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Background: DPP-4 inhibitor has been shown to improve not only blood glucose levels but also dyslipidemia, but the effect remains controversial. Further, there are few reports regarding the influence on Apo B, Apo A-1 and Apo B/Apo A-1 in alogliptin. Objective: Using the alogliptin, we focused on Apo B and Apo A-1, in addition to LDL-C, HDL-C and TG, and investigated the effect of alogliptin on markers predicting cardiovascular events, such as Apo B/Apo A-1 and LDL-C/Apo B. Methods: This study was carried out with a single arm in an open label manner. 45 consecutive cases that could enroll between September 2011 and March 2012 were selected as the subjects for randomization. Alogliptin 25 mg/day was administered for eight weeks and non-fasting blood samples were collected 2-3 hours after breakfast, once at the beginning of the study and once eight weeks later, and changes in glucose and lipid metabolism markers were compared. Results: Administration of alogliptin significantly reduced HbA1c levels and non-fasting blood glucose levels, and reduced LDL-C and non-fasting TG. Apo B was significantly reduced by alogliptin treatment but Apo A-1 was unchanged. The Apo B/Apo A-1 ratio was significantly decreased and the LDL-C/Apo B ratio significantly increased by alogliptin treatment. The change in the pre-administration Apo B/Apo A-1 ratio was positively correlated with body weight, TG, HbA1c, blood CPR and pooled urine CPR and negatively correlated with HDL-C Conclusion: Administration of alogliptin in type 2 diabetic patients significantly improved levels of blood glucose, in addition to those of lipid metabolism markers such as LDL-C and non-fasting TG, as well as sensitive predictive markers for the onset risk of cardiovascular events, such as the Apo B/Apo A-1 ratio and the LDL-C/Apo B ratio. These results suggest that alogliptin could potentially suppress atherosclerosis and prevent cardiovascular events (UMIN 000011470).

We report a case of a seventy-year-old woman with syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and adrenal insufficiency induced by Rathke's cleft cyst. She experienced nausea, vomiting, diarrhea, and headache and disturbance of consciousness induced by hyponatremia at a serum sodium level of 100 mEq/l. In spite of severe hyponatremia, urinary sodium excretion was not suppressed and serum osmolality (270 mOsm/kg) was lower than urine osmolality (304 mOsm/kg), and arginine vasopressin (AVP) remained within normal range. SIADH was diagnosed because she was free from other diseases known to cause hyponatremia such as dehydration, cardiac dysfunction, liver dysfunction, renal dysfunction, hypothyroidism, and adrenal insufficiency. Cranial computed tomographic (CT) scan and cranial magnetic resonance (MR) imaging showed a cystic lesion of approximately 2 cm in diameter in the pituitary gland. These images suggested that the cystic lesion was a Rathke's cleft cyst, which was the cause of SIADH. Water restriction therapy normalized her serum sodium concentration and improved her symptoms. After one year, she suffered from general fatigue, appetite loss, fever, and body weight loss (5 kg/2 months). She had neither hypotension nor hypoglycemia, but her serum sodium level was low and serum cortisol, ACTH, and urine free cortisol were very low. Therefore, secondary adrenal insufficiency was suspected and diagnosed by stimulation tests. After start of hydrocortisone replacement therapy (10 mg/day), her symptoms disappeared. In conclusion, Rathke's cleft cyst should be kept in mind as a potential cause in a patient with SIADH, hypopituitarism, and/or adrenal insufficiency.

種々の免疫異常が報告されているGraves病について,本研究では45名の患者を対象とし末梢血細胞のinterleukin-1 (IL-1), interleukin-2 (IL-2)産生能を健常者と比較し,さらに抗甲状腺剤と甲状線ホルモンのIL-1, IL-2産生に及ぼす影響についても健常人の末梢血細胞を用いて検討した. Lipopolysaccharide刺激単球の培養上清をIL-1測定用, phytohemagglutinin刺激リンパ球の培養上清をIL-2測定用試料とし, IL-1, IL-2共にradioimmunoassayで測定した.甲状腺機能亢進Graves病では健常者より有意なIL-1産生の増加とIL-2産生の低下を認めた.甲状腺機能正常Graves病ではIL-1, IL-2産生共に健常者と差はなかった. Propylthiouracil (PTU)とmethimazole (MMI)は濃度依存性にIL-1を抑制したが, MMIはIL-2を増加させた.一部の健常者では3-5-3'triiodothyronine (T3)はIL-1を増加させた.本研究より甲状腺機能亢進Graves病ではIL-1の増加とIL-2の低下があり,さらに抗甲状腺剤と甲状腺ホルモンがIL-1, IL-2産生に影響する可能性も示唆された.

Diabetic patients tend to show a reduced QOL because of macrovascular complications such as cerebral and myocardial infarction, as well as marked microvascular complications. It is important for the prevention and amelioration of these complications to diagnose diabetes mellitus (DM) early and effectively control glycemia, the blood pressure, lipids, and body weight. We examine fasting plasma glucose (FPG) and HbA1c for a diagnosis of diabetes at any time, but examine 75gOGTT for impaired glucose tolerance or DM. Examination to be necessary for a pathologic classification of DM is islet-associated antibody, namely, GAD antibody, IA-2 antibody and the measurement of IRI, blood/urinary C-peptide to evaluate insulin secretory ability. HOMA-R is an index of insulin resistance, and HOMA-beta is an index of insulin secretory ability which can be calculated from FPG and IRI, but we need to be aware that the insulin secretory ability of the patient may have decreased already. HbA1c is a standard index of glycemic control, but glycoalbumin measurement is suitable for disease states such as anemia and liver cirrhosis, and 1,5-anhydroglucitol is suitable for detecting changes in levels of urinary glucose. Examinations necessary for the evaluation of diabetic nephropathy are microalbumin and 24hr Ccr in the urine, but eGFR has been recently recommended instead of 24hr Ccr. We measure small dense LDL-C, RLP-C, and Lp (a) as well as conduct conventional lipid analyses for dislipidemia combined with DM for qualitative as well as quantitative data. Metabolic syndrome is caused by the life habits of overeating and lack of exercise, leading to atherosclerotic disease, because insulin resistance advances from visceral fat accumulation. TNF-alpha and leptin levels as insulin resistance advances and adiponectin levels as insulin resistance improves are measured as adipocytokines secreted by visceral fat tissue.

Summary 1. In order to study the prevalence of insulin resistance syndrome (syndrome X) in Japanese subjects, inhabitants aged above 40 years living in Osaka-Sayama city from September 1992 through December 1993 were investigated. The population-based study was performed on 2498 subjects (661 males and 1837 females) constituting 10.9% of the total population aged above 40 years. 2. The prevalence of glucose intolerance was 8.7% (n= 218) in 2498 subjects. The prevalence of hypertension was 36.9% (n= 923) and that of hypertriglyceridaemia was 19.0% (n= 475). The prevalence of syndrome X as characterized by an association of glucose intolerance, hypertension and hypertriglyceridaemia was 1.6% (n= 39) in all subjects examined and 17.4% in subjects showing glucose intolerance. 3. Fasting serum insulin levels were significantly higher in patients with syndrome X than in normal subjects. Furthermore, the levels were significantly correlated with blood levels of frucutosamine, fasting glucose and triglyceride, and with body mass index as well. 4. In conclusion, insulin resistance syndrome (syndrome X) is also found among the larger Japanese population, and fasting serum insulin levels can be a useful marker of this metabolic disorder.