The American journal of medicine
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Randomized Controlled Trial Clinical Trial
Addition of pioglitazone or bedtime insulin to maximal doses of sulfonylurea and metformin in type 2 diabetes patients with poor glucose control: a prospective, randomized trial.
To compare the efficacy of adding pioglitazone or bedtime isophane (NPH) insulin to maximal doses of metformin and an insulin secretagogue in patients with poor glucose control. ⋯ Adding pioglitazone or bedtime insulin for 16 weeks improved glycemic control in type 2 diabetic patients with secondary oral agent failure. Pioglitazone was associated with less hypoglycemia and improved HDL cholesterol levels.
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To evaluate the short-term outcome of patients who underwent carotid stenting with the routine use of cerebral protection devices. ⋯ In this uncontrolled study, routine cerebral protection during carotid artery stenting was technically feasible and clinically safe. The incidence of major neurologic complications in this study was lower than in previous reports of carotid artery stenting without cerebral protection.
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Randomized Controlled Trial Clinical Trial
Glycemic control with glyburide/metformin tablets in combination with rosiglitazone in patients with type 2 diabetes: a randomized, double-blind trial.
To assess the efficacy and safety of adding rosiglitazone to an established regimen of glyburide/metformin in patients with type 2 diabetes who had not achieved adequate glycemic control (glycosylated hemoglobin [HbA1C] levels >7.0% and < or =10.0%). ⋯ In patients with inadequate glycemic control despite established glyburide/metformin therapy, the addition of rosiglitazone improves glycemic control, allowing more patients to achieve an HbA1C level <7% and perhaps delaying the need for insulin treatment.
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The renin-angiotensin-aldosterone system regulates renal vasomotor activity, maintains optimal salt and water homeostasis, and controls tissue growth in the kidney. However, pathologic consequences can result from overactivity of this cascade, involving it in the pathophysiology of kidney disease. An activated renin-angiotensin-aldosterone system promotes both systemic and glomerular capillary hypertension, which can induce hemodynamic injury to the vascular endothelium and glomerulus. ⋯ An understanding of this system is important to appreciate that inhibitors of this cascade can reduce the progression of chronic kidney disease in proteinuric disease states. Pharmacologic agents that can interfere with this cascade include angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and aldosterone receptor antagonists. This paper will provide an overview of the renin-angiotensin system, review its role in kidney disease, examine the renal effects of inhibition of this cascade in experimental animal models, and review clinical studies utilizing renin-angiotensin-aldosterone inhibitors in patients with diabetic and nondiabetic nephropathies.
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Recognition of the basal and postprandial components of hyperglycemia, in tandem with the development of new insulins and other clinical research, has led to a reassessment of type 2 diabetes mellitus treatment. In the future, insulin will be used earlier, treatment will intensify as the disease progresses, and combination therapy will be routine. Hyperglycemia can be controlled initially with sulfonylureas and metformin, agents that mainly improve control of fasting and preprandial glucose. ⋯ Although the traditional approach has been to introduce insulin therapy only after very high glucose values have persisted, despite prolonged use of oral agents alone, a more desirable strategy would be to prevent patients from ever experiencing the loss of glycemic control associated with hemoglobin A(1c) (HbA(1c)) elevations >7%. This goal could be achieved by diagnosing type 2 diabetes earlier in its course and by adding basal insulin to oral therapy much earlier. To maintain the recommended <7% HbA(1c) target level of control, treatments that target postprandial hyperglycemia will have to be added to basal insulin later on, as endogenous insulin continues to decline.