The declaration of a state of emergency due to the spread of COVID-19 infection has changed society's lifestyle. Lifestyle changes worsen glycemic control in diabetic patients (DM). The effect of refraining from going out due to a state of emergency on glycemic control in DM is unclear. We investigated the effects of the declaration of a state of emergency on the living conditions and glycemic control of diabetic patients living on remote islands. Although the area was non-endemic, the frequency of outings decreased in about half of both Type 1 and Type 2 DM patients. However, the body mass index and HbA1c values did not change markedly after the emergency declaration in Type 1 and Type 2 DM patients. In addition, the amount of food purchased per trip tended to decrease as the frequency of outings decreased in both types (Type 1 DM: r=−0.340, p=0.057; Type 2 DM: r=−0.32, p=0.034). In this study, no marked change in glycemic control after the declaration of the state of emergency was noted. However, about half of the subjects decreased their frequency of going out, and some changed their food purchasing behavior. It is important to provide dietary guidance while focusing on changes in eating behavior, even in areas without a wide COVID-19 spread.

We report the case of a 95-year-old woman who had been diagnosed with diabetes mellitus with HbA1c 9.7 % and a fasting blood glucose level of 199 mg/dL at 94 years of age. Despite the administration of oral hypoglycemic therapy for 5 months, her blood glucose was poorly controlled. On admission, we found that her HbA1c was 11.0 %, her casual blood glucose was 394 mg/dL and her glutamic acid decarboxylase antibody titer was 1740 U/mL (ELISA); she was then diagnosed with SPIDDM. While the development of SPIDDM is commonly reported in patients in their 40s to 50s, recent studies showed that around 10 % of elderly patients who developed diabetes were diagnosed with SPIDDM. We searched clinical characteristics of latter-stage elderly patients who developed SPIDDM and found that majority were female and showed reduced insulin secretion with poor glycemic control. It is important to consider the possibility of type 1 diabetes, including SPIDDM, even in elderly patients who have developed diabetes with poor glycemic control.

Pheochromocytoma is known to be associated with impaired glucose tolerance, but it rarely leads to diabetic ketoacidosis (DKA). We herein report a patient with asymptomatic pheochromocytoma and DKA who was diagnosed with an adrenal incidentaloma. A 52-year-old man with diabetes was admitted for DKA. Pheochromocytoma was not suspected because the patient had no history of hypertension, physical examination findings were unremarkable, and laboratory results were almost normal except for the presence of an adrenal tumor with a CT value of 48.2 Hounsfield units (HU). After the patient had recovered from DKA, we performed a glucagon challenge test and found that the patient was insulin-dependent. After discharge, 123I-metaiodobenzylguanidine (123I-MIBG) scintigraphy was performed, and pheochromocytoma was diagnosed. After tumor resection, the insulin secretory capacity was re-examined, and the patient was insulin-independent. Reports have been published concerning two patients with pheochromocytoma who developed DKA. In both cases, the adrenal tumor was considered to be non-functioning, and notably, both patients were taking a sodium-glucose co-transporter 2 (SGLT2) inhibitor for treatment of diabetes. The present case was similar to these cases. Physicians should consider undiagnosed pheochromocytoma in patients who have adrenal tumors with a relatively high HU on CT and/or who develop DKA while taking SGLT2 inhibitors.

In general, when patients with hemodialysis develop type 1 diabetes, hyperglycemia has few symptoms, as it is corrected by hemodialysis. We herein report a patient on hemodialysis who developed fulminant type 1 diabetes. A 73-year-old non-diabetic woman had been started on dialysis 1 year ago. Before admission to our hospital, the patient felt thirsty for two days. On the day of admission, she developed nausea at 3: 00 am and vomited during and after dialysis. At admission, her blood glucose level was 497 mg/dL, and hemoglobin A1c was 5.8 %; in addition, she had high anion-gap metabolic acidosis despite dialysis. Continuous intravenous insulin infusion therapy was started immediately. Conventional fluid infusion for diabetic ketoacidosis was not necessary because of oliguria. A glucagon challenge test showed a peak serum C-peptide level of ≤0.03 ng/mL, confirming endogenous insulin deficiency. An islet-related autoantibodies test was negative, and blood pancreatic exocrine enzymes were elevated, so we diagnosed her with fulminant type 1 diabetes. In patients on dialysis who develop fulminant type 1 diabetes, the onset of diabetes may not be predicted, even by regular blood glucose monitoring. Refraining from fluid infusion in diabetic ketoacidosis is recommended in patients with oliguria.

A 53-year-old woman who consumed a substantial amount of sweet soft drinks visited a diabetologist due to thirst and polydipsia. Her blood glucose was 498 mg/dL, and HbA1c was 13.0 %. Insulin therapy was immediately started. Although the fasting serum C peptide level was 0.64 ng/dL, she had been obese, and anti-GAD antibody was negative. Therefore, type 2 diabetes mellitus was diagnosed, and insulin was substituted for oral therapy with metformin and sitagliptin. Although her glycemic control was excellent, her serum potassium level was 2.9 mmol/L with a serum magnesium level of 1.8 mg/dL, urinary potassium 27.0 mmol/g creatinine, urinary calcium 0.01 g/g creatinine, HCO₃^- 30.7 mmol/L on an arterial blood gas analysis, plasma renin activity 6.5 ng/mL/h, and normal blood pressure and renal ultrasound findings. These clinical findings strongly suggested a diagnosis of Gitelman syndrome. Subsequently, we performed genetic testing for comprehensive genetic tubular diseases using a next-generation sequencing-based gene panel. As a result, triple mutations (A569V, L585H, G898W) were identified, which were previously reported as pathogenic missense mutations. Administration of KCL and MgO₂ kept the serum potassium and magnesium levels above 3.5 mmol/L and 1.8 mg/dL, respectively. The effect of coexisting Gitelman syndrome on treatment of diabetes and the development of diabetic complications remains to be elucidated.