Biochemistry Tests
Aspartate aminotransferase (IU/L)30630<35
Alanine aminotransferase (IU/L)3834<40
Lactate dehydrogenase (IU/L)567345120–250
Creatine kinase (IU/L)38359420–140
Hydroxybutyrate dehydrogenase (IU/L)56428372–182
Serum β hydroxybutyric acid (mmol/L)3.570.160.02–0.27
Urea nitrogen (mmol/L)7.63.22.6–7.5
Creatinine (umol/L)686248–79
Sodium (mmol/L)132.3137.3135–148
Chloride (mmol/L)109.3102.798–107
Potassium (mmol/L)2.984.713.5–5.3
Phosphate (mmol/L)0.411.100.85–1.52
blood glucose (mmol/L)50.1910.194.1–5.9
ANCA Test
Anti-Neutrophil Cytoplasmic AntibodyNegative (-)Negative (-)
Anti-Proteinase 3 Antibody (AU/mL)<2.00<20
Anti-Myeloperoxidase Antibody (AU/mL)1.72<20
Autoimmune Screen
Anti-nuclear AntibodyNegative (-)Negative (-)
Anti-double-stranded DNA Antibody (IU/mL)<2.00<30
Anti-U1-nRNP Antibody/Sm AntibodyNegative (-)Negative (-)
Anti-Sm AntibodyNegative (-)Negative (-)
Anti-SS-A AntibodyNegative (-)Negative (-)
Anti-Ro-52 AntibodyNegative (-)Negative (-)
Anti-SS-B AntibodyNegative (-)Negative (-)
Anti-Scl-70 AntibodyNegative (-)Negative (-)
Anti-PM-Scl AntibodyNegative (-)Negative (-)
Anti-Jo-1 AntibodyNegative (-)Negative (-)
Anti-CENP-B AntibodyNegative (-)Negative (-)
Anti-Cell Cycle Protein AntibodyNegative (-)Negative (-)
Anti-Nucleolar AntibodyNegative (-)Negative (-)
Anti-Ribonucleoprotein AntibodyNegative (-)Negative (-)
Anti-Nuclear Phosphoprotein P AntibodyNegative (-)Negative (-)
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MDPI and ACS Style

Swe, T.H.; Ren, Y.; Gong, H.; Li, Z.; Lv, Q.; Ran, X.; Wei, X.; Wang, C. The Diagnostic Challenges of Acute Myocarditis in a Patient with Fulminant Type 1 Diabetes and Transient Elevation of Anti-GAD Antibodies—A Case Report. J. Clin. Med. 2026, 15, 1553. https://doi.org/10.3390/jcm15041553

AMA Style

Swe TH, Ren Y, Gong H, Li Z, Lv Q, Ran X, Wei X, Wang C. The Diagnostic Challenges of Acute Myocarditis in a Patient with Fulminant Type 1 Diabetes and Transient Elevation of Anti-GAD Antibodies—A Case Report. Journal of Clinical Medicine. 2026; 15(4):1553. https://doi.org/10.3390/jcm15041553

Chicago/Turabian Style

Swe, Thet Htar, Yan Ren, Hongping Gong, Zhenyi Li, Qingguo Lv, Xingwu Ran, Xin Wei, and Chun Wang. 2026. "The Diagnostic Challenges of Acute Myocarditis in a Patient with Fulminant Type 1 Diabetes and Transient Elevation of Anti-GAD Antibodies—A Case Report" Journal of Clinical Medicine 15, no. 4: 1553. https://doi.org/10.3390/jcm15041553

APA Style

Swe, T. H., Ren, Y., Gong, H., Li, Z., Lv, Q., Ran, X., Wei, X., & Wang, C. (2026). The Diagnostic Challenges of Acute Myocarditis in a Patient with Fulminant Type 1 Diabetes and Transient Elevation of Anti-GAD Antibodies—A Case Report. Journal of Clinical Medicine, 15(4), 1553. https://doi.org/10.3390/jcm15041553

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