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OBJECTIVES: To examine retinopathy and nephropathy in elderly patients with diabetes mellitus (DM) under intensive multifactorial DM control. DESIGN: Six-year interventional observation study. SETTING: Multicenter study including four hospitals. PARTICIPANTS: Four hundred thirteen elderly (≥65) patients with type 2 DM attending each hospital for 1 year or longer; those receiving hemodialysis or with uncured malignancy were excluded. MEASUREMENTS: Development, worsening, and improvement of retinopathy and nephropathy and respective risk factors. RESULTS: The mean baseline hemoglobin (HbA1c), blood pressure (BP), and total cholesterol were 6.8%, 137/74 mmHg, and 5.13 mmol/L, respectively. Retinopathy developed in 45 of 168 (27%) patients and, of 63 with nonproliferative retinopathy, worsened and improved in 11 (17%) and 23 (37%), respectively. Nephropathy developed in 53 of 227 (23%) patients and improved in 13 of 51 (25%) having it baseline. The mean change in glomerular filtration rate (ΔGFR, baseline GFR–GFR at the end of the study period) in those with nephropathy at baseline was 21.5 mL/min. HbA1c was related to development of retinopathy ( P=.001, odds ratio (OR)=1.91), and serum creatinine ( P=.03, OR=1.02), systolic BP (SBP) ( P=.03, OR=1.22), and prior stroke ( P=.005, OR=3.21) were related to development of nephropathy. In patients with nephropathy at baseline, SBP ( P=.03, Spearman's rho (ρ)=0.310), total cholesterol ( P=.01, ρ=0.361), and low-density lipoprotein cholesterol ( P=.03, ρ=0.322) were correlated with ΔGFR. CONCLUSION: In elderly patients under intensive control for DM, the outcome of microangiopathy is favorable. Modifiable risk factors were hyperglycemia for development of retinopathy and hypertension and hypercholesterolemia for development or worsening of nephropathy; prior stroke was an unmodifiable risk factor for development of nephropathy. [ABSTRACT FROM AUTHOR]

OBJECTIVE -- To clarify mortality and morbidity of intensively managed elderly diabetic individuals and to explore factors predicting mortality and diabetes-related end points. RESEARCH DESIGN AND METHODS -- A total of 390 elderly (≥65 years of age) outpatients with type 2 diabetes (173 men and 217 women, mean age 73.0 years) were analyzed. The mean HbA[sub1c] upon entry was 6.8% (332 receiving oral hypoglycemics and/or insulin) and blood pressure upon entry was 136/74 mmHg (219 receiving antihypertensive drugs). The patients have been followed-up for 3 years with HbA[sub1c] <7.0% and blood pressure <145/80 mmHg as targets, with mortality and an aggregate of fatal and nonfatal diabetes-related events as end points. Mortality rate and causes of mortality, as well as risk factors for mortality and morbidity, were determined. RESULTS -- The mortality rate, 2.9% per year, was comparable to that of the age-and sex-matched general population. Stroke was a leading cause of mortality after malignancy. By the univariate Cox proportional hazards model, only high serum creatinine and prior stroke were highly significant and strong risks for both end points. In those without prior stroke and receiving antihypertensive agents, the incidence of the diabetes-related end point based on their systolic blood pressure (SBP) quartile was U-shaped, with the nadir at the 3rd (SBP, 137-147 mmHg) and the peak at the 1st (SBP ≤ 125 mmHg) quartile. CONCLUSIONS -- In well-controlled elderly diabetic subjects, there was no excessive mortality compared to the age- and sex-matched general population. Renal dysfunction and prior stroke were independent risks for mortality and morbidity. In those without prior stroke, a risk of too much lowering of blood pressure was suggested. [ABSTRACT FROM AUTHOR]

Objective: To report a case of infundibuloneurohypophysitis treated with steroid. Clinical Presentation: A 65-year-old woman who was well until 4 weeks before admission and was not taking any medication presented with acute development of polydipsia and polyuria. Urinary volume was increased to 4,500 ml/day. She showed elevated serum osmolality and low urine osmolality, together with shortage of antidiuretic hormone. Magnetic resonance imaging (MRI) of the pituitary revealed marked nodular thickening of the neurohypophysis. Endocrinologically, anterior pituitary function appeared normal. Based on these examinations, she was diagnosed as having central diabetes insipidus due to lymphocytic infundibuloneurohypophysitis. Intervention: Prednisolone (1 mg/kg/day, p.o.) and D-deaminovasopressin (5 μg/day, intranasal) were commenced. Ten days after the administration of the agents, MRI showed a dramatic improvement in the thickening of the neurohypophysis. Ten weeks later, abnormalities found in earlier MRI had disappeared. The drugs were withdrawn gradually, and diabetes insipidus ceased 25 weeks later. Recurrence was not seen in the subsequent MRI, and the function of the posterior pituitary gland was completely normalized even 7 years after discontinuation of treatments. Conclusion: This case shows that noninvasive diagnosis and appropriate steroid administration can effectively cure lymphocytic infundibuloneurohypophysitis; it is recommended with long-term follow-up. Copyright © 2009 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Proinsulin C-peptide was for long considered to be without biological activity of its own. Recent reports have demonstrated beneficial effects of C-peptide in the diabetic state, including improvements of kidney and nerve function. In this study, we estimated that effects of C-peptide on intracellular signaling mechanisms and crosstalk to insulin signaling in vitro. Physiological dose of C-peptide suppressed basal activity of mitogen-activated protein kinase (MAPK), which is a serine threonine kinase that modulates gene expression, mitosis, and cell proliferation though high dose of C-peptide activated MAPK. Insulin-induced MAPK activity was also suppressed by C-peptide treatment. On the other hand, there was no effect of C-peptide on the basal and insulin-induced activities of Akt, another important serine kinase. C-peptide suppressed the basal and insulin-induced activity of serum response element, one of MAPK-responsive gene element in dose-dependent manner. These suppressive effects of C-peptide may not result from refractory responses against partial MAPK activation of C-peptide as C-peptide inhibited the basal activity of MAPK and its down-stream. Further, C-peptide did not modify insulin-induced glycogen synthesis. These results suggested that C-peptida selectively attenuated proliferative action of insulin signaling These activities of C-peptide might explain the suppressive effect of C-peptide on diabetic complications. [ABSTRACT FROM AUTHOR]