Recent reports have shown that a low level of serum magnesium (SMg), which is frequently observed in patients with diabetes mellitus (DM), can predict the progression of DM nephropathy and that SGLT2 inhibitor treatment increases the SMg levels. We aimed to clarify the effects of canagliflozin, an SGLT2 inhibitor, on the SMg levels, fractional urinary excretion of Mg (FEMg), estimated glomerular filtration rate (eGFR), body mass index (BMI) and HbA1c in 14 out-patients with type 2 DM. After 8.3 months of canagliflozin treatment, the SMg levels and eGFR were significantly increased compared to baseline, while the FEMg, BMI and HbA1c values were decreased. The changes in SMg (ΔSMg) and FEMg (ΔFEMg) were negatively correlated with the baseline SMg and FEMg, respectively. The ΔFEMg in patients with ΔSMg ≥0.21 mg/dL (median) was significantly greater than that in patients with ΔSMg <0.21 mg/dL. These results suggested that enhanced renal tubular Mg reabsorption may be related to an elevation of the canagliflozin-induced SMg level, partially due to an improvement in the glucose metabolism.

The Japan Diabetes Society/Japan Geriatrics Society Joint Committee recommends glycemic targets for elderly patients with diabetes categorized according to comprehensive geriatric assessments. Accordingly, we categorized elderly patients with diabetes and examined their clinical characteristics. We enrolled 341 outpatients with type-2 diabetes ≥65 years of age. We categorized patients using the committee's report, Mini-Mental State Examination (MMSE), Barthel Index (BI), and Tokyo Metropolitan Institute of Gerontology Index (TMIG-I). We examined the association of MMSE≤27, BI≤90, and TMIG-I≤9 with glycated hemoglobin (HbA1c), low-density lipoprotein cholesterol, high-density lipoprotein cholesterol (HDL-C), cerebrovascular disease (CVD) history, diabetic therapy, educational status adjusted for age, sex, diabetes duration, diabetic nephropathy, and estimated glomerular filtration rate. We classified 37.0 %, 49.0 %, and 14.1 % of patients into categories I, II, and III, respectively. The percentage of patients prescribed drugs potentially associated with severe hypoglycemia was 44.9 %. Of these, 60.1 % displayed HbA1c levels below the recommended target. MMSE≤27 was significantly associated with lower HDL-C and educational status. BI≤90 and TMIG-I≤9 were significantly associated with CVD. In summary, 63.0 % of patients were categorized as class II or III, and 27.0 % had a risk of hypoglycemia. The cognitive function was thus found to be associated with the HDL-C level and educational status. The activities of daily living were therefore associated with CVD.

A 72-year-old female had been diagnosed with diabetes 3 years previously and had since been receiving medical treatment; however, her glycemic control was observed to have worsened about 4 months prior to this presentation. She was admitted to the hospital due to acute bronchitis and high HbA1c levels (11.7 %). Abnormally high tumor marker levels of CA19-9 3226.0 U/mL and CEA 41.3 ng/mL were also observed, and abdominal ultrasonography, CT, MRCP, gastroscopy and colonoscopy were performed; however, the primary disease could not be identified. Regarding the patient's diabetes, her blood glucose levels improved after administering intensive insulin therapy, and a further improvement was obtained after administering insulin degludec/aspart and vildagliptin. An increased fluorodeoxyglucose (¹⁸F-FDG) accumulation was identified in the ileocecum on ¹⁸F-FDG-positron emission tomography/computed tomography, and surgery was performed. As a result, mucinous appendiceal adenocarcinoma with metastasis to the lymph nodes was diagnosed. The tumor cells were densely stained by CA19-9 immunostaining, with serum CA19-9 normalizing after carrying out postoperative chemotherapy. Fat cells in the cancer nest showed positive staining for IL-6 and TNFα. A tendency for the blood glucose levels to decrease was observed after carcinectomy, resulting in a reduction in the insulin dose. Subsequently, the patient showed a good recovery, and her HbA1c levels returned to the upper 6 % range.

A 55-year-old man had type I diabetes mellitus pointed out 24 years earlier, and insulin intensive therapy had been given. Because his symptoms of nausea and vomiting had appeared from one week before his hospitalization, we first suspected diabetic keto-acidosis and performed an arterial blood gas assay. The data revealed the development of significant anion gap non-increased-type metabolic acidosis. Bladder urinary tract full extraction and ileal conduit reconstruction had been performed for the treatment of bladder cancer one year earlier, so we considered the disorder of acid excretion in the kidney to be due to diabetic nephropathy or renal tubular acidosis; however, several tests failed to confirm this etiology. Because his intestinal peristalsis had been reduced by diabetic neuropathy, the excretion of bicarbonate was enhanced by urinary retention. In addition, urinary acid excretion by the kidney was affected due to diabetic nephropathy, which might have induced his acidosis. The patient was treated with bicarbonate administration, and all symptoms disappeared. However, the continuous administration of bicarbonate has been needed, based on a blood gas analysis one year later. We should therefore recognize that metabolic acidosis can be induced by urinary diversion through the ileum in patients with diabetic complications.

A 75-year-old man presented due to symptoms of hypoglycemia induced by 22 h of fasting. His serum glucose levels were 40 mg/dL, and his serum immunoreactive insulin and C-peptide levels were 6.9 μU/mL and 1.91 ng/mL, respectively, indicating that hypoglycemia had been induced by the hyperactivity of insulin. We could not detect any tumors in his pancreas using computed tomography, magnetic resonance imaging, or ultrasonography. A selective arterial calcium injection test revealed that the serum insulin levels obtained from the hepatic vein were paradoxically and drastically increased after the injection of calcium into the pancreatic tail artery. Based on these findings, we diagnosed the patient with insulinoma in the pancreatic tail. Hemi-pancreatectomy was performed and resulted in temporary remission of hypoglycemia. However, a histological examination did not reveal any insulinomas in the resected specimen. In addition, no mutations were identified in the ABCC8, KCNJ11, or GCK genes. Six months after the operation, hypoglycemia again occurred in the patient. Therefore, we considered non-insulinoma pancreatogenous hypoglycemia syndrome in the differential diagnosis. A histological reexamination indicated hyperplasia of the islet cells. The oral administration of diazoxide was partially effective in preventing hypoglycemia. However, the monthly administration of a long-acting octreotide completely prevented the occurrence of hypoglycemia in this case.