This study examined the prescribing patterns of oral hypoglycemic agents (OHAs) in drug-naïve patients with type 2 diabetes mellitus (T2DM) as well as the impact of the implementation of a medication flowchart. A retrospective chart review of drug-naïve T2DM patients who started oral hypoglycemic monotherapy between January 1, 2015, and July 31, 2017, was conducted. A medication flowchart, including sitagliptin and metformin, was developed by an endocrinologist and a pharmacist. We simulated the enrollment of patients in the chart review to see if using the flowchart would change the selection of the initial therapy and influence drug costs. Among 168 patients enrolled in the study, 68.5 % started on dipeptidyl peptidase-4 inhibitors, while 20.2 % started on metformin. As a result of the simulation, 83 (49.4 %) prescriptions were changed from other OHAs to metformin, 36 (21.4 %) were changed from other OHAs to sitagliptin, and 49 (29.2 %) showed no change in therapy. The difference of monthly drug cost between pre- and post-utilization of the flowchart was −3,454.8 Japanese yen per patient by switching from DPP-4 inhibitors to metformin and −1,148.6 Japanese yen per patient by switching from DPP-4 inhibitors to sitagliptin. The results of the simulation showed that using the flowchart could promote appropriate initial therapy and reduce drug costs.

Our patient is a 77-year-old man with a history of type 2 diabetes and squamous cell carcinoma of the lung. Five months after initiating treatment with pembrolizumab, he was admitted to our hospital due to conscious disturbance. His HbA1c levels were maintained at 6.0 % to 6.5 % while taking an oral antidiabetic drug. Five days before admission, his blood glucose levels were 249 mg/dL with ketonuria at a regular outpatient visit. He developed malaise three days later. On the day of admission, he visited our emergency room due to impaired consciousness and was diagnosed with diabetic ketoacidosis due to fulminant type 1 diabetes. We administered large amounts of fluid and continuous insulin infusion. However, he succumbed 17 h after the admission. A histopathological analysis revealed pathological changes characteristic of fulminant type 1 diabetes, such as decreased pancreatic β and α cells and CD3-positive T cell infiltration. Additionally, we noted a decreased expression of programmed cell death ligand 1 in the pancreatic islets. When immune checkpoint inhibitors are administered to diabetic patients, it is crucial to notify professional healthcare providers and patients of the risk of immune-related type 1 diabetes development.

We herein report a 57-year-old man with glucagonoma who developed ketosis. He had visited our clinic due to thirst, general fatigue, and weight loss for the past two months. His body mass index was 20.3 kg/m² at the time of his visit. He was diagnosed with diabetic ketosis based on the following findings: blood glucose, 454 mg/dL; HbA1c, 14.1 %; and positive urine ketone bodies, and he was treated with insulin therapy. Computed tomography revealed multiple tumors in the pancreatic tail and liver. His fasting glucagon level of 442 pg/mL on a blood test suggested he had glucagonoma. He was treated with everolimus but developed interstitial pneumonia 15 months later and stopped treatment. After that, streptozocin was started, but it was stopped due to deterioration of the renal function. He underwent distal pancreatectomy at another hospital. The pathological diagnosis was pancreatic neuroendocrine tumor G1, with positive glucagon staining. With regard to diabetes, insulin was able to be withdrawn after discharge, and he was treated with an oral hypoglycemic agent. However, insulin was resumed two months before the onset of interstitial pneumonia and was able to be withdrawn again after surgery. The presence of secondary diabetes should also be borne in mind when diagnosing diabetes.

A 66-year-old man was admitted to our hospital for glycemic control of fulminant type 1 diabetes (T1DM). At 62 years old, a pancreatic tail mass lesion had been noted, and the patient underwent partial pancreatectomy. Hormonal and pathological examinations revealed a non-functioning endocrine tumor. Although his pancreatic volume was reduced, glycemic control was maintained (HbA1c value <6.5 %) without medication for 4 years. At 65 years old, during hospitalization for rehabilitation for orthopedic disease, epigastric pain occurred, and 1 week later, his consciousness deteriorated rapidly. A laboratory examination showed an extremely high blood glucose level (827 mg/dL) accompanied by an increased serum amylase level, while elevation of HbA1c was relatively mild (6.9 %). Insulin therapy was initiated, and the patient was then transferred to our hospital. Serum C-peptide was undetectable, and he was diagnosed with fulminant T1DM. We then re-evaluated the pancreas specimen obtained four years earlier. Pancreatic islets outside the endocrine tumor showed no abnormal findings and no invasion of inflammatory cells, which indicated morphologically normal pancreatic islets four years before the onset of fulminant T1DM. We also document the detailed clinical course of fulminant T1DM in the hospital.