作者: Sharon OʼByrne , John Feely
DOI: 10.2165/00003495-199040020-00003
关键词:
摘要: Non-insulin-dependent diabetes mellitus (NIDDM) is being increasingly diagnosed as its importance a risk factor for the development of cardiovascular disease continues to be recognised. Good metabolic control remains major goal drug therapy it decreases severity and incidence diabetic complications. Many drugs have been known interfere with glucose control, either in beneficial or, more commonly, deleterious fashion. Unfortunately many instances drug-induced effects not looked at specifically NIDDM. Thiazide diuretics shown cause deterioration only general population but especially patients who impaired tolerance. While effect appears less potassium supplementation lower dosage employed nowadays, thiazide are best avoided patients. Loop reported reduce lesser extent than thiazides. Although indapamide would appear blood sugar NIDDM, higher doses that loss may deterioration. β-Adrenoceptor antagonists rise glycosylated haemoglobin The marked on oral hypoglycaemic agents opposed diet alone those concomitant diuretics. greatest was seen propranolol, least cardioselective lipophilic β-blockers. It interest α-blockade prazosin seems antagonise β-adrenoceptor blocker-induced control. calcium differing which structure related. In some, all, studies use dihydropyridines such nifedipine has associated Long term needed assess definitively their Verapamil, other hand, 1 small study found Centrally acting α-agonists antihypertensive clonidine result when used although there isolated case reports. specific agonist guanfacine uncontrolled tolerance Uncontrolled suggest phenothiazines aggravate significance number recent observations fully clear. balance endogenous opioid influences over pancreatic β-cell function NIDDM favours inhibitory met-enkephalin, opiate antagonist naloxone partially restores acute insulin response glucose. Aspirin dual — decreased clearance tissue sensitivity no resultant overall change levels. There also improve A fall 2-hour plasma during treatment angiotensin converting enzyme (ACE) inhibitors captopril (post load) enalapril (postprandial), relatively nonsignificant some studies. reports reduction fasting levels lipid-lowering fibric acid derivatives (clofibrate, bezafibrate fenofibrate) possibly nicotinic derivatives, suggesting increased insulin. gemfibrozil agents. Mebendazole, through secretion, chloroquine, reduced hepatic degradation insulin, 2 induction metabolising activity advanced means improving enhanced peripheral utilisation, date produced contradictory results. both monoamine oxidase (MAOIs) tricyclic antidepressants Close monitoring recommended where abovementioned evidence possible new recognised requirement development, particularly