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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinicians are frequently faced with treating non-insulin-dependent diabetics (NIDDM) who do not exhibit optimal glycemic control on maximal dosages of oral sulfonylurea agents or large dosages of insulin. Sustained hyperglycemia is implicated in the onset and progression of retinopathy, nephropathy, and neuropathy. Recent studies also suggest that hyperinsulinemia contributes to hypertension and altered lipid levels. Hence, the maintenance of euglycemia with minimal circulating insulin concentrations is the prime goal of therapy. Most studies document that the efficacy of combination therapy requires smaller insulin doses, enhances glycemic control without adverse effects on body weight or lipids, and decreases hypoglycemic episodes compared with insulin monotherapy. Therefore, combination therapy may be the optimal therapeutic option in NIDDM clients manifesting secondary failure to oral agents or insulin resistance.
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PMID:Combination sulfonylurea and insulin therapy in non-insulin-dependent diabetes mellitus. 835 Oct 85

The aim of this study was to assess the prevalence of long-term complications in all patients with non-insulin-dependent diabetes mellitus, who were known to their general practitioners (GPs). During one year 19 GPs in the area of Hoogeveen in the Netherlands examined their non-insulin-dependent (NIDDM) patients, including those under specialist's care. A detailed protocol was used; the GPs were trained in the diagnostic procedures. Complications were either already known from the records or newly discovered during screening. In a population of 41,940 14.5/1000 patients with diabetes were identified: 12/1000 NIDDM and 2.5/1000 insulin-dependent diabetes mellitus (IDDM). Of the 509 NIDDM patients, 387 (76%) could be screened for late complications. Signs and symptoms of late complications were found in many patients: retinopathy (14%), nephropathy (57%), neuropathy (68%) and macroangiopathy (53%). The prevalence of serious complications was: proliferative retino- and maculopathy (3.3%); diabetic foot (2.6%); renal failure (2.5%). The systemic screening revealed a high number of previously unknown cases. It is concluded that many patients with NIDDM develop signs and symptoms of late complications. Most cases are identified by systemic screening only. More long-term studies of the prognosis of late complications in NIDDM are needed.
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PMID:Diabetes and its long-term complications in general practice: a survey in a well-defined population. 835 6

Urinary protein excretion rate and clinical and metabolic associates were investigated in a group of 108 patients with Type 2 diabetes mellitus at the time of diagnosis and after 5 years, and also 121 control subjects. The presence of coronary heart disease, neuropathy and retinopathy, cardiovascular risk factors and 24-h urinary excretion rate of albumin, beta-2-microglobulin, and IgG were examined. At the 5-year examination, urinary excretion rate of albumin was higher in diabetic patients than in control subjects (39 +/- 75 vs 16 +/- 28 mg 24 h-1 for men, p < 0.05; 38 +/- 57 vs 22 +/- 42 mg 24(-1) h for women, p < 0.01). Furthermore, increased beta-2-microglobulin excretion rate, a marker of tubular impairment, was observed in diabetic men as compared to control men (0.17 +/- 0.15 vs 0.14 +/- 0.21 mg 24 h-1, p < 0.05). Diabetic patients with increased albumin excretion rate (> 30 mg 24 h-1) showed poorer metabolic control than those with normal albumin excretion rate, but no significant differences in body mass index or in the frequencies of smoking, hypertension, coronary heart disease or retinopathy and neuropathy were observed between the groups. Baseline hyperinsulinaemia was closely associated with increasing albuminuria at the 5-year examination.
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PMID:A prospective study of clinical and metabolic associates of proteinuria in patients with type 2 diabetes mellitus. 836 91

Of the various types of diabetes mellitus, non-insulin-dependent diabetes (NIDDM) is by far the most common and is increasing rapidly in many populations around the world. It is a heterogeneous disorder, characterized by a genetic predisposition and interaction between insulin resistance and decreased pancreatic beta-cell function. There is a strong association between the presence of obesity and low levels of physical exercise and the development of NIDDM. However, NIDDM may also develop in lean individuals and the incidence increases significantly with increasing age. A diagnosis of impaired glucose tolerance or gestational diabetes is a strong predictor for future development of NIDDM and should signal appropriate interventions to prevent or delay the progression to NIDDM. NIDDM is frequently associated with other conditions such as hypertension, hypertriglyceridemia and decreased high-density lipoprotein which are additional risk factors for atherosclerosis and cardiovascular disease. The 'insulin resistance syndrome', which includes obesity, NIDDM, hypertension, hyperinsulinemia and dyslipidemia is a major and increasing cause of morbidity and mortality in many populations. In addition, people with NIDDM and poor glycemic control may develop severe microvascular complications of diabetes, including retinopathy, nephropathy and neuropathy. Appropriate diet, weight control and increased physical activity will increase insulin sensitivity in insulin resistant patients and are effective treatments for patients with NIDDM or may prevent the development of NIDDM in susceptible individuals. If these measures are unsuccessful, then oral hypoglycemic agents or insulin therapy may be required.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:NIDDM--the devastating disease. 852 17

Non-insulin-dependent diabetes (NIDDM) is a common multimetabolic disorder with potential (and potentially severe) long-term complications affecting large and small blood vessels. Where microvascular complications (retinopathy, nephropathy and neuropathy) are concerned, the Diabetes Control and Complications Trial (DCCT), as well as much circumstantial evidence, suggests that hyperglycaemia is the main aetiological factor and this is likely to apply in NIDDM as well as IDDM. Unfortunately, achieving normoglycaemia in NIDDM is not easy and it is unclear whether insulin has advantages over oral hypoglycaemic agents or vice versa. Turning to macrovascular disease, it is unclear which of the many potentially atherogenic abnormalities-hypertension, hyperinsulinaemia, hyperlipidaemia, etc-are most important. A further problem is that macrovascular disease is already well developed in many patients when NIDDM is diagnosed and we do not know whether secondary prevention is effective. Nevertheless, it is sensible to try to reverse the atherogenic milieu and this should be done in the first instance by lifestyle modification rather than drugs. Even if we cannot manipulate the biochemistry to prevent small or large vessel complications, much can still be done; proactive foot care can prevent ulceration, timely laser treatment can prevent visual loss and thrombolytic therapy is relatively more effective in diabetic patients with myocardial infarction than in their non-diabetic peers. Finally, patients with NIDDM need intensive education and each needs an individualised treatment plan and goals.
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PMID:Targets of therapy for NIDDM. 852 19

Non-insulin-dependent diabetes mellitus (NIDDM) may be the most rapidly-growing chronic disease in the world. Its long-term complications, including retinopathy, nephropathy, neuropathy, and accelerated macrovascular disease cause major morbidity and mortality. Although therapy that normalizes glycemia may prevent the development and delay the progression of long-term complications in NIDDM, as has been demonstrated in insulin-dependent diabetes mellitus (IDDM), no direct data exist to support the efficacy of "intensive therapy" in NIDDM. An alternative approach to preventing the development of long-term complications may be to intervene more distally, i.e., inhibit the mechanism(s) by which elevated glucose levels cause complications. Potential pathogenic mechanisms include the accumulation of sorbitol and other biochemical changes in tissues with aldose reductase, and the modification of proteins by glycation. Pharmacologic probes, including aldose reductase inhibitors and glycation inhibitors such as aminoguanidine, are currently under study and may provide an efficient means of preventing complications, independent of the ambient glycemic level.
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PMID:Prevention of long-term complications of non-insulin-dependent diabetes mellitus. 854 21

During long-term treatment of arterial hypertension with calcium antagonists of the dihydropyridine type activation of the sympathetic nervous system and subsequently also of the renin-angiotensin-aldosterone system persists, while the haemodynamic reaction to vasodilatation, manifested by an elevated pulse rate and minute volume from the initial stage of therapy, recedes. In type II diabetics the basal and stimulated response of the renin-angiotensin-aldosterone system is reduced. The administration of calcium antagonists of the dihydropyridine type does not stimulate significantly the renin-angiotensin-aldosterone system as the starting function of the sympathetic nervous system is impaired within the framework of vegetative neuropathy. In almost 20% NIDDM plasma renin activity and aldosterone do not respond to furosemide administration and the vertical posture. In others the response is found but takes place at reduced levels. Hyporeninaemic hypoaldosteronism is thus manifested not so much by a drop of plasma renin and aldosterone beneath the lower range of reference values as by a reduced response to stimulation. Functional hyporeninaemic hypoaldosteronism is another, frequent late complication of diabetes. In advanced forms a further block of the renin-angiotensin-aldosterone system by ACE inhibitors can then produce, even in the absence of diabetic nephropathy, in the stage of chronic renal failure dangerous hyperkaliaemia which may threaten the patient. Dynamic examination of the sympathetic nerve and the renin-angiotensin-aldosterone system makes it possible to predict this condition. In practice it is necessary in diabetics with arterial hypertension after starting with ACE inhibitors during the first days to monitor repeatedly plasma potassium and creatinine. ACE inhibitors and calcium antagonists are otherwise for diabetics drugs of first choice which can arrest the progression of nephropathy, effectively reduced the blood pressure without causing deterioration of insulin resistance and hyperlipoproteinaemia and lead even to regression of hypertrophy of the vascular wall and left ventricle.
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PMID:[The effect of long-term treatment of arterial hypertension with Ca antagonists on the renin-angiotensin-aldosterone system in diabetics. Hyporeninemic hypoaldosteronism]. 857 95

A cross-sectional study was designed to identify a relationship between the presence of symptoms usually related to nervous system involvement as well as other chronic complications of diabetes with three objectively defined degrees of autonomic neuropathy (AN). Symptoms usually related to peripheral sensitive neuropathy and AN were assessed using a questionnaire applied to 132 diabetics (38 IDDM and 94 NIDDM), 65 without and 67 with AN. AN was classified as follows according to 5 cardiovascular autonomic tests described by Ewing: 1) early involvement-1 abnormal test (N = 27); 2) definite involvement-2 or 3 abnormal tests (N = 26); 3) severe involvement-4 or 5 abnormal tests (N = 14). A statistically significant association was observed between degree of autonomic involvement and the presence of the following symptoms: dizziness on standing, dysphagia, vomiting, diarrhea, fecal incontinence, gustatory sweating, urinary retention, numbness and hyperesthesia of the feet or legs. Constipation and cystitis were not significantly related to cardiovascular AN. Only 3% of the patients without neuropathy and with early involvement had four or more than four of the symptoms. The prevalence of proliferative retinopathy and nephropathy was increased among patients with more severe degrees of AN. For IDDM patients there was a positive correlation between the degree of cardiovascular AN and the duration of diabetes. We conclude that: 1) severe cardiovascular AN is usually related to 4 or more of the evaluated symptoms and those patients usually have the other complications of diabetes; 2) severe AN could be a risk factor or an indicator of the same underlying process that determines the beginning of proliferative retinopathy and/or nephropathy.
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PMID:Relationship between the degree of cardiovascular autonomic dysfunction and symptoms of neuropathy and other complications of diabetes mellitus. 858 Aug 65

Little is known about the occurrence and predictive factors of autonomic neuropathy and its relationship to cardiovascular mortality in NIDDM patients, and no long-term follow-up studies including nondiabetic control subjects are available. A total of 133 patients with newly diagnosed NIDDM (70 men) and 144 control subjects (62 men) were examined at baseline and after 5 and 10 years of follow-up. Deep-breathing tests (baseline, 5-year, and 10-year) and active orthostatic tests (5- and 10-year) were performed. Criteria for autonomic neuropathy were parasympathetic (expiration-to-inspiration ratio </- 1.10), sympathetic (systolic blood pressure decrease >/- 30 mmHg in the orthostatic test), and combined autonomic neuropathy (parasympathetic with sympathetic neuropathy). The frequency of parasympathetic neuropathy (NIDDM patients versus control subjects) was 4.9 vs. 2.2% (P = 0.224) at baseline, 19.6 vs. 8.5% (P = 0.017) at 5 years, and 65.0 vs. 28.0% (P < 0.001) at 10 years of follow-up. The frequency of sympathetic neuropathy was 6.8 vs. 5.6% (P = 0.709) at 5 years and 24.4 vs. 9.0% (P = 0.003) at 10 years of follow- up. These figures for combined autonomic neuropathy were 2.1 vs. 1.8% (P = 0.869) at 5 years and 15.2 vs. 4.2% (P = 0.007) at 10 years of follow-up. NIDDM patients with parasympathetic neuropathy at the 10-year examination showed worse glycemic control and higher insulin values than those without parasympathetic neuropathy. Furthermore, in our subjects, women were more prone to have parasympathetic neuropathy than men. Parasympathetic neuropathy at baseline was more frequent in those who died from a cardiovascular cause than those who did not (13 vs. 3%, P = 0.045). Similarly, sympathetic autonomic nervous dysfunction at the 5-year examination predicted the 10-year cardiovascular mortality. In conclusion, the frequency of autonomic neuropathy in NIDDM patients increases sharply with time. The development of autonomic neuropathy is connected with poor glycemic control. Interestingly, a high insulin level seems to have a predictive role in the development of parasympathetic autonomic neuropathy irrespective of obesity and glycemia.
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PMID:Occurrence, predictors, and clinical significance of autonomic neuropathy in NIDDM. Ten-year follow-up from the diagnosis. 859 35

To examine the characteristic features of risk factors for macroangiopathy (MA) in nonobese Japanese NIDDM patients, 899 NIDDM patients with and without MA were registered from 40 facilities. Of these, 386 subjects were identified as having any form of MA (total MA); these included 211 with ischemic heart disease (IHD), 163 with cerebrovascular disease (CVD), and 77 with peripheral vascular disease (PVD). Univariate analyses revealed the following common risk factors for total MA, IHD, CVD, and PVD: age, hypertension, systolic blood pressure (sBP) or diastolic blood pressure (dBP), duration of diabetes, diabetic microangiopathy (retinopathy, nephropathy, and neuropathy), low HDL cholesterol level, and higher LDL cholesterol/HDL cholesterol ratio. Additional significant risk factors for specific conditions were also identified, respectively, as male sex for total MA, IHD, and PVD, smoking for IHD and PVD, and high fasting plasma glucose level for total MA and CVD. With stepwise multivariate logistic regression analysis, older age, duration of diabetes, smoking, and low LDL cholesterol/HDL cholesterol ratio were identified as significant and independent risk factors for total MA, IHD, CVD, and PVD. Other risk factors identified were high dBP for IHD, CVD, and PVD, high sBP for total MA, and low BMI for PVD. These results clearly demonstrated that duration of diabetes, smoking, hypertension, and dyslipidemia are major risk factors for MA in NIDDM patients. Since the mean BMI was similar for both groups (approximately 23 kg/m2) and there were no significant differences in immunoreactive insulin levels before and after 75-g oral glucose challenge testing, obesity and hyperinsulinism at the time of the analyses were not considered to play an important role for the pathogenesis of MA in Japanese NIDDM patients. By using the chi 2 test, cutoff points were determined for six of the most commonly measured risk factors. The cutoff point was the level beyond which a significantly higher prevalence of MA occurred. The cutoff points (rounded slightly upward in some cases) for fasting plasma glucose, sBP, dBP, serum total cholesterol level, serum triglyceride level, and BMI were 140 mg/dl, 140 mmHg, 80 mmHg, 180 mg/dl, 120 mg/dl, and 23 kg/m2, respectively. When these cutoff points were used as control criteria, the prevalence of MA was significantly lower in subjects whose risk factor measurements remained under the proposed control criteria for four or more of the six variables. In conclusion, in nonobese NIDDM patients, age, hypertension, and dyslipidemia were found to be risk factors for MA. Duration of diabetes was also demonstrated as an independent risk factor, indicating the close association of deranged glucose metabolism with the pathogenesis of MA in NIDDM patients. It seems to be crucial to control these risk factors for the prevention of MA in NIDDM patients.
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PMID:Risk factor analyses for macrovascular complication in nonobese NIDDM patients. Multiclinical Study for Diabetic Macroangiopathy (MSDM). 867 83


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