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Query: UMLS:C0011849 (diabetes)
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A retrospective study on the role of pancreatic B-cell insulin secretory capacity in the development of proliferative diabetic retinopathy was performed in 160 diabetic patients with a duration of diabetes of more than 10 years (mean 19.5 +/- 7.9 years). Pancreatic B-cell insulin secretory capacity was assessed in terms of the quantity of C-peptide excreted into urine per day (24-h urinary C-peptide). When the patients were divided into three groups according to the quantity of 24-h urinary C-peptide (group I, C-peptide less than 30 micrograms, n = 49; group II, 30 micrograms less than or equal to C-peptide less than 80 micrograms, n = 76; and group III, C-peptide greater than or equal to 80 micrograms, n = 35), the prevalence of proliferative diabetic retinopathy was much higher in group I (26.5%) than in group II (5.3%) or group III (2.9%). The incidence of proliferative diabetic retinopathy during the follow-up period (mean 9.8 +/- 4.8 years) was also highest in group I (20.0%, 2.7%, and 2.9% in groups I, II, and III, respectively). Other factors which might affect the development of proliferative diabetic retinopathy, including duration of diabetes and past glycemic control, were comparable in these three groups. In contrast, a division of the patients according to glycemic control revealed a strong correlation between glycemic control and background diabetic retinopathy whereas no such correlation was apparent with proliferative diabetic retinopathy. These data are consistent with the view that low pancreatic B-cell insulin secretory capacity may be a risk factor for the development of proliferative diabetic retinopathy.
Diabetes Res Clin Pract 1989 Jan 03
PMID:High prevalence of proliferative retinopathy in diabetic patients with low pancreatic B-cell capacity. 264 41

Quantities of growth hormone (GH) excreted into the urine over 24 h were measured by the highly sensitive sandwich enzyme immunoassay in 63 non-insulin-dependent diabetes mellitus (NIDDM) subjects, 6 insulin-dependent diabetes mellitus (IDDM) subjects, and 17 age-matched nondiabetic control subjects. GH-provocative tests with intravenous infusion of arginine revealed that urinary GH levels are closely correlated with the integrated concentrations of serum GH (r = .931, n = 14, P less than .001). Furthermore, 24-h urinary GH in control and diabetic subjects was inversely related to body mass index (r = .359, n = 80, P less than .001). The mean 24-h urinary GH in NIDDM subjects was 11.1 +/- 1.9 ng/g creatinine (Cr), which was not significantly different from that in nondiabetic control subjects (9.2 +/- 2.7 ng/g Cr). By contrast, the individual values for IDDM subjects varied widely, and their mean values (42.5 +/- 20.8 ng/g Cr) were much greater than those in the control and NIDDM subjects (P less than .01). The degree of glycemic control does not seem to affect 24-h urinary GH in NIDDM. The mean 24-h urinary GH in 7 subjects with proliferative diabetic retinopathy was comparable to that in subjects without retinopathy or with background retinopathy. Thus, the measurement of 24-h urinary GH appears to provide reliable assessments of endogenous GH secretion under physiological conditions and will be a useful tool for obtaining further insight into the role of GH in diabetes.
Diabetes 1989 Dec
PMID:Evaluation and clinical applications of measurement of urinary growth hormone in diabetic subjects. 268 12

The relationship between the macular recovery recorded by nyctometry and the retinal findings was examined in 60 initially pre-pubescent children with insulin-dependent diabetes mellitus during a 6-year period with special reference to the clinical applicability of nyctometry in selecting children and adolescents at risk of developing proliferative diabetic retinopathy. At the end of the study period the mean age of the patients was 21.9 years (range 18-23 years) and the mean diabetes duration 13.2 years (range 8.1-21.2 years). At the initial recording of macular recovery, only 7% of the children showed retinopathy, and this only in the form of a few microaneurysms or dot haemorrhages. During the study period, however, nearly all (93%) developed retinopathy, and in 9 (14%) the disease progressed into proliferative retinopathy. The initially recorded macular recovery time (MRI) of those children developing proliferative retinopathy was significantly lower (616 +/- 95; X +/- SEM) compared to the initial MRT performances (900 +/- 47) of the rest of the children. However, due to a high coefficient of variation in the material; predictive sensitivity showed low (56%) at a specificity level of 90%, suggesting that nyctometry is less suitable for selecting risk patients in children than in adults.
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PMID:Macular recovery during onset and development of diabetic retinopathy in childhood and adolescence. 280 Oct 42

Localization of the site of blood-retinal barrier breakdown in diabetes has been controversial. It has been particularly difficult to make assessments in clinical material where the use of tracer materials may not be practical. In this study, immunohistochemical staining for albumin was performed on paraffin-embedded eyes from patients with no known ocular disease and those with various stages of diabetic retinopathy. No extravascular albumin was detected in the retina or retinal pigment epithelium (RPE) of normal nondiabetics or diabetics with no ocular findings, but it was detected in 12.5% of mildly affected diabetics, 20% of background diabetic retinopathy cases, and 89% of proliferative diabetic retinopathy cases. The inner retinal vasculature appeared to be the primary site of leakage in diabetics because all cases demonstrating extravascular albumin-positivity expressed it in the inner retina. It usually permeated the vessel walls and spread along the inner surface of the retina. Some of these cases also contained albumin in the outer retina and RPE, suggesting that additional leakage also may occur through the RPE. A case of cytomegalovirus (CMV) retinitis showed albumin staining predominantly in the inner retina, whereas a rhegmatogenous retinal detachment showed only outer retina staining. These data suggest immunohistochemical staining for albumin may be a useful technique for localizing blood-retinal barrier breakdown.
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PMID:Immunohistochemical localization of blood-retinal barrier breakdown in human diabetics. 291 45

Population-based epidemiologic data on the incidence and progression of diabetic retinopathy are important in medical counseling and rehabilitative services and for developing approaches to preventing diabetic retinopathy. We performed a population-based study in southern Wisconsin of insulin-taking diabetic persons diagnosed before 30 years of age. Of the 271 who had no retinopathy at the first visit, 160 (59%) developed it by the time they were reexamined four years later, and 75 (11%) of the 713 free of proliferative diabetic retinopathy developed it. Overall, worsening of retinopathy occurred in 41% of the population, whereas improvement occurred in only 7%. The incidence of proliferative retinopathy rose with increasing duration until 13 to 14 years of diabetes, thereafter remaining between 14% and 17%. These incidence data underscore the need for careful ophthalmologic follow-up of these people.
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PMID:The Wisconsin Epidemiologic Study of Diabetic Retinopathy. IX. Four-year incidence and progression of diabetic retinopathy when age at diagnosis is less than 30 years. 291 77

The incidence of proliferative diabetic retinopathy was determined in the Pima Indians of the Gila River Indian Community in Arizona. Over 4 yr, this complication developed in 25 of 953 subjects greater than or equal to 9 yr of age with non-insulin-dependent diabetes. No cases were diagnosed in less than 35-yr-old subjects, and the incidence was strongly related to the duration of diabetes. The cumulative incidence of proliferative retinopathy after 20 yr duration was 14%. All cases of proliferative retinopathy occurred in subjects with background retinopathy. Younger age at diagnosis of diabetes was associated with a higher incidence of proliferation when subjects with diabetes of similar duration were compared. A higher incidence of proliferative retinopathy, after controlling for age, sex, and diabetes duration, was associated with hypertension, proteinuria, renal insufficiency, absence of Achilles tendon reflex, elevated total serum cholesterol concentration, and insulin therapy.
Diabetes 1989 Apr
PMID:Proliferative retinopathy in NIDDM. Incidence and risk factors in Pima Indians. 292 7

A 5-year study on the predictive value of the macular recovery time, as recorded by nyctometry, in the development of proliferative diabetic retinopathy in insulin-dependent diabetes mellitus has been completed. Seventy-seven patients with a median age of 30,8 years and a median duration of the disease of 15,8 years participated. In the follow-up period, 16 out of 20 patients initially showing abnormally prolonged macular recovery time had developed proliferative diabetic retinopathy the median duration from the initial investigation to the diagnosis of retinal neovascularization being 34 months. Contrary to this finding, only 4 out of 57 patients initially showing normal macular recovery had advanced into proliferative retinopathy, and the median duration until diagnosis of this condition was 45 months. It is concluded that nyctometry can serve as an easily performed screening method in selecting those at risk of developing proliferative retinopathy within a few years.
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PMID:Macular recovery time recorded by nyctometry--a screening method for selection of patients who are at risk of developing proliferative diabetic retinopathy. Results of a 5-year follow-up. 300 99

Pancreatic B-cell function in relation to diabetic retinopathy was studied in 195 NIDDM patients with long-standing diabetes. Background diabetic retinopathy (BDR) was present in 95 (48.7%) and proliferative retinopathy (PDR) in 17 (8.7%) of the subjects. There was no significant difference between the BDR, PDR, and non-retinopathy groups with respect to age, age at diagnosis of diabetes and HbA1 values. Mean duration of diabetes was higher in the PDR group (p less than 0.05). Serum C-peptide values showed no correlation with the presence of retinopathy or with the duration of diabetes. The C-peptide values were widely scattered in patients with BDR and PDR showing no association between pancreatic B-cell reserve and occurrence or severity of retinopathy in NIDDM patients. Thus, decreased pancreatic B-cell reserve does not appear to be a risk factor for diabetic retinopathy in NIDDM patients.
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PMID:Pancreatic B-cell function in relation to diabetic retinopathy in Asian Indian NIDDM patients. 306 87

Plasma prorenin, but not renin, is elevated in long-standing diabetes mellitus. Nephropathy and autonomic neuropathy have been implicated as causes. However, we found no arteriovenous difference in prorenin across the kidney, despite high levels of circulating prorenin and a very low renal plasma flow, in five diabetics with combined end-stage nephropathy and proliferative diabetic retinopathy. Moreover, plasma prorenin was normal in 16 non-diabetics with autonomic neuropathy. The presence of a high level of prorenin was closely associated with the presence of diabetic retinopathy, particularly the proliferative type, in 223 consecutive patients. This association was independent of insulin requirements, metabolic control and of the presence of nephropathy or neuropathy. These data are evidence that part of the elevated plasma prorenin in diabetics is produced by an extrarenal source and that perhaps the eye affected by diabetic retinopathy is that source.
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PMID:Association of high plasma prorenin with diabetic retinopathy. 307 86

Several studies report increased growth hormone (GH) responses to provocative stimuli in patients with diabetic retinopathy. We studied GH responses to 1 microgram/kg body wt human pancreatic GH-releasing hormone 1-44 (hpGHRH 1-44) in 33 patients with type I diabetes mellitus, 31 patients with type II diabetes mellitus, and 2 control groups (N = 11 and 8). Based on the results of fundoscopy and fluorescein angiography, the diabetic patients were subdivided into patients without diabetic retinopathy, patients with nonproliferative diabetic retinopathy, and patients with proliferative diabetic retinopathy. Growth hormone responses to hpGHRH 1-44 in diabetic patients with proliferative or nonproliferative retinopathy or without retinopathy were not significantly different regardless of the type of diabetes. Remarkably, GH responses to hpGHRH 1-44 in type I diabetic patients without retinopathy were significantly higher than the matched controls. Our data suggest that diabetic retinopathy in type I and in type II diabetes is not associated with increased GH responsiveness to hpGHRH 1-44, whereas in type I diabetes mellitus without diabetic retinopathy, a GH hyperresponsiveness to hpGHRH seems to occur.
Diabetes 1987 Feb
PMID:No evidence for increased growth hormone responses to growth hormone-releasing hormone in patients with diabetic retinopathy. 310 Mar 67


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