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Cardiovascular complications are the main cause of disability and deaths in insulin dependent diabetic patients. The main aim of the EURODIAB IDDM Complications Study was to assess the prevalence of diabetes complications and of risk factors of these complications. In this study the data on cardiovascular diseases and their risk factors in patients included in the EURODIAB IDDM Complications Study--Krakow are presented. The study population included insulin dependent clinic attenders, aged 15-60 years, diagnosed before the age of 36 years. A random sample of up to 140 patients stratified by age, sex and duration of diabetes was chosen. Within each centre the study population consisted of all eligible IDDM patients living in a defined catchement area, who had attended the center at least once during the preceding 12 months. The studied sample included 120 patients (61 men and 59 women). Mean (sd) age of patients was 34.0 (9.6) years, mean duration of diabetes 14.2 (9.8) years, mean Hb A1c concentration 6.6 (1.5)%. The prevalence of cardiovascular diseases was assessed using standardized questionnaire and resting electrocardiogram. Blood pressure was measured with "random zero" sphygmomanometer. Electrocardiogram was assessed according to Minnesota code. Serum cholesterol and triglyceride concentration were determined by enzymatic methods. Albumin excretion rate was determined in 24 hours urine collection. Albumin concentration was assayed by immunoturbidimetry. Cardiovascular diseases were observed in 8.3% of patients. Arterial hypertension (WHO dfn) was found in 11.7% of patients, systolic blood pressure > or = 140 mm Hg in 9.2% of patients and diastolic blood pressure > or = 90 mm Hg in about 5% of men and 2% of women. Hypercholesterolemia (serum cholesterol > or = 6.5 mmol/l) was found in about 20% of patients, hypertriglyceridemia (serum triglyceride 2.2 mmol/1) in 16.4% of men and 10.2% of women. 41.0% of men and 28.8% of women were current cigarette smokers. Microalbuminuria (defined as albumin excretion rate 20-200 micrograms/min) was observed in 23% of men and 15.3% of women.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Coronary risk factors in a group of patients with insulin dependent diabetes mellitus--examination of the EURODIAB IDDM Complications Study Krakow]. 787 Nov 92

The microvascular complications of retinopathy, nephropathy, and neuropathy are less prevalent, and not as severe, in NIDDM as compared with IDDM for unknown reasons. Macrovascular disease is the greatest challenge in the management of NIDDM because it is the cause of death in 50% to 60% of this patient population. Control of the hyperglycemia is the most important because the prevention of complications is more effective than the treatment of them. Blood glucose control through diet, exercise, and medication is the key to reducing the previously identified complications. Lifestyle modifications of diet and exercise are the most effective treatment to reduce hyperglycemia. It is important to emphasize during the asymptomatic period the serious consequences of the complications and to set goals using the glycosylated hemoglobin. If these goals are not met, treatment should be intensified by more frequent visits or referral for the team approach. The time for intervention is before the complications are present, not after they occur. It is certainly reasonable to reduce as many risk factors as possible that adversely affect the complications of NIDDM. Hypertension can affect the course of coronary artery disease, retinopathy, nephropathy, and neuropathy and should be treated. The avoidance of tobacco is a must for the prevention of vascular disease and is associated with painful neuropathy. Dyslipidemia is seen frequently in NIDDM and should be assessed by fasting lipid panel and treated to lower the LDL cholesterol below 130 mg/dL. Reduction of individual risk factors is the most effective approach to this complex clinical syndrome until such time as a better understanding of the pathophysiology provides a more specific and effective intervention.
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PMID:Noninsulin-dependent diabetes mellitus. The prevention of complications. 787 91

The authors noticed a 50% increase in the incidence of arterial hypertension in diabetic subjects compared with non diabetic ones. Females are more affected in both types of diabetes mellitus and during the first ten years after onset of NIDDM. Diabetic retinopathy is more frequent in IDDM. In hypertensive diabetic females retinopathy is twice as frequent as in non-hypertensive female patients.
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PMID:[Incidence and onset of arterial hypertension and diabetic retinopathy in a population of subjects with diabetes mellitus]. 800 35

There are two types of diabetes mellitus. Type I, insulin-dependent diabetes (IDDM), which becomes manifest before the age of 40, is the result of an absolute deficiency of insulin. Type II, the non-insulin-dependent diabetes (NIDDM), develops in the elderly and is caused by a relative insulin deficiency. Patients with type-I diabetes are prone to the development of ketoacidosis, while type II causes hyperglycaemic, hyperosmolar, nonketotic coma. Apart from these acute metabolic alterations, the long-term complications of diabetes are of concern to the anaesthesiologist. Hypertension, coronary artery disease, renal insufficiency and autonomic neuropathy are common and can result in myocardial ischaemia, cardiovascular instability and gastroparesis, with an increased risk of aspiration. Limited movement of the atlanto-occipital joint can cause difficult intubation. To avoid perioperative metabolic catastrophy, blood glucose concentration should be kept between 6.7 and 10 mmol.l-1 (120-180 mg.dl-1). Hypoglycaemia can result in neurological damage, whereas hyperglycaemia causes impaired wound healing and susceptibility to infections and worsens ischaemic damage to the myocardium and brain. Perioperative diabetes management depends on the severity of the surgical procedure and the type of diabetes. All type-I diabetics, whatever operation being performed, need insulin. The intravenous route is recommended as it allows better adjustment. After determination of the fasting blood glucose level, insulin is given at a dosage of 0.5-1 U.h-1 (at gluc < 11.1 mmol.l-1), 1.5-2 U.h-1 (at gluc 11.1-16.7 mmol.l-1) or 3 U.h-1 (at gluc > 16.7 mmol.l-1). In addition, 5-10 g glucose.h-1 is given. In type-II diabetes the oral antidiabetic drug is withheld. During minor surgery the blood glucose concentration is monitored frequently, and if necessary insulin (with gluc > 13.9 mmol.l-1) or glucose is given. In most cases of major surgery insulin therapy will be necessary. Administration should follow the guidelines listed for type-I diabetes. Whether the intravenous or the subcutaneous route is used for insulin, repeated glucose determinations are mandatory. If ketoacidosis develops the volume depletion is treated with normal saline. For hyperglycaemia and acidosis insulin (3-6 U.h-1) with 10-20 mmol.h-1 potassium phosphate is given. Bicarbonate is only indicated when the serum pH is lower than 7.1. It must be borne in mind that perioperative management of diabetes does not end with postanaesthesia care.
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PMID:[Anesthesia and diabetes mellitus]. 804 63

Hyperinsulinemia is very much in the spotlight. Debate rages as to its significance and role in the etiology not only of NIDDM, but also other morphological and metabolic risk factors for atherosclerotic cardiovascular disease, including upper-body obesity, dyslipidemia, hypertension, and hyperuricemia. Epidemiological data support a key role for hyperinsulinemia in these disorders but it is far from conclusive except for the fact that hyperinsulinemia and insulin resistance may be present many years before the onset of impaired glucose tolerance and NIDDM, and clearly play a role in their etiology. The thrifty genotype hypothesis provides a plausible basis for a better understanding of how hyperinsulinemia and insulin resistance could lead to glucose intolerance and atherosclerotic cardiovascular disease, but the detailed biochemical mechanisms remain elusive. A role for increased sympathetic nervous system activity, resulting from hypothalamic stimulation as a primary event causing hyperinsulinemia, cannot be excluded as a cause of hyperinsulinemia. The current focus on hyperinsulinemia also has resulted in closer examination of the therapy of diabetes and hypertension, emphasizing the need to avoid hyperinsulinemia in both IDDM and NIDDM individuals because of the putative risk of atherosclerotic cardiovascular disease and hypertension. There is still a paucity of epidemiological data to support a role for hyperinsulinemia in the etiology of hypertension. However, clinical practice already is being influenced by the fact that ACE inhibitors have been shown to reduce insulin resistance in clinical research studies. The research reviewed here, particularly that relating to hyperinsulinemia, insulin resistance, and cardiovascular disease risk factors, has opened new vistas for the treatment and prevention of NIDDM and atherosclerotic cardiovascular disease. Appropriate exercise clearly is associated with improved insulin sensitivity, modification of CVD risk factors, and lower prevalence of NIDDM. Upper-body obesity, the latest culprit in the field, can also be reduced by exercise. Hyperinsulinemia and insulin resistance can be detected in children, adolescents, and young adults. NIDDM can be prevented, but clearly, intervention needs to commence in childhood, and intensive risk factor intervention in subjects with NIDDM can reduce the risk of atherosclerotic cardiovascular disease. It seems paradoxical that prevention of NIDDM and atherosclerotic cardiovascular disease are now possible even though the biochemical and molecular basis of these disorders is not fully understood.
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PMID:Hyperinsulinemia--how innocent a bystander? 829 79

The aim of the study was to assess the significance of the renin-angiotensin-aldosterone system (R-A-A) in the pathogenesis of arterial hypertension in patients with diabetes type I (IDDM). Testing was accomplished in the hospital conditions in a group of 131 patients with long-term IDDM, who beside of diabetes mellitus and its chronic complications did not show any symptoms of additional diseases. The patients were divided in 5 groups (A-E) depending on the type of coexisting late diabetic complications. The control group was consisted of 20 healthy persons matched for sex and age. In each case the following tests were performed: measurement of blood pressure in succumbent position, daily profile of glycemia and glucosuria, Hb A1 level, ophthalmoscopy, functional assessment of kidney and autonomic system status. Tenin activity in plasma (ARO) and plasma aldosterone (ALD) were determined in basal (after 6 h of succumbent position) and after i.v. administration of 40 mg of furosemide and 3 h of standing position (reactive values). In all groups under study the significant decrease of average, basal and reactive ARO was found in comparison with the control group. This abnormality was the most distinct in subjects with diabetic nephropathy. The autonomic neuropathy was abolishing this tendency. The mean concentration ob basal ALD was in all diabetic subgroups similar as in the controls. The mean reactive ALD was however significantly decreased. In diabetes complicated by retinopathy the negative correlation between ARO and systolic, diastolic and mean blood pressure existed. In diabetes complicated by nephropathy the dependence between blood pressure and ARO and ALD was not found.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Basal and reactive renin and aldosterone secretion in arterial hypertension of insulin dependent diabetics]. 836 86

Hypertension is known to place the individual with IDDM at high risk for the development of both renal and cardiovascular disease. Recent data suggest that aggressive antihypertensive therapy (angiotensin I converting enzyme inhibitors, prazosin, and calcium channel blockers) have significantly improved overall prognosis and long-term survival for individuals with IDDM. Because in individuals with IDDM the development of both hypertension and renal disease has its roots in childhood, it is important that early and effective antihypertensive treatment begin there.
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PMID:Hypertension in individuals with insulin-dependent diabetes mellitus. 841 12

OBJECTIVE--To describe the natural history of kidney disease in Pima Indians with NIDDM. RESEARCH DESIGN AND METHODS--Review of previous studies describing diabetic kidney disease in this Native-American population and in other populations. RESULTS--NIDDM is the leading cause of renal failure in Pima Indians, among whom the incidence of ESRD is 23 times that of the general U.S. population. The high incidence of NIDDM and its early onset in the Pima undoubtedly contribute to this difference. The incidence of overt nephropathy and ESRD, as a function of diabetes duration, is at least as high in Pima Indians with NIDDM as that reported in other populations with IDDM. Furthermore, nearly all of the excess mortality associated with NIDDM is found in individuals with overt nephropathy. Mild elevations of UAE, which may be present even shortly after the onset of diabetes, predict the development of overt nephropathy in diabetic Pimas. Additional predictors include high blood pressure, level of glycemia, duration of diabetes, family history of diabetic nephropathy, and type of diabetes treatment. CONCLUSIONS--Diabetic kidney disease is a major cause of morbidity and mortality in Pima Indians. The natural history of diabetic kidney disease in this population is similar, in many ways, to the natural history described in individuals with IDDM.
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PMID:Diabetic kidney disease in Pima Indians. 842 5

Most aspects of the nutritional therapy of diabetes mellitus apply equally to IDDM and NIDDM patients and are also appropriate for people with high risk of cardiovascular diseases. A restriction of energy, a reduction of saturated fatty acids as well as of alcoholic drinks and simple sugars are the most important measures. This modification of nutritional intake together with increased fibre consumption is not only appropriate to avoid hyperglycaemia in diabetic patients but has also its benefits in patients presenting with the metabolic syndrome (possible reduction of hyperinsulinaemia, hypertension and hyperlipoproteinaemia). Diabetic patients should have regular screening for microalbuminuria. At first signs of an early stage of nephropathy patients should be advised to restrict their protein intake. About 50% of daily energy intake should be derived from carbohydrates and fat intake should be no more than 35% of total energy (saturated fatty acids less than 10% of energy). Carbohydrate exchange units are usually not necessary in NIDDM patients. In addition diabetes specialty foods are not an essential part of the nutritional therapy. The success of the nutritional therapy in diabetic patients is substantially dependent upon qualified counselling and education of the patients by the physician (as far as possible with the assistance of a dietitian).
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PMID:[Nutritional therapy in diabetes mellitus]. 847 34

On the whole, diabetic microangiopathy can be understood as the clinical renal-retinal syndrome. About 10% of all diabetics die of end-stage renal failure, more frequent in IDDM. With an incidence of 14% diabetic retinopathy is one of the major causes of blindness in adulthood. In the non-proliferative state, the pathological changes are limited to the retina, whereas the alterations affect both retina and vitreous in the proliferative state. Photocoagulation is the treatment of choice. If photocoagulatory treatment is not possible because of cataract, vitreous surgery (pars-plana vitrectomy) could improve visual prognosis. The clinical features hypertension, proteinuria and finally renal failure define the term "diabetic nephropathy". The increased intraglomerular pressure is the main pathological alteration of incipient nephropathy. Microalbuminuria essentially determines the prognosis: in IDDM it concerns the incidence of a manifest nephropathy, in NIDDM the excessively increased incidence of cardiovascular mortality. Sonographically, the kidneys are large with bright and wide parenchyma. Along with the development of end-stage renal disease the kidney size diminishes. According to Mogensen, nephropathy is divided into five stages: Stage 1, the early stage, is defined by hypertrophy and hyperfiltration. Stage 2 shows incipient structural changes without any clinical findings. Stage 3 is characterised by persistent microalbuminuria. Stage 4 leads to increasing renal failure and stage 5 to end-stage renal disease and the necessity of dialysis treatment. Incipient nephropathy demands a strict treatment of both hypertension and diabetes. In the meantime, ACE inhibitors are the treatment of choice. In case of dialysis treatment continuous ambulant peritoneal dialysis (CAPD) is usually preferred.
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PMID:[Diabetic microangiopathy]. 847 38


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