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

Diabetes mellitus and hypertension constitute two powerful independent risk factors for cardiovascular, renal and atherosclerotic disease. The frequent occurrence of the two diseases in the same individual doubles the risk of cardiovascular death, as well as substantially increasing the frequency of transient ischemic attacks, strokes, peripheral vascular disease with lower extremity amputations, as well as end-stage renal disease and blindness. Although hypertension usually occurs in IDDM in association with renal disease, in NIDDM the evolution of hypertension appears to be multifactorial and independent of renal disease. Obesity appears to be dissociable from hypertension and NIDDM with a common link between obesity, hypertension and NIDDM appearing to be hyperinsulinism and insulin resistance. It has been suggested that hyperinsulinism and insulin resistance may lead to hypertension through altered intracellular calcium metabolism, enhanced renal sodium reabsorption, or through an effect of insulin upon lipid and/or catecholamine metabolism. Further, insulin itself may have a direct effect upon the atherosclerotic process in the hypertensive diabetic patient. These considerations have been taken into account in the structuring of antihypertensive therapy in Type I and Type II Diabetes Mellitus.
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PMID:Diabetes and hypertension. 207 56

During the period from 1974 through 1988, we annually examined approximately 225,000 to 386,400 school children residing in Tokyo for glycosuria to detect juvenile diabetes. If the first test was positive for glucose, glycosuria was confirmed by a second test. In children who gave a positive result in both the first and second tests 0-GTT were performed. All 124 patients were diagnosed as NIDDM according to the criteria of the WHO Report on Diabetes of 1985. The incidence of NIDDM in children in Japan has increased in recent years and from 1984 to 1986 was approximately 3.8 per 100,000 per year. The frequency of NIDDM increases with age up to 14 years. In about 84% of cases, the body weight at diagnosis is more than 20% above the ideal weight and the height is often above average. There is a high frequency in families with a history of diabetes. Diet and exercise therapy in newly diagnosed patients irrespective of the presence or absence of obesity may result in remission, but some cases may require insulin therapy or oral administration of a hypoglycemic drug to obtain a better glycemic control. Children with NIDDM are more likely to be complicated by incipient retinopathy within two years after diagnosis than those with IDDM. Therefore, it is important to keep strict glycemic control to prevent diabetic complications in NIDDM children just as in juvenile onset IDDM.
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PMID:Descriptive epidemiology of non-insulin dependent diabetes mellitus detected by urine glucose screening in school children in Japan. 208 75

Currently our knowledge of the role of lipid abnormalities as risk factors for CHD in diabetes is insufficient. We need to define exact risk parameters to target correctly the therapy of lipid disorders and to outline optimum therapeutic strategies. Therefore it is necessary to identify quantitative and qualitative abnormalities of lipoproteins and apoproteins which signify the risk of CHD and to define their predictive power in prospective trials. Obviously we need to know more about the pathophysiology of lipid abnormalities and the action of insulin. Because diabetic patients carry a high inherent risk of CHD, target values recommended for non-diabetic populations may not be optimal for diabetic populations, but should be lower. To date no primary or secondary intervention trials in diabetic populations have been carried out to show that the lowering of lipid values (serum and LDL cholesterol) will reduce the risk of CHD morbidity or mortality or will prevent the progression of CHD in diabetes. Since hypertriglyceridaemia and low HDL levels are typical abnormalities in NIDDM it is a unique target group to test whether lowering of triglycerides and raising of HDL cholesterol levels will reduce the risk of CHD. Therefore there is a pressing need for clinical trials in both IDDM and NIDDM to provide adequate information on the benefits of lipid-lowering therapy and to confirm treatment strategies.
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PMID:Hyperlipidaemia in diabetes. 208 5

The responsiveness of renin-angiotensin and kallikrein-kinin systems to furosemide challenge has been investigated in forty-six diabetic patients (34 NIDDM/12 IDDM), subdivided into Group I (uncomplicated DM), Group II (DM with hypertension), Group III (DM with nephropathy), Group IV (DM with hypertension and nephropathy) and a control group of 10 healthy volunteers. Plasma renin activity (PRA) was estimated by radioimmunoassay in blood samples drawn before and 10 min after furosemide administration (0.5 mg/kg i.v.). Urinary kallikrein levels were measured by bioassay using estrogenized rat uterus preparation in 4h urine samples collected before and after the diuretic. Urinary Na+ and K+ were also measured. The basal PRA in diabetics was not significantly different from controls, whereas, urinary kallikrein levels were markedly low in all patients. Both PRA and kallikrein levels increased after furosemide in controls while in diabetics this response was severely blunted. In a subset of Group I, a paradoxical fall in PRA and kallikrein levels was noted after furosemide, an effect similar to that observed in patients with nephropathy (Group III). This response in absence of clinical and biochemical parameters of nephropathy indicates early derangement of renal hemodynamic mechanisms heralding the onset of nephropathy.
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PMID:Plasma renin activity and urinary kallikrein excretion in response to intravenous furosemide in diabetic patients. 208 34

The widespread and depth-in investigations on the pulmonary change in DM have been documented abroad. Some revealed that the abnormalities of pulmonary function usually exist in DM. There has been no similar report found in China so far. In this study, ventilation, small airway function (V25 and V50), diffusion capacity and artery blood gas studies have been done in 60 DM and 62 healthy subjects respectively. The results have shown that there is a significant difference between NIDDM group and control group (P less than 0.05) in V50, V25, DLCO and the reduced value of PaO2, and there exists remarkably significant difference between the IDDM group and control group (P less than 0.01) in the decreased values of TLC, FEV1.0%, V50, V25, DLCO, PaCO2 and PaO2.
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PMID:[Pulmonary function and artery blood analysis of diabetes mellitus]. 209 57

A. PATIENT SURVIVAL 1. The best cadaver graft patient survival 3-years posttransplant was observed in those whose primary disease was either nephrotic syndrome (98%), renal hypoplasia (98%), renal dysplasia (98%), IgA nephropathy (96%), or medullary cystic disease (97%). The worst survival was in those with Goodpasture's syndrome (88%), hypertensive nephrosclerosis (87%), MPGN (87%), IDDM (86%), and NIDDM (85%). 2. Patient survival correlated inversely with nonimmunologic graft loss. Nonimmunologic graft loss was high in patients with hypertensive nephrosclerosis (21%), polycystic kidney disease (23%), IDDM (27%), and NIDDM (27%). 3. Females with CGN and IDDM had better patient survival than males with the same diseases. The 2-, 3-, and 5-year survivals for females with IDDM were 91%, 89%, and 87% whereas for males, they were 87%, 84%, and 81%, respectively (p = 0.01). For CGN the 2-, 3-, and 5-year survivals were 95%, 94%, and 93% for females and 93%, 91%, and 90% for males (p less than 0.01). Females with Alport's syndrome had lower patient survival rates at 1 year (86%) than males (95%, p = 0.03). B. GRAFT SURVIVAL 1. The best 3-year graft survival was in recipients whose primary pathology was IgA nephropathy with 83% for cadaver grafts and 95% for LRD grafts. This was not secondary to center effects. The worst graft survival at 3 years for cadaver kidney recipients was in those whose primary illness was NIDDM (61%), hypertensive nephrosclerosis (58%), MPGN (59%), and Goodpasture's syndrome (59%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Outcome of kidney transplantation in different diseases. 210 68

The urinary excretion of kappa light chains, beta 2-microglobulin and albumin was examined in patients with newly diagnosed and long-standing insulin-dependent (IDDM) and non-insulin-dependent (NIDDM) diabetes mellitus, and compared to age-matched control subjects. Patients with IDDM diagnosed within two months, presented with normal albumin excretion, whereas the concentrations of beta 2-microglobulin and kappa light chain in urine were higher than in control subjects. The initiation of insulin therapy reduced, but did not completely normalize, the elevated rate of kappa light chain excretion. Patients with IDDM of long duration showed increased urine excretion of kappa light chains and albumin. In keeping with the findings in IDDM, patients with newly diagnosed NIDDM (within one year) showed increased urinary excretion of kappa light chains compared with control subjects. There was, however, no further increase in light chain excretion with longer duration of NIDDM. To study the effect of short-term hyperglycemia on urinary protein excretion, 12 normal subjects participated in a three-step hyperglycemic clamp study, during which their plasma glucose concentration was raised by +50, +125 and +300 mg/dl. The urine excretion of albumin and beta 2-microglobulin rose progressively with each hyperglycemic clamp step, whereas that of kappa light chain excretion was unaffected by hyperglycemia. We conclude that increased urinary excretion of kappa light chain is a consistent finding in all types of diabetes mellitus, and can be observed even when the albumin excretion is normal. Since the serum concentration of kappa light chain is normal in diabetes, the increased urinary excretion of kappa light chains must be of renal origin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Urinary excretion of kappa light chains in patients with diabetes mellitus. 211 17

We randomly administered thyrotropin-releasing hormone (200 micrograms, as an i.v. bolus) or control saline (in isovolumic amount) to 30 male diabetic subjects (23 IDDM, 7 NIDDM) in fair metabolic control (HbA1 9.7 +/- 0.3%, means +/- SEM) and to 12 healthy male controls on two different mornings. While GH in the basal state was similar in IDDM, NIDDM and normal subjects, TRH administration evoked a significant GH release only in a single IDDM individual. The only GH-responder to TRH was a newly-diagnosed (two weeks) IDDM patient, still with a high glycated hemoglobin level (HbA1 11.1%), despite normal plasma glucose levels. Saline infusion did not affect GH concentrations either in normals or in diabetics. Exaggerated GH responses to TRH are uncommon in diabetic patients in good metabolic conditions.
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PMID:Inappropriate growth-hormone (GH) response to thyrotropin-releasing hormone (TRH) occurs infrequently in well-regulated diabetes mellitus. 211 57

Rheography (impedance plethysmography) makes it possible to differentiate the normal condition of arteries of the lower extremity from functional and organic affections. The examination of a group of 325 patients with diabetes mellitus revealed that without the use of rheography, i.e. when relying only on examination of the lower extremities by palpation, the presence of macroangiopathy would escape attention in 46% of the affected subjects. Macroangiopathy of an organic character was found significantly more frequently in type 2 (NIDDM) (35%) than in type 1 (IDDM) (9%; p less than 0.03). Its incidence increased in both types of diabetes with the duration of the disease. Moreover it was significantly associated with hyperlipoproteinaemia. The assembled results drew attention to the great diagnostic value of rheography. It permits also to document objectively the effect of treatment focused on macroangiopathy.
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PMID:[Diagnosis of diabetic macroangiopathy of the lower extremities using rheography]. 213 62

The prevalence of microalbuminuria and persistent proteinuria was studied in a population of 801 diabetic patients (535 with type II and 266 with type I diabetes). Urinary albumin excretion rate (AER) was measured on morning samples by laser nephelometry. Normoalbuminuria, as defined, in the absence of contaminated urine, by an albumin: creatinine (A/C) ratio below 2, was found in 551 patients, microalbuminuria (NC greater than or equal to 2 with AER below 200 mg/l) in 190 patients and persistent proteinuria (AER greater than or equal to 200 mg/l) in 60 patients. Microalbuminuria was present in 48 (18 p. 100) IDDM patients and 142 NIDDM patients. In IDDM patients, AER increased with the duration of the disease with no apparent influence of age at the onset. The prevalence of hypertension was 25 p. 100 and 61 p. 100 in IDDM patients with microalbuminuria and macroproteinuria respectively versus 10 p. 100 in patients with normoalbuminuria. This prevalence increased in NIDDM patients from 39.3 p. 100 with normoalbuminuria to 40.8 p. 100 and 76.2 p. 100 with microalbuminuria or macroproteinuria respectively. Proliferative retinopathy in type I and type II patients with normal AER was 7.4 p. 100 and 1.2 p. 100 respectively increasing to 15.2 p. 100 and 8.9 p. 100 with microalbuminuria and 27.8 p. 100 and 23.1 p. 100 with macroproteinuria. The prevalence of coronary disease increased from 4 to 10.4 p. 100 in patients with type I diabetes and microalbuminuria. The prevalence of cardiac failure increased from 1.5 to 2.1 p. 100 in type I diabetics and from 3.2 to 7.8 p. 100 in type II diabetics in the presence of microalbuminuria. Patients with microalbuminuria had increased levels of glycosylated hemoglobin A 1C but statistical difference was only obtained for patients with type II diabetes. Routine analysis of AER in diabetics allows early detection of diabetic nephropathy and emphasizes the need for tight metabolic and blood pressure control. Hypertension can be detrimental to nephropathy but might also initiate renal lesions in NIDDM patients.
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PMID:[Microalbuminuria and diabetic nephropathy. Detection and correlation with other degenerative complications]. 214 8


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