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Background. Glycemic variability is associated with higher risk of microvascular complications in patients with type 2 diabetes. Aim. To test the hypothesis that glycemic variability can contribute to progression to macroalbuminuria in normal or microalbuminuria in patients with type 2 diabetes. Design. This prospective study enrolled 193 patients with type 2 diabetes at a tertiary medical center. Methods. For each patient, the intrapersonal glycemic variability (mean, SD, and coefficient of variation of HbA1c) was calculated using all measurements obtained three years before the study. Patients were divided into four groups stratified by both urine albumin/creatinine ratio and HbA1c-SD. The presence of macroalbuminuria was assessed with Kaplan–Meier plots and compared by log-rank test. Results. Of the 193 patients, 83 patients were in the macroalbuminuria state. Patients in the initial macroalbuminuria group after enrollment had the highest diabetes duration, mean, CV-HbA1c and HbA1c-SD, and uric acid level, and the lowest estimate glomerular filtration rate, followed by subsequent macroalbuminuria and without macroalbuminuria groups. Patients with microalbuminuria and high HbA1c-SD showed the highest progression rate to macroalbuminuria, after a six-year follow-up study by Kaplan–Meier Plots and compared by log-rank test. Conclusions. Higher HbA1C variability is more likely to progress to macroalbuminuria in those patients who are already in a microalbuminuria state. We recommend that clinicians should aggressively control blood glucose to an acceptable range and avoid blood glucose fluctuations by individualized treatment to prevent renal status progression.

From January 1987 to December 2011, over a total of 25 years, 84 patients with Cushing’s syndrome (CS) were identified at a medical center in southern Taiwan. We observed a higher incidence of ACTH-independent CS (75%) than ACTH-dependent CS (25%). A higher incidence of adrenocortical adenoma (58.3%) than Cushing’s disease (CD, 21.4%) was also found. The sensitivity of the definitive diagnostic tests for CS, including loss of plasma cortisol circadian rhythm, a baseline 24 h urinary free cortisol (UFC) value >80 μg, and overnight and 2-day low-dose dexamethasone suppression test, was between 94.4% and 100%. For the 2-day high-dose dexamethasone suppression test for the differential diagnosis of CD, the sensitivity of 0800 h plasma cortisol and 24 h UFC was 44.4% and 85.7%, respectively. For the differential diagnosis of adrenal CS, the sensitivities of the 0800 h plasma cortisol and 24 h UFC were 95.5% and 88.9%, respectively. In patients with ACTH-independent CS and ACTH-dependent CS, the baseline plasma ACTH levels were all below 29 pg/mL and above 37 pg/mL, respectively. The postsurgical hospitalization stay following retroperitoneoscopic adrenalectomy was shorter than that observed for transabdominal adrenalectomy (4.3 ± 1.6 versus 8.8 ± 3.7 days,P<0.001). It was easy to develop retroperitoneal and peritoneal seeding of adrenocortical carcinoma via laparoscopic adrenalectomy.

Background. Brain-derived neurotrophic factor (BDNF) is associated with sympathetic activation. However, the effects of BDNF on diabetic nephropathy are unknown. The aim of this study was to assess the estimated glomerular filtration rates (eGFRs) and changes in serum BDNF levels in type 2 diabetic subjects treated with antihypertensive medications.Methods. In this randomized, double-blind clinical trial, type 2 diabetic subjects with hypertension were assigned to either the benazepril/amlodipine or valsartan/hydrochlorothiazide treatment groups for a 16-week period. The post hoc analyses were based on increased or decreased serum BDNF levels.Results. Of the 153 enrolled subjects, the changes in eGFR were significantly and inversely correlated with those in BDNF in the 76 subjects treated with valsartan/hydrochlorothiazide (r=-0.264,P=0.021) but not in the 77 subjects treated with benazepril/amlodipine (r=-0.025,P=0.862). The 45 subjects with increased BDNF following valsartan/hydrochlorothiazide treatment exhibited a significantly reduced eGFR (-8.8±14.9 mL/min/1.73 m2;P<0.001). Multivariate regression analysis revealed that increased serum BDNF represents an independent factor for reduced eGFR (95% confidence interval between −0.887 and −0.076,P=0.020).Conclusions. Increased serum BDNF is associated with reduced eGFR in type 2 diabetic subjects treated with valsartan/hydrochlorothiazide but not with amlodipine/benazepril.