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Strategies for the use of oral agents and insulin in NIDDM
West Indian med. j ; 44(Suppl. 1): 9-10, Feb. 1995.
Artigo em Inglês | MedCarib | ID: med-5626
Biblioteca responsável: JM3.1
Localização: JM3.1; R18.W4
ABSTRACT
The goals of chronic treatment of NIDDM are to eliminate or minimize microvascular and neuropathic complications and reduce the incidence of macrovascular complications to that of the non-diabetic. The first goal can be achieved by appropriate glycaemic control while the therapeutic regimens necessary to attain the second goal have yet to be clearly elucidated. Ideal glycaemic regulation would be normal fasting and post-prandial blood glucoses and haemoglobin Alc. Inadequate data are available to ascertain what lesser levels of glycaemic control in NIDDM patients might be adequate to minimize microvascular and neuropathic complications. Since the rate of development and progression of the complications appears to be related to the magnitude and duration of hyperglycaemia, it would seem that, all other factors being equal, the better the chronic glycaemic control achieved in NIDDM patients, the more benefit can be expected. Thus, while one can strive for haemoglobin Alc in the normal range, attaining a level which is no higher than 15 to 20 per cent above the upper limit of normal may be a more practical target. Since hypertension accelerates microvascular disease, a secondary goal should be to maintain a mean arterial pressure < 100 mm of Hg. The strategies employed to achieve glycaemic control in NIDDM patients are dependent on the magnitude of impairment of insulin secretion and the degree of insulin resistance in the individual patient. The quantitative magnitude of the defects differs among NIDDM patients and changes with time in the individual patient. The therapeutic programme must be individually designed and periodically re-evaluated. Four classes of drugs are available for the management of hyperglycaemia in NIDDM patients 1) Inhibitors of carbohydrate digestion such as alpha glucosidase inhibitors. These drugs lower post-prandial glucose rise. 2) Agents that decrease hepatic glucose production. This is the main action of intermediate acting insulin at bedtime. 3) Agents that increase insulin action on the liver and/or peripheral tissues. Metformin and thiazolidandiones are likely to act through this mechanism. 4) Drugs that stimulate insulin secretion. Sulfonylureas are the prototype of this class of drugs. Patients with mild modest fasting hyperglycaemia and significant post-prandial hyperglycaemia respond well to diet plus alpha glucosidase inhibitors. More severe hyperglycaemia usually indicates significant decrease in insulin secretory reserve and is better treated with metformin or sulfonylureas. As insulin secretory deficiency increases, sulfonylureas or sulfonylureas plus metformin are necessary. Progressive insulin secretory deficiency may require bedtime insulin and oral agents during daytime. When insulin secretion is severly impaired, multiple doses of insulin are likely to be needed. This stepwise approach to combination drugs therapy of NIDDM seems the most reasonable approach in 1995 (AU)
Assuntos
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Coleções: Bases de dados internacionais Base de dados: MedCarib Assunto principal: Diabetes Mellitus Tipo 2 / Hiperglicemia Limite: Humanos Idioma: Inglês Revista: West Indian med. j Ano de publicação: 1995 Tipo de documento: Artigo / Congresso e conferência
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Coleções: Bases de dados internacionais Base de dados: MedCarib Assunto principal: Diabetes Mellitus Tipo 2 / Hiperglicemia Limite: Humanos Idioma: Inglês Revista: West Indian med. j Ano de publicação: 1995 Tipo de documento: Artigo / Congresso e conferência
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