A 28-year-old woman visited a surgery clinic due to a skin abscess on her back. She had neither a history of obesity nor alcohol consumption and no family history of diabetes. Her blood glucose was 415 mg/dL, and her HbA1c was 16.1 %. Since her endogenous insulin secretion was severely impaired, intensive insulin therapy was introduced. Imaging revealed hypoplasia of the pancreatic body and tail, and the calculus of the pancreatic head and defects in the main pancreatic duct were suggestive of pancreatolithiasis. The exocrine pancreatic function was also reduced. In addition, she had advanced triopathy, with symptoms such as postural hypotension, preproliferative retinopathy and macroalbuminuira. We herein report a case of juvenile diabetes mellitus associated with advanced diabetic complications and hypoplasia of the dorsal pancreas at presentation, along with bibliographic consideration.

We experienced two cases of spontaneous pneumomediastinum complicated with diabetic ketoacidosis (DKA). In case 1, a 20 year-old male patient presented to the emergency department with a chief complaint of dyspnea after 1 week of malaise, nausea and vomiting. Chest auscultation revealed a positive Hamman's sign. Chest X-ray and computed tomography (CT) showed subcutaneous emphysema and pneumomediastinum. Casual plasma glucose of 553 mg/dL, arterial blood of pH 7.044 and total ketone bodies of 8,340 μmol/L indicated DKA. In case 2, a 27 year-old male patient presented to the outpatient clinic after 3 weeks of thirst, polyposia, nausea and loss of appetite. Chest auscultation revealed a negative Hamman's sign. Chest CT showed pneumomediastinum, which was not apparent in chest X-ray. Casual plasma glucose of 1,268 mg/dL, arterial blood pH of 7.206 and total ketone bodies of 10,957 μmol/L indicated DKA. Pneumomediastinum due to esophagus hiatus often causes severe mediastinitis. In contrast, pneumomediastinum due to DKA rarely cause mediastinitis. Thus, a precise diagnosis should be performed.

A 25-year-old woman with type 1 diabetes was admitted to our hospital 9 hours after deliberate injecting an overdose of insulin glargine (1200 U). She had a history of personality disorder and frequently self-harmed by injecting excessive doses of insulin. On admission, she was mostly alert; however, her blood glucose level was 46 mg/dL. To maintain an adequate blood glucose level, we determined the glucose infusion rate (GIR) according to the hyperinsulinemic euglycemic clamp theory (clamp theory). Her body mass index (BMI) was 17.9 kg/m². There were no other factors that would have influenced her blood glucose level (i.e., infection or the intake of food); thus, we started continuous intravenous infusion of glucose at 10 mg/kg/min, which is the rate at which glucose is administered to insulin-sensitive patients in hyperinsulinemic euglycemic clamp studies. The maximum GIR required to maintain euglycemia was 12.5 mg/kg/min. The continuous intravenous infusion of glucose was necessary until 96 hours after the injection of insulin; the total dose of glucose was 2,805 g. Although there are no established therapeutic strategies for treating insulin overdoses, we obtained stable glucose control by estimating the starting GIR based on the clamp theory, and found that this method was useful for managing hypoglycemia due to an insulin overdose.

The patient in the present case was a 33-year-old woman. She underwent surgery and radiotherapy for optic glioma at 8 years of age. She displayed amenorrhea, obesity, and hyperglycemia at 18 years of age, and was diagnosed with Fröhlich syndrome. She displayed symptoms of hypoglycemia at 27 years of age, and a provocation test revealed a low response of growth hormone (GH). Severe hypoglycemia (plasma glucose 23 mg/dL) was recognized just before her admission, and she was admitted to our hospital for further examination. A 75-gram oral glucose tolerance test revealed an impaired glucose tolerance and the exaggerated secretion of insulin after the glucose load. After admission, episodes of hypoglycemia were recognized before lunch but not during overnight fasting. An insulin tolerance test again demonstrated a blunted GH response. Fröhlich syndrome results in hyperphagia, decreased sympathetic nerve activity, and GH deficiency due to the impairment of the ventromedial hypothalamus nucleus. In this case, hypoglycemia might be induced by the exaggerated secretion of insulin during post-absorptive hyperglycemia and might be exacerbated by GH deficiency.