Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 107 patients with non-insulin dependent diabetes(NIDDM), plasma growth hormone(GH) responses during standard arginine test (0.5 g/kg of body weight) were studied and analyzed in comparison with those in 17 normal subjects. The indices of the responsiveness of GH, peak value of GH, sum of GH values(sigma GH), area of GH curve(integral of GH), sum of GH values above fasting level(sigma delta GH) and area of GH curve above fasting level(integral of delta GH) during the test (2 hr) were calculated. Data were also analyzed with multiple regression analysis using stepwise method for variable selection. Basal level of GH was significantly higher in diabetic patients than in normal subjects (2.1 +/- 1.7 vs. 1.6 +/- 0.5 ng/ml, mean +/- SD, p less than 0.05), and sigma GH and integral of GH were also higher in diabetic patients. There was a significantly positive correlation between fasting plasma glucose(FPG) and basal level of GH (r = 0.24, n = 107, p less than 0.05), and the indices of GH responses except delta GH and GH peak value (r = 0.24 to 0.31, p less than 0.05 to 0.01). Some indices of GH responses (sigma delta GH, sigma GH, integral of delta GH and integral of GH) were significantly higher in the poor control group (patients with FPG above 180 mg/dl, n = 29) of diabetic patients than in the good control group (patients with FPG below 140 mg/dl, n = 59), or in the group with no abnormal findings of retinopathy (n = 46). During the follow-up of retinopathy for 2.5 years on the average, progression of retinopathy was found in 21 out of 107 patients. Significantly higher GH, and GH in the patients with increasing severity of retinopathy were revealed retrospectively compared to the patients without it. However, there were no significant differences in these parameters between both groups matched by FPG or severity of retinopathy. Multiple regression analysis to the basal GH level and GH responses during arginine infusion as criterion variables of various predictor variables (total 44 factors: biochemical laboratory data, indices of glucose and insulin response to oral glucose load, indices of glucose response to arginine, age, age of the onset, obese index, duration of retinopathy, neuropathy, and therapy) were performed in 86 patients using forward and backward method for variable selection. Basal plasma level of GH showed close positive association with therapy and proteinuria and negative association with age and obesity. Five of 6 indices of GH responsiveness showed significant relationship with retinopathy.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Growth hormone response to arginine administration in diabetics--with special reference to the multiple regression analysis in association with diabetic retinopathy]. 279 59

The prevalence of limited joint mobility (LJM) was studied in 110 insulin-dependent (IDDM) and 190 non-insulin-dependent (NIDDM) consecutive Ethiopian African diabetics and 300 age- and sex-matched controls at the Tikur Anbassa Teaching Hospital in Addis Ababa over a period of 18 months. Mean ages +/- S.D. of the IDDM, NIDDM, and controls were 35 +/- 9.9, 49.4 +/- 12.0, and 43.3 +/- 14.0 years, respectively. LJM was found in 44.5% of IDDM, 25.3% of NIDDM, and 6.7% of controls, being significantly commoner in IDDM than NIDDM (p less than 0.001) and in the diabetics than in controls (p less than 0.001). In IDDM those with LJM were significantly younger (p less than 0.05), had a higher prevalence of median fasting blood glucose (FBG) levels of 15 mmol/l and above (p less than 0.01), and retinopathy (p less than 0.05), but did not differ from those without LJM in duration of diabetes, or prevalence of neuropathy and nephropathy. In NIDDM those with LJM had a significantly longer duration of diabetes (p less than 0.005) and a higher prevalence of nephropathy (p less than 0.005), but did not differ from those without LJM in age at onset of diabetes, prevalence of neuropathy, and retinopathy or median FBG level.
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PMID:Limited finger joint mobility in insulin-dependent and non-insulin-dependent Ethiopian diabetics. 295 Oct 96

Short- (3-4 week) and long-term (1-4 yrs) results of the use of intensive insulin therapy schemes were used in 37 patients with severe forms of type I diabetes mellitus. Its beneficial effect on metabolism, remaining secretory beta-cell function, the frequency and expression of hypoglycemic reactions, manifestations of peripheral and visceral neuropathy, diabetic encephalopathy was proved.
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PMID:[Short- and long-term results of intensive insulin therapy in patients with severe forms of diabetes mellitus type I]. 306 38

Of 208 young women with insulin dependent diabetes, 15 (7%) had a clinically apparent eating disorder (anorexia nervosa or bulimia), a much higher prevalence than reported in non-diabetic women. Most, but not all, of these patients had a long history of poor glycaemic control. In contrast with previous suggestions, control did not deteriorate after the onset of the eating disorder. There was a high incidence and an early onset of diabetic complications. Eleven of the 15 patients had retinopathy, six with proliferative changes; six had nephropathy; and six neuropathy. Most strikingly, four patients with anorexia nervosa developed acute painful polyneuropathy. In each case pain started when the eating disorder developed, almost coinciding with the peak of weight reduction. Remission of pain occurred as weight was regained. The symptoms were accompanied by abnormalities in peripheral nerve electrophysiology and autonomic nerve function, some improvements in which accompanied weight recovery. It is suggested that nutritional factors may contribute to the high rate of early onset diabetic complications, particularly neuropathy.
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PMID:Clinically apparent eating disorders in young diabetic women: associations with painful neuropathy and other complications. 310 77

Diabetic microangiopathy may be associated with the pathogenesis and progression of autonomic and peripheral neuropathy. In 17 long-standing type I diabetic patients with peripheral and autonomic cardiovascular neuropathy, several hemorheological and hemostatic alterations were found compared to 13 matched type I patients without neuropathy. In particular, increased plasma von Willebrand factor antigen (p less than 0.001), fibronectin (p less than 0.001) and fibrinogen (p less than 0.001) levels were demonstrated in neuropathic in comparison with non-neuropathic diabetic patients. Moreover negative correlations between these parameters and both motor and sensitive conduction velocity of median, sural and peroneal nerves were observed in diabetic patients with neuropathy. Higher blood viscosity (p less than 0.05 at shear-rate of 450 and 225 s-1; p less than 0.01 at 90 s-1; p less than 0.001 at 4.5 and 2.25 s-1), plasma viscosity (p less than 0.001) and lower erythrocyte filtrability (p less than 0.001) were also found in neuropathic compared to non-neuropathic diabetics. Increased prevalence of retinopathy (p less than 0.01) and nephropathy (p less than 0.001) was finally reported in patients with autonomic and peripheral neuropathy. Microvascular disease may be involved in the development of neuropathy in long-term type I diabetes mellitus.
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PMID:Hemorheologic and hemostatic changes in long-standing insulin-dependent (type I) diabetic patients with peripheral and autonomic cardiovascular neuropathy. 323 50

A retrospective study was done on 109 diabetic patients who had renal biopsies during 1974-1984 to determine factors identifying nondiabetic renal disease in patients with diabetes mellitus presenting with renal dysfunction. Six of 49 (12%) patients with type I and 17 of 60 (28%) with type II diabetes mellitus had other renal diseases, with or without diabetic glomerulosclerosis. Multivariate predictors of other renal disease in type I diabetes mellitus were duration less than 5 years (p less than 0.001), absence of proteinuria (p less than 0.001), and absence of neuropathy (p less than 0.05). In type II diabetes mellitus these were late age of onset (p less than 0.001), absence of neuropathy (p less than 0.05), and Caucasian race (p less than 0.005). Some patients with other diseases appeared to respond to therapy directed at their nondiabetic glomerulosclerosis disease. We emphasize the need to distinguish between the subgroup of diabetic patients with nondiabetic renal disease from the majority who have diabetic glomerulosclerosis alone. The latter group should be spared the discomforts, risks, and costs of a renal biopsy.
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PMID:Clinical identification of nondiabetic renal disease in diabetic patients with type I and type II disease presenting with renal dysfunction. 323 94

Nine insulin-dependent diabetic (IDDM) patients (aged 25-37 yr) with no symptoms of autonomic neuropathy and 15 healthy control subjects (aged 26-39 yr) were studied at rest and during tests of Valsalva maneuver, deep breathing, cold pressor, and postural change from sitting to standing. Continuous (beat-to-beat) measures were taken of heart rate, systolic blood pressure, diastolic blood pressure, and skin conductance. The diabetic patients were differentiated from the control group by the following: less variability in diastolic blood pressure during deep breathing, failure to exhibit diastolic blood pressure decreases during recovery from a cold pressor stimulus, a flatter blood pressure response pattern when changing from sitting to standing, and a smaller standing ratio (maximum/minimum) for R-R interval. Among the patients, age was negatively correlated with systolic and diastolic standing ratios and diastolic blood pressure variability during deep breathing. By use of the tracking cuff, a method of continuously recording blood pressure noninvasively, we have been able to assess subtle blood pressure changes, thereby revealing signs of sympathetic dysfunction in a group of relatively young diabetic patients with no symptoms of neuropathy. The tracking-cuff method of recording blood pressure has potential in further research on autonomic functioning in diabetic patients.
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PMID:Beat-to-beat blood pressure response in asymptomatic IDDM subjects. 324 97

Early in the course of type 1 diabetes mellitus, hypertrophy of the kidney is a consistent finding that is easily diagnosed using current noninvasive methods, especially ultrasonography. Renal functional changes occur in association with hypertrophy, most notably glomerular hyperfiltration. The structural counterpart of this functional change is an early increase in capillary filtration surface area. In most forms of nondiabetic renal hypertrophy, kidney size is closely linked to GFR. In contrast, in diabetes, persistence of hypertrophy after the clinical onset of overt kidney disease (microalbuminuria, hypertension, decreased GFR, etc.) suggests that sustained release of one or more growth factors may continue even after kidney function declines. The fact that growth factors can act in both an autocrine and paracrine fashion raises the possibility that the local effects of such substances may act as local mediators of kidney growth. Failure of renal hypertrophy to reverse following strict glycemic control for a few months may turn out to be an important prognostic indicator of future progression of the renal disease, but this remains to be established. Prospective studies of kidney size in patients with newly diagnosed type 1 diabetes, using accurate noninvasive methods, may be helpful in establishing whether irreversible ("autonomous") hypertrophy of the kidney is indeed a useful prognostic indicator. As therapies are developed that target the different microvascular complications of diabetes (retinopathy, nephropathy, neuropathy), a noninvasive estimation of kidney size may be a cost-effective method of predicting ultimate renal involvement. Since microalbuminuria occurs relatively late in the disease process, early and persistent hypertrophy of the kidney may become a useful prognostic test in the earliest stages of the disease.
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PMID:Prognostic implications of renal hypertrophy in diabetes mellitus. 328 9

Extensive multiple neuropathies were observed in four patients after prolonged stay in intensive care units. Date of onset of the multiple disorders was difficult to determine due to disturbed consciousness of all patients during the first few weeks of intensive care: it was probably between the 10th and 30th days. Electrophysiological examinations in the 4 patients, and ultrastructural study of musculocutaneous nerve of leg in 2 cases, suggested an acute axonal lesion. All patients survived the causal affection which had justified prolonged intensive care, 3 recovering from the multiple neuropathy within 3 to 4 months, the last patient having marked neuromuscular sequelae. Several factors can be incriminated at the origin of this multiple neuropathy. Whereas retrospective studies allowed exclusion of a toxic, infectious or drug-related cause, severe nutritional deficiencies existed; proteins in all cases and vitamins in one patient despite enteral re-nutrition judged as satisfactory. Additionally, a role for a previous lesion of peripheral nerves from chronic hypoxia was possible in 2 cases as well as for a non-insulin dependent diabetes in one of these two patients. A rarely reported but probably not exceptional complication, diagnosis is assisted by early electrophysiologic exploration. Correction of nutritional disorders may require parenteral feeding exclusively, this possibly accelerating neurologic recovery, as proposed in the several rare studies reported in the literature.
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PMID:[Polyneuropathies during prolonged stays in resuscitation]. 332 11

Altered sorbitol and myo-inositol metabolism, (Na,K)-ATPase function, electrochemical sodium gradients, axonal swelling, and distortion and disruption of the node of Ranvier ("axo-glial dysjunction") directly implicate hyperglycemia in the pathogenesis of neuropathy in diabetic rats, but the relevance of this sequence to clinical neuropathy in heterogeneous groups of diabetic patients remains to be established. Fascicular sural nerve morphometry in 11 patients with neuropathy complicating insulin-dependent diabetes revealed a pattern of interrelated structural changes strikingly similar to that of the diabetic rat when compared to age-matched controls. 17 older non-insulin-dependent diabetic patients with comparable duration and severity of hyperglycemia and severity of neuropathy, displayed similar nerve fiber loss, paranodal demyelination, paranodal remyelination and segmental demyelination compared to age-matched controls, but axo-glial dysjunction was replaced by Wallerian degeneration as the primary manifestation of fiber damage, and fiber loss occurred in a spatial pattern consistent with an ischemic component. The mechanistic model developed from the diabetic rat does indeed appear to apply to human diabetic neuropathy, but superimposed hormonal, metabolic, vascular, and/or age-related effects alter the morphologic expression of the neuropathy in non-insulin dependent diabetes.
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PMID:Histopathological heterogeneity of neuropathy in insulin-dependent and non-insulin-dependent diabetes, and demonstration of axo-glial dysjunction in human diabetic neuropathy. 333 24


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