Fulminant type 1 diabetes is recognized as a novel subtype of type 1 diabetes, which is a non-autoimmune disorder characterized by a sudden onset, several days duration of diabetic symptoms, the absence of islet-related autoantibodies, exhausted beta-cell function, and elevated pancreatic enzymes in the serum [1,2]. Although, the precise mechanisms by which beta-cell destruction occurs in fulminant type 1 diabetes are still unknown, an abrupt onset accompanied by flu-like symptoms, infiltration of lymphocytes and macrophages to pancreata and the presence of enterovirus-capsid protein in affected pancreata [3] abstract. This report presents the case of a 47-year-old female patient with fulminant type 1 diabetes mellitus and myocarditis. Following a high fever, nausea, vomiting and diarrhea, diabetic ketoacidosis occurred and she was transferred to the hospital. The plasma glucose level was 63.6mmol/L and HbA1c was 7.0%. C-peptide was undetectable in her plasma. Blood gas analysis showed a pH of 6.99. Antibodies to glutamic acid decarboxylase nor insulinoma associated antigen-2 were not detected. She was diagnosed to have fulminant type 1 diabetes mellitus. Her electrocardiogram showed diffuse ST-segment elevations on the second day of admission, along with a positive troponin test. However coronary angiography revealed neither occlusion nor stenosis of the cardiac arteries. An endomyocardial biopsy revealed hypertrophic cardiomyocytes with a disarrangement of myofibers and the focal accumulation of mononuclear cells in the stroma, thus suggesting myocarditis or mild myocarditic change. Viruses are an important cause of myocarditis and the preceding flulike symptoms indicate the association of viral infection with myocarditis in this case. The mechanisms by which fulminant type 1 diabetes mellitus occurs is still uncertain, but the presence of islet injury accompanied by myocardial inflammation in the current case suggested that a viral infection accounted for the onset of this type of diabetes.