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E Miki

Publications and source records attributed to E Miki.

At least 19 recordsLinked to original sources
PubMed2001

The appearance of retinopathy and progression to proliferative retinopathy: the WHO Multinational Study of Vascular Disease in Diabetes.

AIMS/HYPOTHESIS: We aimed to estimate incidences of any retinopathy and proliferative diabetic retinopathy (PDR) by direct ophthalmoscopy and relate them to baseline risk factors in re-examined diabetic survivors from 10 centres of the WHO Multinational Study of Vascular Disease in Diabetes. METHODS: After a mean follow-up of 8.4years (11.7 years in Oklahoma), 2877 (71.6%) survivors were resubmitted to standardised direct ophthalmoscopy as at baseline. The presence of any retinopathy and PDR were recorded at each centre and their incidence estimated in those without retinopathy and PDR at baseline. The independent associations of these incidences with baseline risk factors are expressed as odds ratios derived from multiple logistic regression analyses, within individual centres (which included fasting plasma glucose in 8 and triglyceride in 5) and in pooled data. RESULTS: Of the 4662 original patients, 465 (10.4%) of those without and 77 (43.0%) of those with baseline PDR had died (p < 0.001). Any retinopathy was newly reported at follow-up in 47.7 % and PDR in 9.7 % of those free of them at baseline, with reported incidences varying substantially among centres. Incident retinopathy appeared earlier in the known course of diabetes but incidence rates rose more slowly with duration in patients with Type II (non-insulin-dependent) diabetes mellitus than in those with Type I (insulin-dependent) diabetes mellitus. In pooled data and in some individual centres, any retinopathy incidence gave significantly positive odds ratios with age, diabetes duration, systolic pressure, plasma cholesterol, BMI, insulin treatment and proteinuria, and with fasting plasma glucose in the centres where it was measured. Positive odds ratios for PDR were similarly obtained for age, duration, insulin treatment, cholesterol, proteinuria and fasting glycaemia. Smoking status odds ratios were negative for both outcomes. CONCLUSION/INTERPRETATION: Incidence of ophthalmoscopically ascertained any retinopathy varied about twofold and of PDR about threefold among centres. Although, in part attributable to differences between observers, variation in incidence in all centres and in some cases within centres was associated with a number of baseline risk factors. Such associations are not likely due to observer variation or selection biases and emerged despite the imprecision of clinical ophthalmoscopy. Improved detection and control of these risk factors should reduce the impact of diabetic retinopathy and its consequences.

Age Factors↗
PubMed2001

The incidence of visual impairment and its determinants in the WHO Multinational Study of Vascular Disease in Diabetes.

AIMS/HYPOTHESIS: Incidence of severe visual impairment and the ultimate prevalence of all grades of impairment were estimated in the 10 centres of the WHO Multinational Study of Vascular Disease in Diabetes (WHO MSVDD) participating in the follow-up. METHODS: Visual function was ascertained at follow-up in 2994 (77.9 %) of the 3845 eligible participating survivors of the 4709 originally recruited for the WHO MSVDD using the same baseline enquiry method. The associations between incident severe visual impairment, follow-up prevalence of all grades of impairment and baseline risk factors were examined by univariate and stepwise multiple logistic regression analysis. RESULTS: Overall, 8.4 year incidence of severe visual impairment was 1.94 % and showed statistically significant univariate correlations with age at diagnosis, diabetes duration, systolic blood pressure, fasting blood glucose and cholesterol, insulin treatment and strongly with baseline retinopathy. Baseline retinopathy, systolic pressure and cholesterol were statistically significant in multivariable analysis. Differences between centres (0.3% to 3.45%) were not significant. Ultimate prevalence of all grades of impairment differed between centres and within almost all of them was correlated in multivariable analysis with baseline retinopathy and proteinuria. CONCLUSION/INTERPRETATION: Comparisons of incident severe visual impairment between centres are restricted by selective mortality, low incidence rates and relatively small numbers in each centre but before retinopathy, baseline systolic pressure and cholesterol predicted severe visual impairment. Follow-up prevalence of all degrees of impairment varied among centres and were associated with prior retinopathy and renal disease at baseline.

Adult↗
PubMed1994

Diabetic retinopathy and control of diabetes with special reference to blood glucose levels.

Data concerning diabetic retinopathy were collected prospectively in the Diabetes Clinic of the Third Department of Internal Medicine, University of Tokyo, from the beginning of the Clinic in 1957 until 1985. These data are analyzed here. The prevalence and severity of the retinopathy at the initial visit was strongly related to the duration of diabetes before examination. Pretreatment fasting blood glucose levels were also significantly related. During follow-up, the incidence of retinopathy was most strongly influenced by the degree of control of blood glucose, followed by other factors like blood pressure, age at diagnosis, etc. The effectiveness of sulfonylurea on retinopathy was not inferior to insulin so long as good control was obtained. It was deduced from the analysis of the chain of events that dot hemorrhage is the initial component of diabetic retinopathy, followed by hard exudate, blot hemorrhage, soft exudate and proliferative retinopathy. A six-year fluorescein angiography follow-up of well-controlled non-insulin dependent cases with mild retinopathy showed that microaneurysms disappear rapidly during the first year and more slowly thereafter. The avascular areas once formed seem to progress despite the degree of control exerted here. The other Japanese results are discussed.

Blood Glucose↗
PubMed1982

Interrelationships of microangiopathy, plasma glucose and other risk factors in 3583 diabetic patients: a multinational study.

In a multinational study, fasting plasma glucose values in 3583 diabetic patients, aged 34-56 years, were related to the characteristics of these subjects and to the presence and severity of microangiopathy as ascertained by standardised methods. The patients were from nine different populations and ranged in number from 193 to 686 per population (London, Warsaw, Berlin (FRG), New Delhi, Tokyo, Havana, Oklahoma Indians, Arizona Pima Indians, and a national sample in Switzerland). In the total group, mean fasting plasma glucose was 8.1 mmol/l for those on diet alone, 9.7 mmol/l for those on oral agents, and 12.7 mmol/l for insulin-treated patients, of whom 25% had values exceeding 16.5 mmol/l. Since many variables were measured in each patient, it was possible to take into account many confounding factors in evaluating the relationship of plasma glucose levels to retinopathy and nephropathy.

Adult↗
PubMed1977

Insulin secretion in hypoglycemia after adrenal vein ligature or splachnicotomy.

During bonito insulin-induced hypoglycemia in dogs, pancreatic venous dog insulin concentration (IRI), radioimmunoassayed differentially from bonito insulin, was progressively diminished in response to local glucose infusion (0.6 mg/kg - min) for 4 min into the superior pancreaticoduodenal artery. Basal arterial plasma glucose was significantly lower after bilateral splanchnicotomy (BSNC) than after bilateral adrenal vein ligature (BAVL). During local glucose infusion in both normoglycemia and hypoglycemia, the increment of pancreatic venous IRI was significantly greater after BAVL or BSNC than in the controls, and the increment of pancreatic venous glucose was also significantly greater after BAVL than in the controls or after BSNC. It is suggested that under the stress of major surgery the splanchnic nerves partially suppress insulin secretion in normoglycemia as well as in hypoglycemia, and epinephrine released from the adrenal medulla may interfere with glucose-mediated insulin secretion in profound hypoglycemia.

Adrenal Glands↗
PubMed1975

Demonstration of anti-"a-component" antibody--a possible means to differentiate patients with auto-antibodies to endogenous insulin from insulin-treated patients.

The presence of anti-"a-component" antibody was examined in sera of 4 groups of patients with or without anti-insulin antibody, using 125I-a-component and the polyethylene glycol precipitation method. 125I-a-component crossreacted with insulin antibody. This cross-reactivity was abolished after preincubation of these sera with monocomponent insulin. The specificanti-"a-component" antibody could be estimated in this procedure. After preincubation with monocomponent insulin, significant binding of 125I-a-component was demonstrated in sera of most patients treated with ordinary commercial insulin, but not in sera of 2 hypoglycemic patients suspected of an insulin autoimmune syndrome. Some cases treated with commercial insulin for less than one year and all cases treated with monocomponent insulin for 7-10 months did not have significant anti-"a-component" antibody. The test for the presence of anti-"a-component" antibody is not definitive but if positive it differentiates "auto-antibodies" from the antibodies produced by injections of commercial insulin.

Animals↗
PubMed1975

Effect of beta and beta2 adrenoreceptor stimulants infused intrapancreatically on glucagon and insulin secretion.

L-Isoproterenol was infused at a dose of 20 pmol/kg/min for 10 min into the cranial pancreaticoduodenal artery in anesthetized dogs. Arterial plasma glucose, blood flow, and plasma concentrations of both glucagon and insulin in the cranial pancreaticoduodenal vein were significantly enhanced during the infusion, resulting in a greater increase of bihormonal output. Intrapancreatic pretreatment with propranolol abolished all of the isoproterenol-induced increases except for glucagon secretion which was suppressed only in part. Pretreatment with practolol, a specific receptor blocker of the beta1 type, did not exert any discernible inhibiting effect upon the isoproterenol-induced enhancement. Intrapancreatic infusion of trimetoquinol, a selective receptor stimulant of the beta2 type in some mammals, at an equimolar dose caused similar increases in plasma glucose, pancreatic venous blood flow, and bihormonal output when compared to those induced by isoproterenol. Pretreatment with a larger dose of propranolol totally abolished the trimetoquinol-induced enhancement of both glucagon and insulin secretion. Pretreatment with an isomolar dose of practolol, in contrast, did not show any suppressive effect on the parameters investigated. There was a dose-dependency in the bihormonal responses to trimetoquinol. Another beta2 receptor agonist, salbutamol, also significantly raised plasma glucose, pancreatic venous blood flothough to a lesser extent than did trimetoquinol. These results indicate that the adrenergic control over the function of the endocrine pancreas through beta adrenoreceptors may be mediated mainly via those of the beta2 type.

Adrenergic beta-Agonists↗
PubMed1972

[Diabetes].

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Animals↗