We performed a retrospective study on the HbA1c lowering effect of a personal health record (PHR) application, Health2Sync, in the treatment of patients with type 1 and type 2 diabetes mellitus (T1DM and T2DM). We analyzed 49 patients (35 patients with T1DM and 14 with T2DM) using Health2Sync to examine changes in HbA1c, body weight, body mass index (BMI), and insulin dose for four months after the initiation of treatment. The changes were also reviewed according to frequency of application usage (<15 or ≥15 times per month). Overall, HbA1c values improved significantly, from 7.65±0.83 % at the initiation of the study to 7.50±0.87 % at four months. The frequent user group continued to maintain a significant decrease in HbA1c (the greatest decrease was 0.28 %) for four months after the initiation of therapy, without showing any changes in insulin dose or BMI. The study suggests that the PHR application may help improve HbA1c values in patients under insulin treatment regardless of the type of diabetes.

A 58-year-old woman was admitted to the emergency department due to anorexia, vomiting, and dizziness. Despite a high glycosylated hemoglobin level (10.4 %), ketonuria (3+), and metabolic acidosis, the blood glucose level on admission was relatively low (281 mg/dL). At this point, she was diagnosed with euglycemic diabetic ketoacidosis (euDKA). Furthermore, based on the elevation of thyroid hormones (FT4 6.72 ng/dL, FT3 14.01 pg/mL), gastroenterological symptoms, and tachycardia, she was also diagnosed with thyrotoxicosis and impending thyroid storm. Under the application of insulin and fluid infusion, the acidosis improved. For the thyrotoxicosis, a beta-blocker and potassium iodide were prescribed. She was diagnosed with Grave's disease and started treatment with thiamazole. During hospitalization, the fasting blood C-peptide level was 3.2 ng/mL, and both the anti-glutamic acid decarboxylase (GAD) antibody and anti-insulinoma-associated antigen-2 (IA-2) antibody value were negative. These data suggested that she had type 2 diabetes mellitus. This is an extremely rare case of type 2 diabetes mellitus in a patient diagnosed with euDKA and concomitant impending thyroid storm. Furthermore, our patient had no history of taking sodium glucose cotransporter 2 (SGLT2) inhibitors, which have recently been suggested to possibly cause euDKA.

A 29-year-old man presented with a disturbance of consciousness, malaise and vomiting. He had been diagnosed with type 2 diabetes mellitus, dyslipidemia, and obesity 4 years previously; however, he stopped receiving treatment. A laboratory examination revealed hyperglycemia (1243 mg/dL). An arterial blood gas analysis revealed a pH of 7.27 and a bicarbonate concentration of 8.9 mmol/L, which was consistent with metabolic acidosis. The beta-hydroxybutyrate concentration was 13144 μmol/L, which indicated a state of diabetic ketoacidosis (DKA). Chest CT demonstrated pneumomediastinum and increased mediastinal fat tissue density with diffuse thickening of the thoracic esophagus, thus confirming an esophageal rupture. Computed tomography of the abdomen revealed swelling of the distal pancreas with edema in the surrounding areas, consistent with acute pancreatitis. The patient received intravenous fluids for DKA and acute pancreatitis, intravenous insulin infusion for DKA, antibiotic and proton pump inhibitor treatment, and nasogastric tube insertion for the esophageal rupture. He recovered well and was discharged on day 19. We describe a rare case of DKA complicated by acute pancreatitis and spontaneous esophageal rupture.

We experienced a case in which a novel hemoglobin modification mechanism was implicated in a falsely high HbA1c value. The patient was a 72-year-old man. He visited our department because his HbA1c value, as measured by high-performance liquid chromatography (HPLC) (HA-8180, Arkry Inc. ), was as high as 7.9 %. Although his fasting plasma glucose level was within the reference range, a 75 g oral glucose tolerance test showed a diabetic type result. His HbA1c did not decrease with guidance on lifestyle improvement and administration of antidiabetic drugs. Since the HbA1c value measured by enzymatic assay was 5.2 % in the medical examination, antidiabetic drugs were discontinued and detailed examinations were performed. The patient's HbA1c values measured by an enzymatic assay, immunoassay, and affinity assay, as well as his glycated albumin value and 1,5-anhydroglucitol value were all within the reference range. An analysis by high-resolution HPLC revealed an abnormal peak eluting earlier than HbA1c. However, variant hemoglobin was ruled out because no mutation was found in any of the globin genes. This case suggested the existence of a novel mechanism of hemoglobin modification.

Case 1 was a 56-year-old female. She was diagnosed with diabetes 2 years previously and had an HbA1c of approximately 7 %. Laboratory analyses when she was transferred to our hospital due to consciousness disturbance revealed the following: blood glucose, 1,407 mg/dL; HbA1c, 17.1 %; positive urine ketone bodies, blood gas pH, 7.15; and S-amylase, 2,506 U/L. Based on these findings, she was diagnosed with DKA and acute pancreatitis. Her S-CPR was <0.03 ng/mL, but she was diagnosed with DKA due to acute pancreatitis because she was anti-islet autoantibody-negative and her postprandial CPR improved to 3.49 ng/mL after insulin treatment. Case 2 was a 24-year-old female. She visited a nearby doctor due to epigastralgia that had persisted for 1 week. She was diagnosed with acute pancreatitis due to an S-amylase of 729 U/L and pancreatic swelling, and was referred to our hospital 3 days later. Her blood glucose level at the previous doctor was 166 mg/dL, but at the time of admission, she was diagnosed with DKA because of a high blood glucose level (682 mg/dL), positive urine ketone bodies, with a blood gas pH value of 7.24. Furthermore, her HbA1c value was 5.8 %, S-CPR was undetectable, and a test for anti-islet autoantibodies was negative. Since her CPR levels were undetectable even after insulin therapy, she was diagnosed with fulminant type 1 diabetes. It is important to evaluate endogenous insulin secretion over time in order to differentiate the etiology of DKA in patients with DKA accompanied by acute pancreatitis.

The diagnostic criteria for slowly progressive type 1 diabetes mellitus (slowly progressive insulin-dependent diabetes mellitus; SPIDDM) have been revised by the "Committee on Type 1 Diabetes" of the Japan Diabetes Society. The following three criteria are all required for a definitive diagnosis of SPIDDM: 1) the presence of islet-associated autoantibody at some time point during the disease course; 2) the absence of ketosis or ketoacidosis at the diagnosis of diabetes and no need for insulin treatment to correct hyperglycemia immediately after the diagnosis principally; and 3) a gradual decrease in insulin secretion over time, with insulin treatment required more than 3 months after the diagnosis of diabetes, and the exhaustion of endogenous insulin secretion (fasting serum C-peptide < 0.6 ng/mL) at the last observed time point. Should a patient meet only criteria 1 and 2 but not 3, they should be diagnosed with "slowly progressive type 1 diabetes mellitus (probable)" because of their non-insulin-dependent diabetic state.