The effects of split meal serving were examined in middle-aged overweight males working at night at the same company. All of the subjects consumed a large dinner late at night without breakfast; therefore, they had metabolic problems, including visceral fat accumulation, fatty liver, high serum TG levels and low adiponectin levels. Their dinner was divided into two meals with the same total energy count: a light supper in the evening (around 7 pm) and a smaller dinner at night. Eating breakfast, consuming less sweets and engaging in light physical exercise were also recommended. The subjects reduced both their body mass and BMI. The serum TG levels and fatty liver significantly improved, and the serum adiponectin levels increased after eight weeks of intervention. Therefore, the use of split dinner servings is suggested to be effective for controlling obesity and related syndromes.
Variant hemoglobin may lead to errors in assessing glycemic control due to abnormal HbA1c values. We herein report five patients with variant hemoglobin that was discovered based on abnormally low HbA1c values (<4.2 %) during routine medical examinations. In patients with abnormally low HbA1c values measured using the high-pressure liquid chromatography (HPLC) method (HPLC-HbA1c), the glycated albumin (GA) and HbA1c levels were measured using an immunoassay (IA-HbA1c). All five nondiabetic patients with a discrepancy between the HPLC-HbA1c values and the GA and IA-HbA1c values had a heterozygous mutation in the β-globin chain (Hb Shizuoka in one patient, Hb Moriguchi in two patients and Hb G-Szuhu in two patients). Therefore, in cases of abnormally low HPLC-HbA1c levels that are discrepant with the GA and IA-HbA1c levels, a diagnosis of variant hemoglobin should be strongly suspected. We also present a flowchart that we use to diagnose variant hemoglobin in patients with abnormally low HPLC-HbA1c values.
We herein describe a rare case of spontaneous rupture of the ureter in a 20-year-old male patient with diabetes. The patient was admitted to our university hospital due to right abdominal pain and marked hyperglycemia. A computed tomography scan showed massive leakage of urine into the right perirenal and retroperitoneal space with mild right hydronephrosis. The plasma glucose level was 1,430 mg/dl and the HbA1c level was 14.9 % (NGSP value), while antibodies to glutamic acid decarboxylase and Insulinoma-associated antigen-2 were negative. A double J ureteral stent was inserted into the right ureter. The extravasation of urine into the perirenal space disappeared immediately. Basal and bolus insulin therapy was initiated to control the hyperglycemia. A microarray analysis showed a hemizygous whole gene deletion of hepatocyte nuclear factor (HNF) -1β on chromosome 17q12, and the patient was diagnosed with MODY 5. We speculate that the occurrence of spontaneous rupture of the ureter is associated with the phenotype of MODY 5.
A 74-year-old female diagnosed with type 1 diabetes at 42 years of age who had a history of poor glycemic control was admitted to our hospital with abdominal pain, nausea and anorexia. Since the laboratory data on admission showed a plasma glucose level of 461 mg/dl, a finding of 3+for urinary ketone bodies and an increased inflammatory response, infectious gastroenteritis and diabetic ketosis were diagnosed. On hospital day 2, computed tomography of the abdomen was performed following a rise in the blood amylase levels. The results indicated inflammation of the head of the pancreas and edematous thickening of the duodenum. The patient's symptoms were relieved with conservative treatment. On hospital day 8, upper gastrointestinal endoscopy revealed areas of shallow multifocal erosion, ulceration and edema in the duodenum. The patient had taken neither antibiotics nor nonsteroidal anti-inflammatory drugs prior to the onset of illness. In addition, because the endoscopic and histological findings showed ischemic changes in the duodenum, ischemic duodenitis was strongly suspected. The duodenum is supplied by both the celiac and superior mesenteric arteries; therefore, ischemia is not often encountered. As no previous reports have described diabetic ketosis associated with ischemic duodenitis, we herein report this very rare case with reference to the pertinent literature.
A 65-year-old male with a chief complaint of right leg spasms was examined in our hospital. His HbA1c (NGSP) level was 8.7 %, and urinary ketone bodies were positive (1+). Therefore, he was diagnosed as suffering from diabetic ketosis. Later, he was hospitalized because the spasms occurred frequently. On the fifth hospital day, right spastic pain and numbness progressed upward to the right arm. At the same time, a disturbance of consciousness, aphasia and hemiplegia developed. A brain computed tomography (CT) scan performed on admission showed no particular findings, except for brain atrophy. However, on the sixth hospital day, the patient was diagnosed as having a subdural abscess, as high-density and high-intensity areas were observed on the medial side of the left motor cortex and at the circumference of the right lateral ventricle on both a brain CT scan and magnetic resonance imaging. Thereafter, craniotomy was performed to reduce the brain pressure, and the abscess was removed. To the best of our knowledge, there are no reports of cases of type 2 diabetes with a subdural abscess without an antecedent infection or head trauma.
Two patients with impaired glucose tolerance at our clinic exhibited a high urine glucose concentration despite a normal HbA1c level (5.4-5.5 %). We performed 75-g oral glucose tolerance tests (OGTTs) to assess the pathophysiological mechanisms in the two cases (Cases 1 and 2). We also performed 75g-OGTTs in two randomly selected cases as a control group (Cases 3 and 4). One of the two control subjects was a healthy person with a normal HbA1c level, while the other had borderline diabetes mellitus. In the two cases (Cases 1 and 2), blood glucose curves showed the borderline type. The patients also exhibited a low response in the early phase of insulin secretion. The insulinogenic index was 0.18-0.25. Additional secretion in the two cases reactively increased, with a peak at 120 minutes. The urine glucose concentrations were remarkably increased compared with those observed in the serum at 60 minutes and 120 minutes after glucose intake. We infer from the results that the renal glucose threshold was low in the two borderline patients compared with that observed in the two control subjects who demonstrated normal glycosuria. These results shed new light on the threshold for renal glycosuria, which differs from that outlined in the former definition of renal glycosuria. High urine glucose excretion hindering the glycation of serum blood may lower the HbA1c level. The HbA1c level is an essential tool for diagnosing diabetes mellitus, and the urine glucose level may become another criterion for the diagnosis of diabetes mellitus.
Remitting seronegative symmetrical synovitis with pitting edema (abbreviated RS3PE) is a syndrome characterized by symmetric polyarthritis, synovitis and acute pitting edema of the hands and feet that primarily occurs in elderly patients. Recently, the number of case reports of RS3PE syndrome associated with diabetes has increased, especially in cases involving DPP-4 inhibitors. We herein report the cases of two patients with RS3PE syndrome, one of whom was treated with a DPP-4 inhibitor and the other was not, who showed different clinical courses. Case 1 involved a 79-year-old female with type 2 diabetes who suffered from bilateral edema of the hands and feet with upper arm pain in whom deterioration of diabetes control subsequently occurred. She had been prescribed a DPP-4 inhibitor five months earlier. We made a diagnosis of RS3PE syndrome and initiated steroid therapy; however, the patient was refractory to the treatment and consecutively required high-dose steroids. Case 2 involved a 63-year-old female with type 2 diabetes who was prescribed insulin treatment without a DPP-4 inhibitor. She complained of bilateral stiff fingers, knee joint pain and edema of the hands and feet. After receiving a diagnosis of RS3PE syndrome, the patient was treated with steroid therapy. Since her symptoms disappeared quickly, the dose of steroids was gradually tapered and stopped three years after the initiation of treatment.
We herein describe the case of an 87-year-old female with type 2 diabetes treated with sitagliptin who developed bullous pemphigoid (BP). Approximately one month after the administration of sitagliptin, she was admitted with erythema multiforme spreading from the lower legs. Five days after admission, blisters appeared on the patient's palms and thighs. She was diagnosed with BP based on the results of a pathological examination and an elevated BP antigen level in the serum. The BP was controlled after withdrawing the suspected medication and administering steroid therapy. Recently, the development of BP has been reported in patients treated with DPP-4 inhibitors. We also report a case of BP that developed following the administration of a DPP-4 inhibitor.
A 65-year-old male was diagnosed with type 2 diabetes five years before admission and discontinued his prescribed oral medications on his own initiative two years before admission. He experienced a disturbance of consciousness while working in the hot sun. Upon being transferred to the hospital by ambulance, his chief complaint was vomiting. A plasma glucose level of 1,516 mg/dl, positive results for blood and urine ketones, metabolic acidosis and severe dehydration were noted. Diabetic ketoacidosis was diagnosed, and the patient was admitted to the hospital. On the second day after admission, a decreased level of consciousness indicated low blood pressure and poor oxygenation due to hypovolemic shock secondary to dehydration. Contrast-enhanced computed tomography of the abdomen showed portal venous gas and extensive intramural intestinal gas. In addition, bloody ascites fluid with an abnormal odor was sampled via an abdominal tap. Subsequently, nonocclusive mesenteric ischemia (NOMI) associated with intestinal necrosis was diagnosed. Life-saving emergency extended right hemicolectomy was performed. NOMI has a high mortality rate. Making an immediate and proper diagnosis is critical for providing appropriate treatment, although accurately diagnosing the condition is difficult due to the lack of characteristic abdominal findings.
We retrospectively investigated the dose regulation of sulfonylurea (SU) agents in 219 patients who received dipeptidyl peptidase-4 (DPP-4) inhibitors in addition to SU-based treatment. Of 169 patients who received sitagliptin in addition to SU-based treatment without reducing the dose of the SU agent, 46 (27 %) patients required a reduction of the SU agent within three months for hypoglycemia or to prevent hypoglycemia. Moreover, hypoglycemia occurred in nine (20 %) patients who had been treated with an SU agent at a dose lower than the recommended dose when a DPP-4 inhibitor was added without reducing the dose of the SU agent. However, in 50 patients, when the SU agent was reduced to approximately half the dose, no hypoglycemia was observed, regardless of the previous dose, although the HbA1c-lowering effect was not significantly different from that observed in the patients treated without dose reduction (-0.9 %vs-0.9 %, p=0.95). Therefore, we consider that the dose of SU agents should be halved when a DPP-4 inhibitor is added, regardless of the previous dose of the SU agent.